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Venetoclax-Obinutuzumab: CLL’s New Power Duo?
TOPLINE:
METHODOLOGY:
- A total of 432 patients with previously untreated CLL and coexisting conditions were enrolled in the study.
- Participants were randomized 1:1 to receive either 12 cycles of venetoclax with 6 cycles of obinutuzumab or 12 cycles of chlorambucil with 6 cycles of obinutuzumab.
- The primary endpoint was PFS, with secondary endpoints including TTNT, overall survival (OS), and adverse events.
- Minimal residual disease was assessed in peripheral blood and bone marrow at the end of treatment and at several follow-up points.
- The study was conducted across multiple centers and was registered with clinical trial identifiers NCT02242942 and EudraCT 2014-001810-24.
TAKEAWAY:
- The 6-year PFS rate was significantly higher in the venetoclax-obinutuzumab group (53%) than in the chlorambucil-obinutuzumab group (21.7%) (P < .0001).
- The TTNT rate was 65.2% in the venetoclax-obinutuzumab group vs 37.1% in the chlorambucil-obinutuzumab group (P < .0001).
- The OS rate at 6 years was 78.7% in the venetoclax-obinutuzumab group and 69.2% in the chlorambucil-obinutuzumab group (P = .052).
- Patients in the venetoclax-obinutuzumab group reported better quality of life and less fatigue than those in the chlorambucil-obinutuzumab group.
IN PRACTICE:
“Patients treated with the venetoclax-obinutuzumab combination showed a statistically significant sustained prolongation of PFS, compared with patients treated with chlorambucil-obinutuzumab (76.2 vs 36.4 months). Overall, the PFS rate was 53% in the venetoclax-obinutuzumab group vs 21.7% after chlorambucil-obinutuzumab,” the study’s authors wrote.
In a related article, Silvia Deaglio, University of Turin in Italy, noted: “A second important observation of the study is that in the venetoclax-obinutuzumab arm, patients who relapsed more frequently presented with unmutated IGHV genes, deletion of 17p, or TP53 mutations.”
SOURCE:
This study was led by Othman Al-Sawaf, Sandra Robrecht, and Can Zhang, University of Cologne in Germany. It was published online on October 31 in Blood.
LIMITATIONS:
This study’s limitations included the relatively small sample size and the short duration of follow-up for some endpoints. Additionally, the study population was limited to older adult patients with coexisting conditions, which may limit the generalizability of the findings to a broader CLL population.
DISCLOSURES:
This study was supported by F. Hoffmann-La Roche and AbbVie. Al-Sawaf disclosed receiving grants from BeiGene, AbbVie, Janssen, and Roche. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- A total of 432 patients with previously untreated CLL and coexisting conditions were enrolled in the study.
- Participants were randomized 1:1 to receive either 12 cycles of venetoclax with 6 cycles of obinutuzumab or 12 cycles of chlorambucil with 6 cycles of obinutuzumab.
- The primary endpoint was PFS, with secondary endpoints including TTNT, overall survival (OS), and adverse events.
- Minimal residual disease was assessed in peripheral blood and bone marrow at the end of treatment and at several follow-up points.
- The study was conducted across multiple centers and was registered with clinical trial identifiers NCT02242942 and EudraCT 2014-001810-24.
TAKEAWAY:
- The 6-year PFS rate was significantly higher in the venetoclax-obinutuzumab group (53%) than in the chlorambucil-obinutuzumab group (21.7%) (P < .0001).
- The TTNT rate was 65.2% in the venetoclax-obinutuzumab group vs 37.1% in the chlorambucil-obinutuzumab group (P < .0001).
- The OS rate at 6 years was 78.7% in the venetoclax-obinutuzumab group and 69.2% in the chlorambucil-obinutuzumab group (P = .052).
- Patients in the venetoclax-obinutuzumab group reported better quality of life and less fatigue than those in the chlorambucil-obinutuzumab group.
IN PRACTICE:
“Patients treated with the venetoclax-obinutuzumab combination showed a statistically significant sustained prolongation of PFS, compared with patients treated with chlorambucil-obinutuzumab (76.2 vs 36.4 months). Overall, the PFS rate was 53% in the venetoclax-obinutuzumab group vs 21.7% after chlorambucil-obinutuzumab,” the study’s authors wrote.
In a related article, Silvia Deaglio, University of Turin in Italy, noted: “A second important observation of the study is that in the venetoclax-obinutuzumab arm, patients who relapsed more frequently presented with unmutated IGHV genes, deletion of 17p, or TP53 mutations.”
SOURCE:
This study was led by Othman Al-Sawaf, Sandra Robrecht, and Can Zhang, University of Cologne in Germany. It was published online on October 31 in Blood.
LIMITATIONS:
This study’s limitations included the relatively small sample size and the short duration of follow-up for some endpoints. Additionally, the study population was limited to older adult patients with coexisting conditions, which may limit the generalizability of the findings to a broader CLL population.
DISCLOSURES:
This study was supported by F. Hoffmann-La Roche and AbbVie. Al-Sawaf disclosed receiving grants from BeiGene, AbbVie, Janssen, and Roche. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- A total of 432 patients with previously untreated CLL and coexisting conditions were enrolled in the study.
- Participants were randomized 1:1 to receive either 12 cycles of venetoclax with 6 cycles of obinutuzumab or 12 cycles of chlorambucil with 6 cycles of obinutuzumab.
- The primary endpoint was PFS, with secondary endpoints including TTNT, overall survival (OS), and adverse events.
- Minimal residual disease was assessed in peripheral blood and bone marrow at the end of treatment and at several follow-up points.
- The study was conducted across multiple centers and was registered with clinical trial identifiers NCT02242942 and EudraCT 2014-001810-24.
TAKEAWAY:
- The 6-year PFS rate was significantly higher in the venetoclax-obinutuzumab group (53%) than in the chlorambucil-obinutuzumab group (21.7%) (P < .0001).
- The TTNT rate was 65.2% in the venetoclax-obinutuzumab group vs 37.1% in the chlorambucil-obinutuzumab group (P < .0001).
- The OS rate at 6 years was 78.7% in the venetoclax-obinutuzumab group and 69.2% in the chlorambucil-obinutuzumab group (P = .052).
- Patients in the venetoclax-obinutuzumab group reported better quality of life and less fatigue than those in the chlorambucil-obinutuzumab group.
IN PRACTICE:
“Patients treated with the venetoclax-obinutuzumab combination showed a statistically significant sustained prolongation of PFS, compared with patients treated with chlorambucil-obinutuzumab (76.2 vs 36.4 months). Overall, the PFS rate was 53% in the venetoclax-obinutuzumab group vs 21.7% after chlorambucil-obinutuzumab,” the study’s authors wrote.
In a related article, Silvia Deaglio, University of Turin in Italy, noted: “A second important observation of the study is that in the venetoclax-obinutuzumab arm, patients who relapsed more frequently presented with unmutated IGHV genes, deletion of 17p, or TP53 mutations.”
SOURCE:
This study was led by Othman Al-Sawaf, Sandra Robrecht, and Can Zhang, University of Cologne in Germany. It was published online on October 31 in Blood.
LIMITATIONS:
This study’s limitations included the relatively small sample size and the short duration of follow-up for some endpoints. Additionally, the study population was limited to older adult patients with coexisting conditions, which may limit the generalizability of the findings to a broader CLL population.
DISCLOSURES:
This study was supported by F. Hoffmann-La Roche and AbbVie. Al-Sawaf disclosed receiving grants from BeiGene, AbbVie, Janssen, and Roche. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Popular Weight Loss Drugs Now for Patients With Cancer?
Demand for new weight loss drugs has surged over the past few years.
Led by the antiobesity drugs semaglutide (Wegovy) and tirzepatide (Zepbound), these popular medications — more commonly known as glucagon-like peptide 1 (GLP-1) agonists — have become game changers for shedding excess pounds.
Aside from obesity indications, both drugs have been approved to treat type 2 diabetes under different brand names and have a growing list of other potential benefits, such as reducing inflammation and depression.
While there’s limited data to support the use of GLP-1 agonists for weight loss in cancer, some oncologists have begun carefully integrating the antiobesity agents into care and studying their effects in this patient population.
The reason: Research suggests that obesity can reduce the effectiveness of cancer therapies, especially in patients with breast cancer, and can increase the risk for treatment-related side effects.
The idea is that managing patients’ weight will improve their cancer outcomes, explained Lajos Pusztai, MD, PhD, a breast cancer specialist and professor of medicine at Yale School of Medicine in New Haven, Connecticut.
Although Dr. Pusztai and his oncology peers at Yale don’t yet use GPL-1 agonists, Neil Iyengar, MD, and colleagues have begun doing so to help some patients with breast cancer manage their weight. Dr. Iyengar estimates that a few hundred — almost 40% — of his patients are on the antiobesity drugs.
“For a patient who has really tried to reduce their weight and who is in the obese range, that’s where I think the use of these medications can be considered,” said Dr. Iyengar, a breast cancer oncologist at Memorial Sloan Kettering Cancer Center in New York City.
Why GLP-1s in Cancer?
GLP-1 is a hormone that the small intestine releases after eating. GLP-1 agonists work by mimicking GLP-1 to trigger the release of insulin and reduce the production of glucagon — two processes that help regulate blood sugar.
These agents, such as Wegovy (or Ozempic when prescribed for diabetes), also slow gastric emptying and can make people feel fuller longer.
Zebound (or Mounjaro for type 2 diabetes) is considered a dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, which may enhance its weight loss benefits.
In practice, however, these drugs can increase nausea and vomiting from chemotherapy, so Dr. Iyengar typically has patients use them afterwards, during maintenance treatment.
Oncologists don’t prescribe the drugs themselves but instead refer patients to endocrinologists or weight management centers that then write the prescriptions. Taking these drugs involves weekly subcutaneous injections patients can administer themselves.
Endocrinologist Emily Gallagher, MD, PhD, of Mount Sinai Hospital in New York City, estimates she has prescribed the antiobesity drugs to a few hundred patients with cancer and, like Dr. Iyengar, uses the drugs during maintenance treatment with hormone therapy for breast cancer. She also has used these agents in patients with prostate and endometrial cancers and has found the drugs can help counter steroid weight gain in multiple myeloma.
But, to date, the evidence for using GPL-1 agonists in cancer remains limited and the practice has not yet become widespread.
Research largely comes down to a few small retrospective studies in patients with breast cancer receiving aromatase inhibitors. Although no safety issues have emerged so far, these initial reports suggest that the drugs lead to significantly less weight loss in patients with cancer compared to the general population.
Dr. Iyengar led one recent study, presented at the 2024 annual meeting of the American Society of Clinical Oncology, in which he and his team assessed outcomes in 75 women with breast cancer who received a GLP-1 agonist. Almost 80% of patients had diabetes, and 60% received hormone therapy, most commonly an aromatase inhibitor. Patients’ median body mass index (BMI) at baseline was 34 kg/m2 (range, 23-50 kg/m2).
From baseline, patients lost 6.2 kg, on average, or about 5% of their total body weight, 12 months after initiating GLP-1 therapy.
In contrast, phase 3 trials show much higher mean weight loss — about two times — in patients without cancer.
Another recent study also reported modest weight loss results in patients with breast cancer undergoing endocrine therapy. The researchers reported that, at 12 months, Wegovy led to 4.34% reduction in BMI, compared with a 14% change reported in the general population. Zebound, however, was associated with a 2.31% BMI increase overall — though some patients did experience a decrease — compared with a 15% reduction in the general population.
“These findings indicate a substantially reduced weight loss efficacy in breast cancer patients on endocrine therapy compared to the general population,” the authors concluded.
It’s unclear why the drugs appear to not work as well in patients with cancer. It’s possible that hormone therapy or metabolic changes interfere with their effectiveness, given that some cancer therapies lead to weight gain. Steroids and hormone therapies, for instance, often increase appetite, and some treatments can slow patients’ metabolism or lead to fatigue, which can make it harder to exercise.
Patients with cancer may need a higher dose of GLP-1 agonists to achieve similar weight loss to the general population, Dr. Iyengar noted.
However, Dr. Gallagher said, in her own experience, she hasn’t found the drugs to be less effective in patients with cancer, especially the newer agents, like Wegovy and Zepbound.
As for safety, Wegovy and Zepbound both carry a black box warning for thyroid C-cell tumors, including medullary thyroid carcinoma. (Recent research, however, has found that GLP-1 agonists do not increase thyroid cancer risk).
These antiobesity agents are also contraindicated in patients with a personal or family history of medullary thyroid carcinoma and in patients who have multiple endocrine neoplasia syndrome type 2, which is associated with medullary thyroid carcinoma.
Dr. Gallagher hasn’t seen any secondary tumors — thyroid or otherwise — in her patients with cancer, but she follows the labeling contraindications. Dr. Iyengar also noted that more recent and larger data sets have shown no impact on this risk, which may not actually exist, he said
Dr. Gallagher remains cautious about using GPL-1 agonists in patients who have had bariatric surgery because these agents can compound the slower gastric emptying and intestinal transit from surgery, potentially leading to gastrointestinal obstructions.
Looking ahead, GPL-1 manufacturers are interested in adding cancer indications to the drug labeling. Both Dr. Iyengar and Dr. Gallagher said their institutions are in talks with companies to participate in large, multicenter, global phase 3 trials.
Dr. Iyengar welcomes the efforts, not only to test the effectiveness of GPL-1 agonists in oncology but also to “nail down” their safety in cancer.
“I don’t think that there’s mechanistically anything that’s particularly worrisome,” and current observations suggest that these drugs are likely to be safe, Dr. Iyengar said. Even so, “GLP-1 agonists do a lot of things that we don’t fully understand yet.”
The bigger challenge, Dr. Iyengar noted, is that companies will have to show a sizable benefit to using these drugs in patients with cancer to get the Food and Drug Administration’s approval. And to move the needle on cancer-specific outcomes, these antiobesity drugs will need to demonstrate significant, durable weight loss in patients with cancer.
But if these drugs can do that, “I think it’s going to be one of the biggest advances in medicine and oncology given the obesity and cancer epidemic,” Dr. Iyengar said.
Dr. Iyengar has adviser and/or researcher ties with companies that make or are developing GPL-1 agonists, including AstraZeneca, Novartis, Gilead, and Pfizer. Dr. Gallagher is a consultant for Novartis, Flare Therapeutics, Reactive Biosciences, and Seagen.
A version of this article first appeared on Medscape.com.
Demand for new weight loss drugs has surged over the past few years.
Led by the antiobesity drugs semaglutide (Wegovy) and tirzepatide (Zepbound), these popular medications — more commonly known as glucagon-like peptide 1 (GLP-1) agonists — have become game changers for shedding excess pounds.
Aside from obesity indications, both drugs have been approved to treat type 2 diabetes under different brand names and have a growing list of other potential benefits, such as reducing inflammation and depression.
While there’s limited data to support the use of GLP-1 agonists for weight loss in cancer, some oncologists have begun carefully integrating the antiobesity agents into care and studying their effects in this patient population.
The reason: Research suggests that obesity can reduce the effectiveness of cancer therapies, especially in patients with breast cancer, and can increase the risk for treatment-related side effects.
The idea is that managing patients’ weight will improve their cancer outcomes, explained Lajos Pusztai, MD, PhD, a breast cancer specialist and professor of medicine at Yale School of Medicine in New Haven, Connecticut.
Although Dr. Pusztai and his oncology peers at Yale don’t yet use GPL-1 agonists, Neil Iyengar, MD, and colleagues have begun doing so to help some patients with breast cancer manage their weight. Dr. Iyengar estimates that a few hundred — almost 40% — of his patients are on the antiobesity drugs.
“For a patient who has really tried to reduce their weight and who is in the obese range, that’s where I think the use of these medications can be considered,” said Dr. Iyengar, a breast cancer oncologist at Memorial Sloan Kettering Cancer Center in New York City.
Why GLP-1s in Cancer?
GLP-1 is a hormone that the small intestine releases after eating. GLP-1 agonists work by mimicking GLP-1 to trigger the release of insulin and reduce the production of glucagon — two processes that help regulate blood sugar.
These agents, such as Wegovy (or Ozempic when prescribed for diabetes), also slow gastric emptying and can make people feel fuller longer.
Zebound (or Mounjaro for type 2 diabetes) is considered a dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, which may enhance its weight loss benefits.
In practice, however, these drugs can increase nausea and vomiting from chemotherapy, so Dr. Iyengar typically has patients use them afterwards, during maintenance treatment.
Oncologists don’t prescribe the drugs themselves but instead refer patients to endocrinologists or weight management centers that then write the prescriptions. Taking these drugs involves weekly subcutaneous injections patients can administer themselves.
Endocrinologist Emily Gallagher, MD, PhD, of Mount Sinai Hospital in New York City, estimates she has prescribed the antiobesity drugs to a few hundred patients with cancer and, like Dr. Iyengar, uses the drugs during maintenance treatment with hormone therapy for breast cancer. She also has used these agents in patients with prostate and endometrial cancers and has found the drugs can help counter steroid weight gain in multiple myeloma.
But, to date, the evidence for using GPL-1 agonists in cancer remains limited and the practice has not yet become widespread.
Research largely comes down to a few small retrospective studies in patients with breast cancer receiving aromatase inhibitors. Although no safety issues have emerged so far, these initial reports suggest that the drugs lead to significantly less weight loss in patients with cancer compared to the general population.
Dr. Iyengar led one recent study, presented at the 2024 annual meeting of the American Society of Clinical Oncology, in which he and his team assessed outcomes in 75 women with breast cancer who received a GLP-1 agonist. Almost 80% of patients had diabetes, and 60% received hormone therapy, most commonly an aromatase inhibitor. Patients’ median body mass index (BMI) at baseline was 34 kg/m2 (range, 23-50 kg/m2).
From baseline, patients lost 6.2 kg, on average, or about 5% of their total body weight, 12 months after initiating GLP-1 therapy.
In contrast, phase 3 trials show much higher mean weight loss — about two times — in patients without cancer.
Another recent study also reported modest weight loss results in patients with breast cancer undergoing endocrine therapy. The researchers reported that, at 12 months, Wegovy led to 4.34% reduction in BMI, compared with a 14% change reported in the general population. Zebound, however, was associated with a 2.31% BMI increase overall — though some patients did experience a decrease — compared with a 15% reduction in the general population.
“These findings indicate a substantially reduced weight loss efficacy in breast cancer patients on endocrine therapy compared to the general population,” the authors concluded.
It’s unclear why the drugs appear to not work as well in patients with cancer. It’s possible that hormone therapy or metabolic changes interfere with their effectiveness, given that some cancer therapies lead to weight gain. Steroids and hormone therapies, for instance, often increase appetite, and some treatments can slow patients’ metabolism or lead to fatigue, which can make it harder to exercise.
Patients with cancer may need a higher dose of GLP-1 agonists to achieve similar weight loss to the general population, Dr. Iyengar noted.
However, Dr. Gallagher said, in her own experience, she hasn’t found the drugs to be less effective in patients with cancer, especially the newer agents, like Wegovy and Zepbound.
As for safety, Wegovy and Zepbound both carry a black box warning for thyroid C-cell tumors, including medullary thyroid carcinoma. (Recent research, however, has found that GLP-1 agonists do not increase thyroid cancer risk).
These antiobesity agents are also contraindicated in patients with a personal or family history of medullary thyroid carcinoma and in patients who have multiple endocrine neoplasia syndrome type 2, which is associated with medullary thyroid carcinoma.
Dr. Gallagher hasn’t seen any secondary tumors — thyroid or otherwise — in her patients with cancer, but she follows the labeling contraindications. Dr. Iyengar also noted that more recent and larger data sets have shown no impact on this risk, which may not actually exist, he said
Dr. Gallagher remains cautious about using GPL-1 agonists in patients who have had bariatric surgery because these agents can compound the slower gastric emptying and intestinal transit from surgery, potentially leading to gastrointestinal obstructions.
Looking ahead, GPL-1 manufacturers are interested in adding cancer indications to the drug labeling. Both Dr. Iyengar and Dr. Gallagher said their institutions are in talks with companies to participate in large, multicenter, global phase 3 trials.
Dr. Iyengar welcomes the efforts, not only to test the effectiveness of GPL-1 agonists in oncology but also to “nail down” their safety in cancer.
“I don’t think that there’s mechanistically anything that’s particularly worrisome,” and current observations suggest that these drugs are likely to be safe, Dr. Iyengar said. Even so, “GLP-1 agonists do a lot of things that we don’t fully understand yet.”
The bigger challenge, Dr. Iyengar noted, is that companies will have to show a sizable benefit to using these drugs in patients with cancer to get the Food and Drug Administration’s approval. And to move the needle on cancer-specific outcomes, these antiobesity drugs will need to demonstrate significant, durable weight loss in patients with cancer.
But if these drugs can do that, “I think it’s going to be one of the biggest advances in medicine and oncology given the obesity and cancer epidemic,” Dr. Iyengar said.
Dr. Iyengar has adviser and/or researcher ties with companies that make or are developing GPL-1 agonists, including AstraZeneca, Novartis, Gilead, and Pfizer. Dr. Gallagher is a consultant for Novartis, Flare Therapeutics, Reactive Biosciences, and Seagen.
A version of this article first appeared on Medscape.com.
Demand for new weight loss drugs has surged over the past few years.
Led by the antiobesity drugs semaglutide (Wegovy) and tirzepatide (Zepbound), these popular medications — more commonly known as glucagon-like peptide 1 (GLP-1) agonists — have become game changers for shedding excess pounds.
Aside from obesity indications, both drugs have been approved to treat type 2 diabetes under different brand names and have a growing list of other potential benefits, such as reducing inflammation and depression.
While there’s limited data to support the use of GLP-1 agonists for weight loss in cancer, some oncologists have begun carefully integrating the antiobesity agents into care and studying their effects in this patient population.
The reason: Research suggests that obesity can reduce the effectiveness of cancer therapies, especially in patients with breast cancer, and can increase the risk for treatment-related side effects.
The idea is that managing patients’ weight will improve their cancer outcomes, explained Lajos Pusztai, MD, PhD, a breast cancer specialist and professor of medicine at Yale School of Medicine in New Haven, Connecticut.
Although Dr. Pusztai and his oncology peers at Yale don’t yet use GPL-1 agonists, Neil Iyengar, MD, and colleagues have begun doing so to help some patients with breast cancer manage their weight. Dr. Iyengar estimates that a few hundred — almost 40% — of his patients are on the antiobesity drugs.
“For a patient who has really tried to reduce their weight and who is in the obese range, that’s where I think the use of these medications can be considered,” said Dr. Iyengar, a breast cancer oncologist at Memorial Sloan Kettering Cancer Center in New York City.
Why GLP-1s in Cancer?
GLP-1 is a hormone that the small intestine releases after eating. GLP-1 agonists work by mimicking GLP-1 to trigger the release of insulin and reduce the production of glucagon — two processes that help regulate blood sugar.
These agents, such as Wegovy (or Ozempic when prescribed for diabetes), also slow gastric emptying and can make people feel fuller longer.
Zebound (or Mounjaro for type 2 diabetes) is considered a dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, which may enhance its weight loss benefits.
In practice, however, these drugs can increase nausea and vomiting from chemotherapy, so Dr. Iyengar typically has patients use them afterwards, during maintenance treatment.
Oncologists don’t prescribe the drugs themselves but instead refer patients to endocrinologists or weight management centers that then write the prescriptions. Taking these drugs involves weekly subcutaneous injections patients can administer themselves.
Endocrinologist Emily Gallagher, MD, PhD, of Mount Sinai Hospital in New York City, estimates she has prescribed the antiobesity drugs to a few hundred patients with cancer and, like Dr. Iyengar, uses the drugs during maintenance treatment with hormone therapy for breast cancer. She also has used these agents in patients with prostate and endometrial cancers and has found the drugs can help counter steroid weight gain in multiple myeloma.
But, to date, the evidence for using GPL-1 agonists in cancer remains limited and the practice has not yet become widespread.
Research largely comes down to a few small retrospective studies in patients with breast cancer receiving aromatase inhibitors. Although no safety issues have emerged so far, these initial reports suggest that the drugs lead to significantly less weight loss in patients with cancer compared to the general population.
Dr. Iyengar led one recent study, presented at the 2024 annual meeting of the American Society of Clinical Oncology, in which he and his team assessed outcomes in 75 women with breast cancer who received a GLP-1 agonist. Almost 80% of patients had diabetes, and 60% received hormone therapy, most commonly an aromatase inhibitor. Patients’ median body mass index (BMI) at baseline was 34 kg/m2 (range, 23-50 kg/m2).
From baseline, patients lost 6.2 kg, on average, or about 5% of their total body weight, 12 months after initiating GLP-1 therapy.
In contrast, phase 3 trials show much higher mean weight loss — about two times — in patients without cancer.
Another recent study also reported modest weight loss results in patients with breast cancer undergoing endocrine therapy. The researchers reported that, at 12 months, Wegovy led to 4.34% reduction in BMI, compared with a 14% change reported in the general population. Zebound, however, was associated with a 2.31% BMI increase overall — though some patients did experience a decrease — compared with a 15% reduction in the general population.
“These findings indicate a substantially reduced weight loss efficacy in breast cancer patients on endocrine therapy compared to the general population,” the authors concluded.
It’s unclear why the drugs appear to not work as well in patients with cancer. It’s possible that hormone therapy or metabolic changes interfere with their effectiveness, given that some cancer therapies lead to weight gain. Steroids and hormone therapies, for instance, often increase appetite, and some treatments can slow patients’ metabolism or lead to fatigue, which can make it harder to exercise.
Patients with cancer may need a higher dose of GLP-1 agonists to achieve similar weight loss to the general population, Dr. Iyengar noted.
However, Dr. Gallagher said, in her own experience, she hasn’t found the drugs to be less effective in patients with cancer, especially the newer agents, like Wegovy and Zepbound.
As for safety, Wegovy and Zepbound both carry a black box warning for thyroid C-cell tumors, including medullary thyroid carcinoma. (Recent research, however, has found that GLP-1 agonists do not increase thyroid cancer risk).
These antiobesity agents are also contraindicated in patients with a personal or family history of medullary thyroid carcinoma and in patients who have multiple endocrine neoplasia syndrome type 2, which is associated with medullary thyroid carcinoma.
Dr. Gallagher hasn’t seen any secondary tumors — thyroid or otherwise — in her patients with cancer, but she follows the labeling contraindications. Dr. Iyengar also noted that more recent and larger data sets have shown no impact on this risk, which may not actually exist, he said
Dr. Gallagher remains cautious about using GPL-1 agonists in patients who have had bariatric surgery because these agents can compound the slower gastric emptying and intestinal transit from surgery, potentially leading to gastrointestinal obstructions.
Looking ahead, GPL-1 manufacturers are interested in adding cancer indications to the drug labeling. Both Dr. Iyengar and Dr. Gallagher said their institutions are in talks with companies to participate in large, multicenter, global phase 3 trials.
Dr. Iyengar welcomes the efforts, not only to test the effectiveness of GPL-1 agonists in oncology but also to “nail down” their safety in cancer.
“I don’t think that there’s mechanistically anything that’s particularly worrisome,” and current observations suggest that these drugs are likely to be safe, Dr. Iyengar said. Even so, “GLP-1 agonists do a lot of things that we don’t fully understand yet.”
The bigger challenge, Dr. Iyengar noted, is that companies will have to show a sizable benefit to using these drugs in patients with cancer to get the Food and Drug Administration’s approval. And to move the needle on cancer-specific outcomes, these antiobesity drugs will need to demonstrate significant, durable weight loss in patients with cancer.
But if these drugs can do that, “I think it’s going to be one of the biggest advances in medicine and oncology given the obesity and cancer epidemic,” Dr. Iyengar said.
Dr. Iyengar has adviser and/or researcher ties with companies that make or are developing GPL-1 agonists, including AstraZeneca, Novartis, Gilead, and Pfizer. Dr. Gallagher is a consultant for Novartis, Flare Therapeutics, Reactive Biosciences, and Seagen.
A version of this article first appeared on Medscape.com.
Dr. Rogers’ Neighborhood: Guinea Pigs and Groundbreaking Cancer Care
Sometimes, however, Dr. Rogers’ guinea pigs pay visits to her workplace. Every Halloween, she dresses them up and shows off their photos to just about everyone. Patients, coworkers, and even random people in the elevator get glimpses of the furry pair, who pose as dinosaurs, bats, aquarium shrimp, sharks, spiders, and bumblebees.
“Being in the hospital is not funny, but guinea pigs dressed up for Halloween is incredibly funny,” Dr. Rogers said. “They make a lot of people smile.”
For physician-scientist Dr. Rogers, a native of suburban Chicago, quality of life for patients is a priority, even when she’s not trying to entertain them and lift their spirits.
The field of hematology “is trying to figure out not only what’s biologically effective for disease, but also what might be best for people living with the condition,” she said. “This is especially true in terms of patient preference for a treatment you complete vs an ongoing or continuous treatment. I really like this idea of having more attention paid to what matters to patients, which the field of medicine sometimes forgets.”
In an interview, Dr. Rogers spoke about the appeal of storytelling in medicine, advances in treatment for CLL and hairy cell leukemia, and the challenges of college football loyalty.
How did you get drawn to medicine?
Ever since I was a kid, I thought, “Oh, I really want to be a doctor. That sounds fun.” At its core, medicine blends things I really like: science, helping people with a problem, and storytelling.
The practice of medicine is a lot about stories — talking to people, figuring out what they’re telling you about what’s going on, then explaining what you know in a way that makes sense to them.
What changes have you seen in leukemia care during your career?
The biggest change is the move from chemotherapies to targeted agents. When I first did a fellowship here at Ohio State, we had studies of ibrutinib, the first-in-class covalent Bruton tyrosine kinase (BTK) inhibitor. We’d see patients who’d been on chemotherapy for the past 10 or 15 years, and then they got in a clinical trial. Ibrutinib worked better than any of the chemotherapy, and they felt better and had fewer side effects.
Now, chemoimmunotherapy is not recommended for CLL, and you can see the impact of targeted agents on the lives of patients. Instead of telling people they need to put aside work and personal plans to take intensive chemotherapy for 6 months, you say: “You’ve got to come to some more appointments to make sure the treatment is going well, and you don’t have too many side effects. But you can expect to continue to work full-time and go to your niece’s wedding out of state or whatever else you want to do.”
What are you most excited about working on?
I’m the principal investigator of a study combining obinutuzumab, ibrutinib, and venetoclax for a fixed duration, a defined treatment course of a little over a year. I just reported the median progression-free survival for phase 2 at the European Hematology Association meeting this spring. It was over 7 years for both patients who had prior treatment and those who hadn’t.
The idea that people could take a year of treatment and get a huge benefit after completing it is quite important. The regimen has gone into phase 3 testing, and we’re now trying to understand the impact in terms of which patients got longer responses or which didn’t.
What are some challenges that remain in CLL?
There are still patients whose CLL becomes resistant to our two most commonly used classes of agents: BTK inhibitors and the BLC2 inhibitor, venetoclax. There are some more BCL2 inhibitors in development, but venetoclax is the only one currently approved.
I am also principal investigator on another study that added venetoclax to ibrutinib when resistance mutations developed that would predict ultimate resistance to ibrutinib. The median progression-free survival in that study was 40.7 months, whereas the expectation with venetoclax alone is 24 months. So, it really improved the amount of time people were in remission. This study is ongoing.
We’ve just started a phase 2 study to have patients take pirtobrutinib, a noncovalent BTK inhibitor, in combination with venetoclax in cases where CLL has become resistant to a covalent BTK inhibitor. Patients will take this combination for about a year and a half.
It’s been really exciting to see the impact of some of these combinations both as first-line CLL treatment and in CLL that’s become resistant. But trying to understand what predicts response is a harder thing. I wish I knew the answers for what causes this synergy between those two classes of drugs.
You also specialize in hairy cell leukemia. Could you talk about what it is?
CLL is the most prevalent adult leukemia in the Western world, whereas hairy cell leukemia is very rare. It’s a slow-growing B-cell cancer that got its name because under the microscope, the cells have hairy projections on them.
It had a survival of only about 2-4 years before the development of purine analogs. After a course of pentostatin or cladribine (2-chlordeoxyadenosine), some people never need treatment again in our natural lifespan.
But some patients don’t benefit from purine analogs, either because they have a devastating infection that makes them unsuitable or for another reason. Or they end up needing treatment every 2-3 years, which isn’t something you want to do for 30 years of someone’s lifespan.
What are some challenges in hairy cell leukemia?
It’s a rare condition, so it can be hard to do a really large clinical trial. A lot of physicians think that the prognosis is good and miss out on an opportunity for better treatment and to generate new knowledge.
Also, some people perceive that it’s not actually a problem for people living with it. Cladribine and pentostatin are not terrible chemotherapies, and most people tolerate them very well. But we can make treatment for hairy cell more effective and more tolerable for our patients if we put more effort into researching it.
I’ve heard that you’re a big college football fan. How do you balance your history as a University of Michigan medical school alum with your work for archrival Ohio State?
I went to Northwestern for undergrad, as did several people in my family. So, I usually just claim Northwestern is my football affiliation. It doesn’t inspire much vitriol if you cheer for Northwestern!
And I understand that you live with a pair of guinea pigs. Do tell.
I adopted guinea pigs as pets in medical school. They’re cute and friendly, and they make all this noise for you when you come home. 
Once, one of my clinic patients said, “I don’t want to be your guinea pig.” I thought, “you should be so lucky.” They have quite a lifestyle: They’ve trained me to bring them vegetables, they nap most of the time, and they have a play space, a guinea pig playground.
I thought I liked the guinea pigs more than they liked me. But last fall, I was gone for about 10 days. When I got back, I’d never heard them make so much noise. They were extremely happy to see me. Then for the next 48 hours, one would randomly start whistling for me to come over. I thought, “oh, these things do like me a little bit.”
Dr. Rogers disclosed receiving research funding from Genentech, AbbVie, Novartis, and AstraZeneca and consulting/advisory relationships with AstraZeneca, AbbVie, Genentech, Janssen, Pharmacyclics, BeiGene, Loxo@Lilly, and Alpine Immune Sciences.
A version of this article first appeared on Medscape.com.
Sometimes, however, Dr. Rogers’ guinea pigs pay visits to her workplace. Every Halloween, she dresses them up and shows off their photos to just about everyone. Patients, coworkers, and even random people in the elevator get glimpses of the furry pair, who pose as dinosaurs, bats, aquarium shrimp, sharks, spiders, and bumblebees.
“Being in the hospital is not funny, but guinea pigs dressed up for Halloween is incredibly funny,” Dr. Rogers said. “They make a lot of people smile.”
For physician-scientist Dr. Rogers, a native of suburban Chicago, quality of life for patients is a priority, even when she’s not trying to entertain them and lift their spirits.
The field of hematology “is trying to figure out not only what’s biologically effective for disease, but also what might be best for people living with the condition,” she said. “This is especially true in terms of patient preference for a treatment you complete vs an ongoing or continuous treatment. I really like this idea of having more attention paid to what matters to patients, which the field of medicine sometimes forgets.”
In an interview, Dr. Rogers spoke about the appeal of storytelling in medicine, advances in treatment for CLL and hairy cell leukemia, and the challenges of college football loyalty.
How did you get drawn to medicine?
Ever since I was a kid, I thought, “Oh, I really want to be a doctor. That sounds fun.” At its core, medicine blends things I really like: science, helping people with a problem, and storytelling.
The practice of medicine is a lot about stories — talking to people, figuring out what they’re telling you about what’s going on, then explaining what you know in a way that makes sense to them.
What changes have you seen in leukemia care during your career?
The biggest change is the move from chemotherapies to targeted agents. When I first did a fellowship here at Ohio State, we had studies of ibrutinib, the first-in-class covalent Bruton tyrosine kinase (BTK) inhibitor. We’d see patients who’d been on chemotherapy for the past 10 or 15 years, and then they got in a clinical trial. Ibrutinib worked better than any of the chemotherapy, and they felt better and had fewer side effects.
Now, chemoimmunotherapy is not recommended for CLL, and you can see the impact of targeted agents on the lives of patients. Instead of telling people they need to put aside work and personal plans to take intensive chemotherapy for 6 months, you say: “You’ve got to come to some more appointments to make sure the treatment is going well, and you don’t have too many side effects. But you can expect to continue to work full-time and go to your niece’s wedding out of state or whatever else you want to do.”
What are you most excited about working on?
I’m the principal investigator of a study combining obinutuzumab, ibrutinib, and venetoclax for a fixed duration, a defined treatment course of a little over a year. I just reported the median progression-free survival for phase 2 at the European Hematology Association meeting this spring. It was over 7 years for both patients who had prior treatment and those who hadn’t.
The idea that people could take a year of treatment and get a huge benefit after completing it is quite important. The regimen has gone into phase 3 testing, and we’re now trying to understand the impact in terms of which patients got longer responses or which didn’t.
What are some challenges that remain in CLL?
There are still patients whose CLL becomes resistant to our two most commonly used classes of agents: BTK inhibitors and the BLC2 inhibitor, venetoclax. There are some more BCL2 inhibitors in development, but venetoclax is the only one currently approved.
I am also principal investigator on another study that added venetoclax to ibrutinib when resistance mutations developed that would predict ultimate resistance to ibrutinib. The median progression-free survival in that study was 40.7 months, whereas the expectation with venetoclax alone is 24 months. So, it really improved the amount of time people were in remission. This study is ongoing.
We’ve just started a phase 2 study to have patients take pirtobrutinib, a noncovalent BTK inhibitor, in combination with venetoclax in cases where CLL has become resistant to a covalent BTK inhibitor. Patients will take this combination for about a year and a half.
It’s been really exciting to see the impact of some of these combinations both as first-line CLL treatment and in CLL that’s become resistant. But trying to understand what predicts response is a harder thing. I wish I knew the answers for what causes this synergy between those two classes of drugs.
You also specialize in hairy cell leukemia. Could you talk about what it is?
CLL is the most prevalent adult leukemia in the Western world, whereas hairy cell leukemia is very rare. It’s a slow-growing B-cell cancer that got its name because under the microscope, the cells have hairy projections on them.
It had a survival of only about 2-4 years before the development of purine analogs. After a course of pentostatin or cladribine (2-chlordeoxyadenosine), some people never need treatment again in our natural lifespan.
But some patients don’t benefit from purine analogs, either because they have a devastating infection that makes them unsuitable or for another reason. Or they end up needing treatment every 2-3 years, which isn’t something you want to do for 30 years of someone’s lifespan.
What are some challenges in hairy cell leukemia?
It’s a rare condition, so it can be hard to do a really large clinical trial. A lot of physicians think that the prognosis is good and miss out on an opportunity for better treatment and to generate new knowledge.
Also, some people perceive that it’s not actually a problem for people living with it. Cladribine and pentostatin are not terrible chemotherapies, and most people tolerate them very well. But we can make treatment for hairy cell more effective and more tolerable for our patients if we put more effort into researching it.
I’ve heard that you’re a big college football fan. How do you balance your history as a University of Michigan medical school alum with your work for archrival Ohio State?
I went to Northwestern for undergrad, as did several people in my family. So, I usually just claim Northwestern is my football affiliation. It doesn’t inspire much vitriol if you cheer for Northwestern!
And I understand that you live with a pair of guinea pigs. Do tell.
I adopted guinea pigs as pets in medical school. They’re cute and friendly, and they make all this noise for you when you come home.
Once, one of my clinic patients said, “I don’t want to be your guinea pig.” I thought, “you should be so lucky.” They have quite a lifestyle: They’ve trained me to bring them vegetables, they nap most of the time, and they have a play space, a guinea pig playground.
I thought I liked the guinea pigs more than they liked me. But last fall, I was gone for about 10 days. When I got back, I’d never heard them make so much noise. They were extremely happy to see me. Then for the next 48 hours, one would randomly start whistling for me to come over. I thought, “oh, these things do like me a little bit.”
Dr. Rogers disclosed receiving research funding from Genentech, AbbVie, Novartis, and AstraZeneca and consulting/advisory relationships with AstraZeneca, AbbVie, Genentech, Janssen, Pharmacyclics, BeiGene, Loxo@Lilly, and Alpine Immune Sciences.
A version of this article first appeared on Medscape.com.
Sometimes, however, Dr. Rogers’ guinea pigs pay visits to her workplace. Every Halloween, she dresses them up and shows off their photos to just about everyone. Patients, coworkers, and even random people in the elevator get glimpses of the furry pair, who pose as dinosaurs, bats, aquarium shrimp, sharks, spiders, and bumblebees.
“Being in the hospital is not funny, but guinea pigs dressed up for Halloween is incredibly funny,” Dr. Rogers said. “They make a lot of people smile.”
For physician-scientist Dr. Rogers, a native of suburban Chicago, quality of life for patients is a priority, even when she’s not trying to entertain them and lift their spirits.
The field of hematology “is trying to figure out not only what’s biologically effective for disease, but also what might be best for people living with the condition,” she said. “This is especially true in terms of patient preference for a treatment you complete vs an ongoing or continuous treatment. I really like this idea of having more attention paid to what matters to patients, which the field of medicine sometimes forgets.”
In an interview, Dr. Rogers spoke about the appeal of storytelling in medicine, advances in treatment for CLL and hairy cell leukemia, and the challenges of college football loyalty.
How did you get drawn to medicine?
Ever since I was a kid, I thought, “Oh, I really want to be a doctor. That sounds fun.” At its core, medicine blends things I really like: science, helping people with a problem, and storytelling.
The practice of medicine is a lot about stories — talking to people, figuring out what they’re telling you about what’s going on, then explaining what you know in a way that makes sense to them.
What changes have you seen in leukemia care during your career?
The biggest change is the move from chemotherapies to targeted agents. When I first did a fellowship here at Ohio State, we had studies of ibrutinib, the first-in-class covalent Bruton tyrosine kinase (BTK) inhibitor. We’d see patients who’d been on chemotherapy for the past 10 or 15 years, and then they got in a clinical trial. Ibrutinib worked better than any of the chemotherapy, and they felt better and had fewer side effects.
Now, chemoimmunotherapy is not recommended for CLL, and you can see the impact of targeted agents on the lives of patients. Instead of telling people they need to put aside work and personal plans to take intensive chemotherapy for 6 months, you say: “You’ve got to come to some more appointments to make sure the treatment is going well, and you don’t have too many side effects. But you can expect to continue to work full-time and go to your niece’s wedding out of state or whatever else you want to do.”
What are you most excited about working on?
I’m the principal investigator of a study combining obinutuzumab, ibrutinib, and venetoclax for a fixed duration, a defined treatment course of a little over a year. I just reported the median progression-free survival for phase 2 at the European Hematology Association meeting this spring. It was over 7 years for both patients who had prior treatment and those who hadn’t.
The idea that people could take a year of treatment and get a huge benefit after completing it is quite important. The regimen has gone into phase 3 testing, and we’re now trying to understand the impact in terms of which patients got longer responses or which didn’t.
What are some challenges that remain in CLL?
There are still patients whose CLL becomes resistant to our two most commonly used classes of agents: BTK inhibitors and the BLC2 inhibitor, venetoclax. There are some more BCL2 inhibitors in development, but venetoclax is the only one currently approved.
I am also principal investigator on another study that added venetoclax to ibrutinib when resistance mutations developed that would predict ultimate resistance to ibrutinib. The median progression-free survival in that study was 40.7 months, whereas the expectation with venetoclax alone is 24 months. So, it really improved the amount of time people were in remission. This study is ongoing.
We’ve just started a phase 2 study to have patients take pirtobrutinib, a noncovalent BTK inhibitor, in combination with venetoclax in cases where CLL has become resistant to a covalent BTK inhibitor. Patients will take this combination for about a year and a half.
It’s been really exciting to see the impact of some of these combinations both as first-line CLL treatment and in CLL that’s become resistant. But trying to understand what predicts response is a harder thing. I wish I knew the answers for what causes this synergy between those two classes of drugs.
You also specialize in hairy cell leukemia. Could you talk about what it is?
CLL is the most prevalent adult leukemia in the Western world, whereas hairy cell leukemia is very rare. It’s a slow-growing B-cell cancer that got its name because under the microscope, the cells have hairy projections on them.
It had a survival of only about 2-4 years before the development of purine analogs. After a course of pentostatin or cladribine (2-chlordeoxyadenosine), some people never need treatment again in our natural lifespan.
But some patients don’t benefit from purine analogs, either because they have a devastating infection that makes them unsuitable or for another reason. Or they end up needing treatment every 2-3 years, which isn’t something you want to do for 30 years of someone’s lifespan.
What are some challenges in hairy cell leukemia?
It’s a rare condition, so it can be hard to do a really large clinical trial. A lot of physicians think that the prognosis is good and miss out on an opportunity for better treatment and to generate new knowledge.
Also, some people perceive that it’s not actually a problem for people living with it. Cladribine and pentostatin are not terrible chemotherapies, and most people tolerate them very well. But we can make treatment for hairy cell more effective and more tolerable for our patients if we put more effort into researching it.
I’ve heard that you’re a big college football fan. How do you balance your history as a University of Michigan medical school alum with your work for archrival Ohio State?
I went to Northwestern for undergrad, as did several people in my family. So, I usually just claim Northwestern is my football affiliation. It doesn’t inspire much vitriol if you cheer for Northwestern!
And I understand that you live with a pair of guinea pigs. Do tell.
I adopted guinea pigs as pets in medical school. They’re cute and friendly, and they make all this noise for you when you come home.
Once, one of my clinic patients said, “I don’t want to be your guinea pig.” I thought, “you should be so lucky.” They have quite a lifestyle: They’ve trained me to bring them vegetables, they nap most of the time, and they have a play space, a guinea pig playground.
I thought I liked the guinea pigs more than they liked me. But last fall, I was gone for about 10 days. When I got back, I’d never heard them make so much noise. They were extremely happy to see me. Then for the next 48 hours, one would randomly start whistling for me to come over. I thought, “oh, these things do like me a little bit.”
Dr. Rogers disclosed receiving research funding from Genentech, AbbVie, Novartis, and AstraZeneca and consulting/advisory relationships with AstraZeneca, AbbVie, Genentech, Janssen, Pharmacyclics, BeiGene, Loxo@Lilly, and Alpine Immune Sciences.
A version of this article first appeared on Medscape.com.
Does Medicare Advantage Offer Higher-Value Chemotherapy?
TOPLINE:
METHODOLOGY:
- Private Medicare Advantage plans enroll more than half of the Medicare population, but it is unknown if or how the cost restrictions they impose affect chemotherapy, which accounts for a large portion of cancer care costs.
- Researchers conducted a cohort study using national Medicare data from January 2015 to December 2019 to look at Medicare Advantage enrollment and treatment patterns for patients with cancer receiving chemotherapy.
- The study included 96,501 Medicare Advantage enrollees and 206,274 traditional Medicare beneficiaries who initiated chemotherapy between January 2016 and December 2019 (mean age, ~73 years; ~56% women; Hispanic individuals, 15% and 8%; Black individuals, 15% and 8%; and White individuals, 75% and 86%, respectively).
- Resource use and care quality were measured during a 6-month period following chemotherapy initiation, and survival days were measured 18 months after beginning chemotherapy.
- Resource use measures included hospital inpatient services, outpatient care, prescription drugs, hospice services, and chemotherapy services. Quality measures included chemotherapy-related emergency visits and hospital admissions, as well as avoidable emergency visits and preventable hospitalizations.
TAKEAWAY:
- Medicare Advantage plans had lower resource use than traditional Medicare per enrollee with cancer undergoing chemotherapy ($8718 lower; 95% CI, $8343-$9094).
- The lower resource use was largely caused by fewer chemotherapy visits and less expensive chemotherapy per visit in Medicare Advantage plans ($5032 lower; 95% CI, $4772-$5293).
- Medicare Advantage enrollees had 2.5 percentage points fewer chemotherapy-related emergency department visits and 0.7 percentage points fewer chemotherapy-related hospitalizations than traditional Medicare beneficiaries.
- There was no clinically meaningful difference in survival between Medicare Advantage and traditional Medicare beneficiaries during the 18 months following chemotherapy initiation.
IN PRACTICE:
“Our new finding is that MA [Medicare Advantage] plans had lower resource use than TM [traditional Medicare] among enrollees with cancer undergoing chemotherapy — a serious condition managed by specialists and requiring expensive treatments. This suggests that MA’s cost advantages over TM are not limited to conditions for which low-cost primary care management can avoid costly services,” the authors wrote.
SOURCE:
The study was led by Yamini Kalidindi, PhD, McDermott+ Consulting, Washington, DC. It was published online on September 20, 2024, in JAMA Network Open (doi: 10.1001/jamanetworkopen.2024.34707), with a commentary.
LIMITATIONS:
The study’s findings may be affected by unobserved patient characteristics despite the use of inverse-probability weighting. The exclusion of Medicare Advantage enrollees in contracts with incomplete encounter data limits the generalizability of the results. The study does not apply to beneficiaries without Part D drug coverage. Quality measures were limited to those available from claims and encounter data, lacking information on patients’ cancer stage. The 18-month measure of survival might not adequately capture survival differences associated with early-stage cancers. The study did not measure whether patient care followed recommended guidelines.
DISCLOSURES:
Various authors reported grants from the National Institute on Aging, the National Institutes of Health, The Commonwealth Fund, Arnold Ventures, the National Cancer Institute, the Department of Defense, and the National Institute of Health Care Management. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Private Medicare Advantage plans enroll more than half of the Medicare population, but it is unknown if or how the cost restrictions they impose affect chemotherapy, which accounts for a large portion of cancer care costs.
- Researchers conducted a cohort study using national Medicare data from January 2015 to December 2019 to look at Medicare Advantage enrollment and treatment patterns for patients with cancer receiving chemotherapy.
- The study included 96,501 Medicare Advantage enrollees and 206,274 traditional Medicare beneficiaries who initiated chemotherapy between January 2016 and December 2019 (mean age, ~73 years; ~56% women; Hispanic individuals, 15% and 8%; Black individuals, 15% and 8%; and White individuals, 75% and 86%, respectively).
- Resource use and care quality were measured during a 6-month period following chemotherapy initiation, and survival days were measured 18 months after beginning chemotherapy.
- Resource use measures included hospital inpatient services, outpatient care, prescription drugs, hospice services, and chemotherapy services. Quality measures included chemotherapy-related emergency visits and hospital admissions, as well as avoidable emergency visits and preventable hospitalizations.
TAKEAWAY:
- Medicare Advantage plans had lower resource use than traditional Medicare per enrollee with cancer undergoing chemotherapy ($8718 lower; 95% CI, $8343-$9094).
- The lower resource use was largely caused by fewer chemotherapy visits and less expensive chemotherapy per visit in Medicare Advantage plans ($5032 lower; 95% CI, $4772-$5293).
- Medicare Advantage enrollees had 2.5 percentage points fewer chemotherapy-related emergency department visits and 0.7 percentage points fewer chemotherapy-related hospitalizations than traditional Medicare beneficiaries.
- There was no clinically meaningful difference in survival between Medicare Advantage and traditional Medicare beneficiaries during the 18 months following chemotherapy initiation.
IN PRACTICE:
“Our new finding is that MA [Medicare Advantage] plans had lower resource use than TM [traditional Medicare] among enrollees with cancer undergoing chemotherapy — a serious condition managed by specialists and requiring expensive treatments. This suggests that MA’s cost advantages over TM are not limited to conditions for which low-cost primary care management can avoid costly services,” the authors wrote.
SOURCE:
The study was led by Yamini Kalidindi, PhD, McDermott+ Consulting, Washington, DC. It was published online on September 20, 2024, in JAMA Network Open (doi: 10.1001/jamanetworkopen.2024.34707), with a commentary.
LIMITATIONS:
The study’s findings may be affected by unobserved patient characteristics despite the use of inverse-probability weighting. The exclusion of Medicare Advantage enrollees in contracts with incomplete encounter data limits the generalizability of the results. The study does not apply to beneficiaries without Part D drug coverage. Quality measures were limited to those available from claims and encounter data, lacking information on patients’ cancer stage. The 18-month measure of survival might not adequately capture survival differences associated with early-stage cancers. The study did not measure whether patient care followed recommended guidelines.
DISCLOSURES:
Various authors reported grants from the National Institute on Aging, the National Institutes of Health, The Commonwealth Fund, Arnold Ventures, the National Cancer Institute, the Department of Defense, and the National Institute of Health Care Management. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Private Medicare Advantage plans enroll more than half of the Medicare population, but it is unknown if or how the cost restrictions they impose affect chemotherapy, which accounts for a large portion of cancer care costs.
- Researchers conducted a cohort study using national Medicare data from January 2015 to December 2019 to look at Medicare Advantage enrollment and treatment patterns for patients with cancer receiving chemotherapy.
- The study included 96,501 Medicare Advantage enrollees and 206,274 traditional Medicare beneficiaries who initiated chemotherapy between January 2016 and December 2019 (mean age, ~73 years; ~56% women; Hispanic individuals, 15% and 8%; Black individuals, 15% and 8%; and White individuals, 75% and 86%, respectively).
- Resource use and care quality were measured during a 6-month period following chemotherapy initiation, and survival days were measured 18 months after beginning chemotherapy.
- Resource use measures included hospital inpatient services, outpatient care, prescription drugs, hospice services, and chemotherapy services. Quality measures included chemotherapy-related emergency visits and hospital admissions, as well as avoidable emergency visits and preventable hospitalizations.
TAKEAWAY:
- Medicare Advantage plans had lower resource use than traditional Medicare per enrollee with cancer undergoing chemotherapy ($8718 lower; 95% CI, $8343-$9094).
- The lower resource use was largely caused by fewer chemotherapy visits and less expensive chemotherapy per visit in Medicare Advantage plans ($5032 lower; 95% CI, $4772-$5293).
- Medicare Advantage enrollees had 2.5 percentage points fewer chemotherapy-related emergency department visits and 0.7 percentage points fewer chemotherapy-related hospitalizations than traditional Medicare beneficiaries.
- There was no clinically meaningful difference in survival between Medicare Advantage and traditional Medicare beneficiaries during the 18 months following chemotherapy initiation.
IN PRACTICE:
“Our new finding is that MA [Medicare Advantage] plans had lower resource use than TM [traditional Medicare] among enrollees with cancer undergoing chemotherapy — a serious condition managed by specialists and requiring expensive treatments. This suggests that MA’s cost advantages over TM are not limited to conditions for which low-cost primary care management can avoid costly services,” the authors wrote.
SOURCE:
The study was led by Yamini Kalidindi, PhD, McDermott+ Consulting, Washington, DC. It was published online on September 20, 2024, in JAMA Network Open (doi: 10.1001/jamanetworkopen.2024.34707), with a commentary.
LIMITATIONS:
The study’s findings may be affected by unobserved patient characteristics despite the use of inverse-probability weighting. The exclusion of Medicare Advantage enrollees in contracts with incomplete encounter data limits the generalizability of the results. The study does not apply to beneficiaries without Part D drug coverage. Quality measures were limited to those available from claims and encounter data, lacking information on patients’ cancer stage. The 18-month measure of survival might not adequately capture survival differences associated with early-stage cancers. The study did not measure whether patient care followed recommended guidelines.
DISCLOSURES:
Various authors reported grants from the National Institute on Aging, the National Institutes of Health, The Commonwealth Fund, Arnold Ventures, the National Cancer Institute, the Department of Defense, and the National Institute of Health Care Management. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
AACR Cancer Progress Report: Big Strides and Big Gaps
The AACR’s 216-page report — an annual endeavor now in its 14th year — focused on the “tremendous” strides made in cancer care, prevention, and early detection and highlighted areas where more research and attention are warranted.
One key area is funding. For the first time since 2016, federal funding for the National Institutes of Health (NIH) and National Cancer Institute (NCI) decreased in the past year. The cuts followed nearly a decade of funding increases that saw the NIH budget expand by nearly $15 billion, and that allowed for a “rapid pace and broad scope” of advances in cancer, AACR’s chief executive officer Margaret Foti, MD, PhD, said during a press briefing.
These recent cuts “threaten to curtail the medical progress seen in recent years and stymie future advancements,” said Dr. Foti, who called on Congress to commit to funding cancer research at significant and consistent levels to “maintain the momentum of progress against cancer.”
Inside the Report: Big Progress
Overall, advances in prevention, early detection, and treatment have helped catch more cancers earlier and save lives.
According to the AACR report, the age-adjusted overall cancer death rate in the United States fell by 33% between 1991 and 2021, meaning about 4.1 million cancer deaths were averted. The overall cancer death rate for children and adolescents has declined by 24% in the past 2 decades. The 5-year relative survival rate for children diagnosed with cancer in the US has improved from 58% for those diagnosed in the mid-1970s to 85% for those diagnosed between 2013 and 2019.
The past fiscal year has seen many new approvals for cancer drugs, diagnostics, and screening tests. From July 1, 2023, to June 30, 2024, the Food and Drug Administration (FDA) approved 15 new anticancer therapeutics, as well as 15 new indications for previously approved agents, one new imaging agent, several artificial intelligence (AI) tools to improve early cancer detection and diagnosis, and two minimally invasive tests for assessing inherited cancer risk or early cancer detection, according to the report.
“Cancer diagnostics are becoming more sophisticated,” AACR president Patricia M. LoRusso, DO, PhD, said during the briefing. “New technologies, such as spatial transcriptomics, are helping us study tumors at a cellular level, and helping to unveil things that we did not initially even begin to understand or think of. AI-based approaches are beginning to transform cancer detection, diagnosis, clinical decision-making, and treatment response monitoring.”
The report also highlights the significant progress in many childhood and adolescent/young adult cancers, Dr. LoRusso noted. These include FDA approvals for two new molecularly targeted therapeutics: tovorafenib for children with certain types of brain tumor and repotrectinib for children with a wide array of cancer types that have a specific genetic alteration known as NTRK gene fusion. It also includes an expanded approval for eflornithine to reduce the risk for relapse in children with high-risk neuroblastoma.
“Decades — decades — of basic research discoveries, have led to these clinical breakthroughs,” she stressed. “These gains against cancer are because of the rapid progress in our ability to decode the cancer genome, which has opened new and innovative avenues for drug development.”
The Gaps
Even with progress in cancer prevention, early detection, and treatment, cancer remains a significant issue.
“In 2024, it is estimated that more than 2 million new cases of cancer will be diagnosed in the United States. More than 611,000 people will die from the disease,” according to the report.
The 2024 report shows that incidence rates for some cancers are increasing in the United States, including vaccine-preventable cancers such as human papillomavirus (HPV)–associated oral cancers and, in young adults, cervical cancers. A recent analysis also found that overall cervical cancer incidence among women aged 30-34 years increased by 2.5% a year between 2012 and 2019.
Furthermore, despite clear evidence demonstrating that the HPV vaccine reduces cervical cancer incidence, uptake has remained poor, with only 38.6% of US children and adolescents aged 9-17 years receiving at least one dose of the vaccine in 2022.
Early-onset cancers are also increasing. Rates of breast, colorectal, and other cancers are on the rise in adults younger than 50 years, the report noted.
The report also pointed to data that 40% of all cancer cases in the United States can be attributed to preventable factors, such as smoking, excess body weight, and alcohol. However, our understanding of these risk factors has improved. Excessive levels of alcohol consumption have, for instance, been shown to increase the risk for six different types of cancer: certain types of head and neck cancer, esophageal squamous cell carcinoma, and breast, colorectal, liver, and stomach cancers.
Financial toxicity remains prevalent as well.
The report explains that financial hardship following a cancer diagnosis is widespread, and the effects can last for years. In fact, more than 40% of patients can spend their entire life savings within the first 2 years of cancer treatment. Among adult survivors of childhood cancers, 20.7% had trouble paying their medical bills, 29.9% said they had been sent to debt collection for unpaid bills, 14.1% had forgone medical care, and 26.8% could not afford nutritious meals.
For young cancer survivors, the lifetime costs associated with a diagnosis of cancer are substantial, reaching an average of $259,324 per person.
On a global level, it is estimated that from 2020 to 2050, the cumulative economic burden of cancer will be $25.2 trillion.
The Path Forward
Despite these challenges, Dr. LoRusso said, “it is unquestionable that we are in a time of unparalleled opportunities in cancer research.
“I am excited about what the future holds for cancer research, and especially for patient care,” she said.
However, funding commitments are needed to avoid impeding this momentum and losing a “talented and creative young workforce” that has brought new ideas and new technologies to the table.
Continued robust funding will help “to markedly improve cancer care, increase cancer survivorship, spur economic growth, and maintain the United States’ position as the global leader in science and medical research,” she added.
The AACR report specifically calls on Congress to:
- Appropriate at least $51.3 billion in fiscal year 2025 for the base budget of the NIH and at least $7.934 billion for the NCI.
- Provide $3.6 billion in dedicated funding for Cancer Moonshot activities through fiscal year 2026 in addition to other funding, consistent with the President’s fiscal year 2025 budget.
- Appropriate at least $472.4 million in fiscal year 2025 for the CDC’s Division of Cancer Prevention to support comprehensive cancer control, central cancer registries, and screening and awareness programs for specific cancers.
- Allocate $55 million in funding for the Oncology Center of Excellence at FDA in fiscal year 2025 to provide regulators with the staff and tools necessary to conduct expedited review of cancer-related medical products.
By working together with Congress and other stakeholders, “we will be able to accelerate the pace of progress and make major strides toward the lifesaving goal of preventing and curing all cancers at the earliest possible time,” Dr. Foti said. “I believe if we do that ... one day we will win this war on cancer.”
A version of this article first appeared on Medscape.com.
The AACR’s 216-page report — an annual endeavor now in its 14th year — focused on the “tremendous” strides made in cancer care, prevention, and early detection and highlighted areas where more research and attention are warranted.
One key area is funding. For the first time since 2016, federal funding for the National Institutes of Health (NIH) and National Cancer Institute (NCI) decreased in the past year. The cuts followed nearly a decade of funding increases that saw the NIH budget expand by nearly $15 billion, and that allowed for a “rapid pace and broad scope” of advances in cancer, AACR’s chief executive officer Margaret Foti, MD, PhD, said during a press briefing.
These recent cuts “threaten to curtail the medical progress seen in recent years and stymie future advancements,” said Dr. Foti, who called on Congress to commit to funding cancer research at significant and consistent levels to “maintain the momentum of progress against cancer.”
Inside the Report: Big Progress
Overall, advances in prevention, early detection, and treatment have helped catch more cancers earlier and save lives.
According to the AACR report, the age-adjusted overall cancer death rate in the United States fell by 33% between 1991 and 2021, meaning about 4.1 million cancer deaths were averted. The overall cancer death rate for children and adolescents has declined by 24% in the past 2 decades. The 5-year relative survival rate for children diagnosed with cancer in the US has improved from 58% for those diagnosed in the mid-1970s to 85% for those diagnosed between 2013 and 2019.
The past fiscal year has seen many new approvals for cancer drugs, diagnostics, and screening tests. From July 1, 2023, to June 30, 2024, the Food and Drug Administration (FDA) approved 15 new anticancer therapeutics, as well as 15 new indications for previously approved agents, one new imaging agent, several artificial intelligence (AI) tools to improve early cancer detection and diagnosis, and two minimally invasive tests for assessing inherited cancer risk or early cancer detection, according to the report.
“Cancer diagnostics are becoming more sophisticated,” AACR president Patricia M. LoRusso, DO, PhD, said during the briefing. “New technologies, such as spatial transcriptomics, are helping us study tumors at a cellular level, and helping to unveil things that we did not initially even begin to understand or think of. AI-based approaches are beginning to transform cancer detection, diagnosis, clinical decision-making, and treatment response monitoring.”
The report also highlights the significant progress in many childhood and adolescent/young adult cancers, Dr. LoRusso noted. These include FDA approvals for two new molecularly targeted therapeutics: tovorafenib for children with certain types of brain tumor and repotrectinib for children with a wide array of cancer types that have a specific genetic alteration known as NTRK gene fusion. It also includes an expanded approval for eflornithine to reduce the risk for relapse in children with high-risk neuroblastoma.
“Decades — decades — of basic research discoveries, have led to these clinical breakthroughs,” she stressed. “These gains against cancer are because of the rapid progress in our ability to decode the cancer genome, which has opened new and innovative avenues for drug development.”
The Gaps
Even with progress in cancer prevention, early detection, and treatment, cancer remains a significant issue.
“In 2024, it is estimated that more than 2 million new cases of cancer will be diagnosed in the United States. More than 611,000 people will die from the disease,” according to the report.
The 2024 report shows that incidence rates for some cancers are increasing in the United States, including vaccine-preventable cancers such as human papillomavirus (HPV)–associated oral cancers and, in young adults, cervical cancers. A recent analysis also found that overall cervical cancer incidence among women aged 30-34 years increased by 2.5% a year between 2012 and 2019.
Furthermore, despite clear evidence demonstrating that the HPV vaccine reduces cervical cancer incidence, uptake has remained poor, with only 38.6% of US children and adolescents aged 9-17 years receiving at least one dose of the vaccine in 2022.
Early-onset cancers are also increasing. Rates of breast, colorectal, and other cancers are on the rise in adults younger than 50 years, the report noted.
The report also pointed to data that 40% of all cancer cases in the United States can be attributed to preventable factors, such as smoking, excess body weight, and alcohol. However, our understanding of these risk factors has improved. Excessive levels of alcohol consumption have, for instance, been shown to increase the risk for six different types of cancer: certain types of head and neck cancer, esophageal squamous cell carcinoma, and breast, colorectal, liver, and stomach cancers.
Financial toxicity remains prevalent as well.
The report explains that financial hardship following a cancer diagnosis is widespread, and the effects can last for years. In fact, more than 40% of patients can spend their entire life savings within the first 2 years of cancer treatment. Among adult survivors of childhood cancers, 20.7% had trouble paying their medical bills, 29.9% said they had been sent to debt collection for unpaid bills, 14.1% had forgone medical care, and 26.8% could not afford nutritious meals.
For young cancer survivors, the lifetime costs associated with a diagnosis of cancer are substantial, reaching an average of $259,324 per person.
On a global level, it is estimated that from 2020 to 2050, the cumulative economic burden of cancer will be $25.2 trillion.
The Path Forward
Despite these challenges, Dr. LoRusso said, “it is unquestionable that we are in a time of unparalleled opportunities in cancer research.
“I am excited about what the future holds for cancer research, and especially for patient care,” she said.
However, funding commitments are needed to avoid impeding this momentum and losing a “talented and creative young workforce” that has brought new ideas and new technologies to the table.
Continued robust funding will help “to markedly improve cancer care, increase cancer survivorship, spur economic growth, and maintain the United States’ position as the global leader in science and medical research,” she added.
The AACR report specifically calls on Congress to:
- Appropriate at least $51.3 billion in fiscal year 2025 for the base budget of the NIH and at least $7.934 billion for the NCI.
- Provide $3.6 billion in dedicated funding for Cancer Moonshot activities through fiscal year 2026 in addition to other funding, consistent with the President’s fiscal year 2025 budget.
- Appropriate at least $472.4 million in fiscal year 2025 for the CDC’s Division of Cancer Prevention to support comprehensive cancer control, central cancer registries, and screening and awareness programs for specific cancers.
- Allocate $55 million in funding for the Oncology Center of Excellence at FDA in fiscal year 2025 to provide regulators with the staff and tools necessary to conduct expedited review of cancer-related medical products.
By working together with Congress and other stakeholders, “we will be able to accelerate the pace of progress and make major strides toward the lifesaving goal of preventing and curing all cancers at the earliest possible time,” Dr. Foti said. “I believe if we do that ... one day we will win this war on cancer.”
A version of this article first appeared on Medscape.com.
The AACR’s 216-page report — an annual endeavor now in its 14th year — focused on the “tremendous” strides made in cancer care, prevention, and early detection and highlighted areas where more research and attention are warranted.
One key area is funding. For the first time since 2016, federal funding for the National Institutes of Health (NIH) and National Cancer Institute (NCI) decreased in the past year. The cuts followed nearly a decade of funding increases that saw the NIH budget expand by nearly $15 billion, and that allowed for a “rapid pace and broad scope” of advances in cancer, AACR’s chief executive officer Margaret Foti, MD, PhD, said during a press briefing.
These recent cuts “threaten to curtail the medical progress seen in recent years and stymie future advancements,” said Dr. Foti, who called on Congress to commit to funding cancer research at significant and consistent levels to “maintain the momentum of progress against cancer.”
Inside the Report: Big Progress
Overall, advances in prevention, early detection, and treatment have helped catch more cancers earlier and save lives.
According to the AACR report, the age-adjusted overall cancer death rate in the United States fell by 33% between 1991 and 2021, meaning about 4.1 million cancer deaths were averted. The overall cancer death rate for children and adolescents has declined by 24% in the past 2 decades. The 5-year relative survival rate for children diagnosed with cancer in the US has improved from 58% for those diagnosed in the mid-1970s to 85% for those diagnosed between 2013 and 2019.
The past fiscal year has seen many new approvals for cancer drugs, diagnostics, and screening tests. From July 1, 2023, to June 30, 2024, the Food and Drug Administration (FDA) approved 15 new anticancer therapeutics, as well as 15 new indications for previously approved agents, one new imaging agent, several artificial intelligence (AI) tools to improve early cancer detection and diagnosis, and two minimally invasive tests for assessing inherited cancer risk or early cancer detection, according to the report.
“Cancer diagnostics are becoming more sophisticated,” AACR president Patricia M. LoRusso, DO, PhD, said during the briefing. “New technologies, such as spatial transcriptomics, are helping us study tumors at a cellular level, and helping to unveil things that we did not initially even begin to understand or think of. AI-based approaches are beginning to transform cancer detection, diagnosis, clinical decision-making, and treatment response monitoring.”
The report also highlights the significant progress in many childhood and adolescent/young adult cancers, Dr. LoRusso noted. These include FDA approvals for two new molecularly targeted therapeutics: tovorafenib for children with certain types of brain tumor and repotrectinib for children with a wide array of cancer types that have a specific genetic alteration known as NTRK gene fusion. It also includes an expanded approval for eflornithine to reduce the risk for relapse in children with high-risk neuroblastoma.
“Decades — decades — of basic research discoveries, have led to these clinical breakthroughs,” she stressed. “These gains against cancer are because of the rapid progress in our ability to decode the cancer genome, which has opened new and innovative avenues for drug development.”
The Gaps
Even with progress in cancer prevention, early detection, and treatment, cancer remains a significant issue.
“In 2024, it is estimated that more than 2 million new cases of cancer will be diagnosed in the United States. More than 611,000 people will die from the disease,” according to the report.
The 2024 report shows that incidence rates for some cancers are increasing in the United States, including vaccine-preventable cancers such as human papillomavirus (HPV)–associated oral cancers and, in young adults, cervical cancers. A recent analysis also found that overall cervical cancer incidence among women aged 30-34 years increased by 2.5% a year between 2012 and 2019.
Furthermore, despite clear evidence demonstrating that the HPV vaccine reduces cervical cancer incidence, uptake has remained poor, with only 38.6% of US children and adolescents aged 9-17 years receiving at least one dose of the vaccine in 2022.
Early-onset cancers are also increasing. Rates of breast, colorectal, and other cancers are on the rise in adults younger than 50 years, the report noted.
The report also pointed to data that 40% of all cancer cases in the United States can be attributed to preventable factors, such as smoking, excess body weight, and alcohol. However, our understanding of these risk factors has improved. Excessive levels of alcohol consumption have, for instance, been shown to increase the risk for six different types of cancer: certain types of head and neck cancer, esophageal squamous cell carcinoma, and breast, colorectal, liver, and stomach cancers.
Financial toxicity remains prevalent as well.
The report explains that financial hardship following a cancer diagnosis is widespread, and the effects can last for years. In fact, more than 40% of patients can spend their entire life savings within the first 2 years of cancer treatment. Among adult survivors of childhood cancers, 20.7% had trouble paying their medical bills, 29.9% said they had been sent to debt collection for unpaid bills, 14.1% had forgone medical care, and 26.8% could not afford nutritious meals.
For young cancer survivors, the lifetime costs associated with a diagnosis of cancer are substantial, reaching an average of $259,324 per person.
On a global level, it is estimated that from 2020 to 2050, the cumulative economic burden of cancer will be $25.2 trillion.
The Path Forward
Despite these challenges, Dr. LoRusso said, “it is unquestionable that we are in a time of unparalleled opportunities in cancer research.
“I am excited about what the future holds for cancer research, and especially for patient care,” she said.
However, funding commitments are needed to avoid impeding this momentum and losing a “talented and creative young workforce” that has brought new ideas and new technologies to the table.
Continued robust funding will help “to markedly improve cancer care, increase cancer survivorship, spur economic growth, and maintain the United States’ position as the global leader in science and medical research,” she added.
The AACR report specifically calls on Congress to:
- Appropriate at least $51.3 billion in fiscal year 2025 for the base budget of the NIH and at least $7.934 billion for the NCI.
- Provide $3.6 billion in dedicated funding for Cancer Moonshot activities through fiscal year 2026 in addition to other funding, consistent with the President’s fiscal year 2025 budget.
- Appropriate at least $472.4 million in fiscal year 2025 for the CDC’s Division of Cancer Prevention to support comprehensive cancer control, central cancer registries, and screening and awareness programs for specific cancers.
- Allocate $55 million in funding for the Oncology Center of Excellence at FDA in fiscal year 2025 to provide regulators with the staff and tools necessary to conduct expedited review of cancer-related medical products.
By working together with Congress and other stakeholders, “we will be able to accelerate the pace of progress and make major strides toward the lifesaving goal of preventing and curing all cancers at the earliest possible time,” Dr. Foti said. “I believe if we do that ... one day we will win this war on cancer.”
A version of this article first appeared on Medscape.com.
Cancer Risk: Are Pesticides the New Smoking?
Pesticides have transformed modern agriculture by boosting production yields and helping alleviate food insecurity amid rapid global population growth. However, from a public health perspective, exposure to pesticides has been linked to numerous harmful effects, including neurologic disorders like Parkinson’s disease, weakened immune function, and an increased risk for cancer.
thus offering a limited perspective.
A comprehensive assessment of how pesticide use affects cancer risk across a broader population has yet to be conducted.
A recent population-level study aimed to address this gap by evaluating cancer risks in the US population using a model that accounts for pesticide use and adjusts for various factors. The goal was to identify regional disparities in exposure and contribute to the development of public health policies that protect populations from potential harm.
Calculating Cancer Risk
Researchers developed a model using several data sources to estimate the additional cancer risk from agricultural pesticide use. Key data included:
- Pesticide use data from the US Geological Survey in 2019, which covered 69 agricultural pesticides across 3143 counties
- Cancer incidence rates per 100,000 people, which were collected between 2015 and 2019 by the National Institutes of Health and the Centers for Disease Control and Prevention; these data covered various cancers, including bladder, colorectal, leukemia, lung, non-Hodgkin lymphoma, and pancreatic cancers
- Covariates, including smoking prevalence, the Social Vulnerability Index, agricultural land use, and total US population in 2019
Pesticide use profile patterns were developed using latent class analysis, a statistical method used to identify homogeneous subgroups within a heterogeneous population. A generalized linear model then estimated how these pesticide use patterns and the covariates affected cancer incidence.
The model highlighted regions with the highest and lowest “additional” cancer risks linked to pesticide exposure, calculating the estimated increase in cancer cases per year that resulted from variations in agricultural pesticide use.
Midwest Most Affected
While this model doesn’t establish causality or assess individual risk, it reveals regional trends in the association between pesticide use patterns and cancer incidence from a population-based perspective.
The Midwest, known for its high corn production, emerged as the region most affected by pesticide use. Compared with regions with the lowest risk, the Midwest faced an additional 154,541 cancer cases annually across all types. For colorectal and pancreatic cancers, the yearly increases were 20,927 and 3835 cases, respectively. Similar trends were observed for leukemia and non-Hodgkin lymphoma.
Pesticides vs Smoking
The researchers also estimated the additional cancer risk related to smoking, using the same model. They found that pesticides contributed to a higher risk for cancer than smoking in several cases.
The most significant difference was observed with non-Hodgkin lymphoma, where pesticides were linked to 154.1% more cases than smoking. For all cancers combined, as well as bladder cancer and leukemia, the increases were moderate: 18.7%, 19.3%, and 21.0%, respectively.
This result highlights the importance of considering pesticide exposure alongside smoking when studying cancer risks.
Expanding Scope of Research
Some limitations of this study should be noted. Certain counties lacked complete data, and there was heterogeneity in the size and population of the counties studied. The research also did not account for seasonal and migrant workers, who are likely to be heavily exposed. In addition, the data used in the study were not independently validated, and they could not be used to assess individual risk.
The effect of pesticides on human health is a vast and critical field of research, often focusing on a limited range of pesticides or specific cancers. This study stands out by taking a broader, more holistic approach, aiming to highlight regional inequalities and identify less-studied pesticides that could be future research priorities.
Given the significant public health impact, the authors encouraged the authorities to share these findings with the most vulnerable communities to raise awareness.
This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Pesticides have transformed modern agriculture by boosting production yields and helping alleviate food insecurity amid rapid global population growth. However, from a public health perspective, exposure to pesticides has been linked to numerous harmful effects, including neurologic disorders like Parkinson’s disease, weakened immune function, and an increased risk for cancer.
thus offering a limited perspective.
A comprehensive assessment of how pesticide use affects cancer risk across a broader population has yet to be conducted.
A recent population-level study aimed to address this gap by evaluating cancer risks in the US population using a model that accounts for pesticide use and adjusts for various factors. The goal was to identify regional disparities in exposure and contribute to the development of public health policies that protect populations from potential harm.
Calculating Cancer Risk
Researchers developed a model using several data sources to estimate the additional cancer risk from agricultural pesticide use. Key data included:
- Pesticide use data from the US Geological Survey in 2019, which covered 69 agricultural pesticides across 3143 counties
- Cancer incidence rates per 100,000 people, which were collected between 2015 and 2019 by the National Institutes of Health and the Centers for Disease Control and Prevention; these data covered various cancers, including bladder, colorectal, leukemia, lung, non-Hodgkin lymphoma, and pancreatic cancers
- Covariates, including smoking prevalence, the Social Vulnerability Index, agricultural land use, and total US population in 2019
Pesticide use profile patterns were developed using latent class analysis, a statistical method used to identify homogeneous subgroups within a heterogeneous population. A generalized linear model then estimated how these pesticide use patterns and the covariates affected cancer incidence.
The model highlighted regions with the highest and lowest “additional” cancer risks linked to pesticide exposure, calculating the estimated increase in cancer cases per year that resulted from variations in agricultural pesticide use.
Midwest Most Affected
While this model doesn’t establish causality or assess individual risk, it reveals regional trends in the association between pesticide use patterns and cancer incidence from a population-based perspective.
The Midwest, known for its high corn production, emerged as the region most affected by pesticide use. Compared with regions with the lowest risk, the Midwest faced an additional 154,541 cancer cases annually across all types. For colorectal and pancreatic cancers, the yearly increases were 20,927 and 3835 cases, respectively. Similar trends were observed for leukemia and non-Hodgkin lymphoma.
Pesticides vs Smoking
The researchers also estimated the additional cancer risk related to smoking, using the same model. They found that pesticides contributed to a higher risk for cancer than smoking in several cases.
The most significant difference was observed with non-Hodgkin lymphoma, where pesticides were linked to 154.1% more cases than smoking. For all cancers combined, as well as bladder cancer and leukemia, the increases were moderate: 18.7%, 19.3%, and 21.0%, respectively.
This result highlights the importance of considering pesticide exposure alongside smoking when studying cancer risks.
Expanding Scope of Research
Some limitations of this study should be noted. Certain counties lacked complete data, and there was heterogeneity in the size and population of the counties studied. The research also did not account for seasonal and migrant workers, who are likely to be heavily exposed. In addition, the data used in the study were not independently validated, and they could not be used to assess individual risk.
The effect of pesticides on human health is a vast and critical field of research, often focusing on a limited range of pesticides or specific cancers. This study stands out by taking a broader, more holistic approach, aiming to highlight regional inequalities and identify less-studied pesticides that could be future research priorities.
Given the significant public health impact, the authors encouraged the authorities to share these findings with the most vulnerable communities to raise awareness.
This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Pesticides have transformed modern agriculture by boosting production yields and helping alleviate food insecurity amid rapid global population growth. However, from a public health perspective, exposure to pesticides has been linked to numerous harmful effects, including neurologic disorders like Parkinson’s disease, weakened immune function, and an increased risk for cancer.
thus offering a limited perspective.
A comprehensive assessment of how pesticide use affects cancer risk across a broader population has yet to be conducted.
A recent population-level study aimed to address this gap by evaluating cancer risks in the US population using a model that accounts for pesticide use and adjusts for various factors. The goal was to identify regional disparities in exposure and contribute to the development of public health policies that protect populations from potential harm.
Calculating Cancer Risk
Researchers developed a model using several data sources to estimate the additional cancer risk from agricultural pesticide use. Key data included:
- Pesticide use data from the US Geological Survey in 2019, which covered 69 agricultural pesticides across 3143 counties
- Cancer incidence rates per 100,000 people, which were collected between 2015 and 2019 by the National Institutes of Health and the Centers for Disease Control and Prevention; these data covered various cancers, including bladder, colorectal, leukemia, lung, non-Hodgkin lymphoma, and pancreatic cancers
- Covariates, including smoking prevalence, the Social Vulnerability Index, agricultural land use, and total US population in 2019
Pesticide use profile patterns were developed using latent class analysis, a statistical method used to identify homogeneous subgroups within a heterogeneous population. A generalized linear model then estimated how these pesticide use patterns and the covariates affected cancer incidence.
The model highlighted regions with the highest and lowest “additional” cancer risks linked to pesticide exposure, calculating the estimated increase in cancer cases per year that resulted from variations in agricultural pesticide use.
Midwest Most Affected
While this model doesn’t establish causality or assess individual risk, it reveals regional trends in the association between pesticide use patterns and cancer incidence from a population-based perspective.
The Midwest, known for its high corn production, emerged as the region most affected by pesticide use. Compared with regions with the lowest risk, the Midwest faced an additional 154,541 cancer cases annually across all types. For colorectal and pancreatic cancers, the yearly increases were 20,927 and 3835 cases, respectively. Similar trends were observed for leukemia and non-Hodgkin lymphoma.
Pesticides vs Smoking
The researchers also estimated the additional cancer risk related to smoking, using the same model. They found that pesticides contributed to a higher risk for cancer than smoking in several cases.
The most significant difference was observed with non-Hodgkin lymphoma, where pesticides were linked to 154.1% more cases than smoking. For all cancers combined, as well as bladder cancer and leukemia, the increases were moderate: 18.7%, 19.3%, and 21.0%, respectively.
This result highlights the importance of considering pesticide exposure alongside smoking when studying cancer risks.
Expanding Scope of Research
Some limitations of this study should be noted. Certain counties lacked complete data, and there was heterogeneity in the size and population of the counties studied. The research also did not account for seasonal and migrant workers, who are likely to be heavily exposed. In addition, the data used in the study were not independently validated, and they could not be used to assess individual risk.
The effect of pesticides on human health is a vast and critical field of research, often focusing on a limited range of pesticides or specific cancers. This study stands out by taking a broader, more holistic approach, aiming to highlight regional inequalities and identify less-studied pesticides that could be future research priorities.
Given the significant public health impact, the authors encouraged the authorities to share these findings with the most vulnerable communities to raise awareness.
This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Treatment Options in MCL: What Are the Best Practices?
In the frontline setting, findings suggest that regimens should differ significantly on the basis of whether patients are older or younger, whereas more data are needed to understand whether treatment can overcome poor prognoses in patients with TP53 mutations, lymphoma specialist Nina Wagner-Johnston, MD, of Johns Hopkins University School of Medicine, Baltimore, said in a presentation at the annual meeting of the Society of Hematologic Oncology (SOHO) 2024 in Houston, Texas.
On the relapsed/refractory front, patients need better options after treatment with Bruton tyrosine kinase inhibitors or chimeric antigen receptor (CAR) T-cell therapy, Krish Patel, MD, a lymphoma specialist with Swedish Cancer Institute in Seattle, said in an adjoining presentation. Fortunately, he said, some treatments are showing early promise.
Here’s a closer look at the presentations by Dr. Wagner-Johnston and Dr. Patel.
Frontline MCL: Age Helps Determine Best Approach
“For older and less fit patients, the standard approach has typically been bendamustine (Bendeka, Treanda) and rituximab (Rituxan), and the median progression-free survival is about 4 years, with overall survival not reached at a median 5 years of follow-up,” Dr. Wagner-Johnston said.
Low doses of the chemotherapy drug cytarabine have been added to the bendamustine-rituximab regimen, with encouraging results, she said. “Certainly there’s more toxicity associated even with lower doses, but those data look fairly promising.”
For younger and fit patients, “the standard of care approach has been to administer intensive chemoimmunotherapy that contains high-dose cytarabine, and then that’s typically followed with an autologous stem cell transplant,” she said. A 2016 study reported median progression-free survival of 8.5 years and median overall survival of 12.7 years.
Now, second-generation Bruton tyrosine kinase inhibitors “look very promising” in the frontline setting, Dr. Wagner-Johnston said.
The road has been rocky, however. The SHINE trial of more than 500 patients aged over 65 found that adding ibrutinib to bendamustine-rituximab improved progression-free survival. “However, progression-free survival did not [connect] to an overall survival benefit, and that’s likely due to the toxicity seen with ibrutinib,” she said.
“It’s not surprising to many of you that ibrutinib has been removed from the FDA label for mantle cell lymphoma,” she said. However, “second-generation [Bruton tyrosine kinase inhibitors] are known to be associated with less toxicity and potentially increased potency.”
What about Bruton tyrosine kinase inhibitors in younger and fitter patients? The TRIANGLE trial demonstrated their benefit, Dr. Wagner-Johnston said, linking ibrutinib to improvement in progression-free survival.
However, “it’s really too early to evaluate the statistical significance for overall survival.” And while the study looks at therapy without stem cell transplant, she believes it’s too early to know whether that’s a good option.
Dr. Wagner-Johnston tackled another topic: Can Bruton tyrosine kinase inhibitors overcome the poor prognosis seen with MCL with TP53 mutation? For now, the limitations of research makes it “hard to know,” she said, although early results of the BOVen trial are promising.
Relapsed/Refractory MCL: Better Options Are Still Needed
In his presentation, Dr. Patel spoke about therapy in patients with MCL and relapsed/refractory disease. “We know that outcomes for patients who progress on covalent [Bruton tyrosine kinase inhibitors] is really dismal,” he said. “This has been shown by multiple groups now across the globe.”
Noncovalent Bruton tyrosine kinase inhibitors are now an option, he noted. “We do understand that they work for some patients, and it can be quite useful, but even noncovalent [Bruton tyrosine kinase inhibitors] themselves are susceptible to resistance mutations. We’ve seen that in the [chronic lymphocytic leukemia] world.”
Dr. Patel asked the audience, “Why not just give everybody CAR T-cells, post-[Bruton tyrosine kinase inhibitors]? You get a CAR T-cell! You get a CAR T-cell! Everybody gets one.”
However, he noted, “Unfortunately, mantle cell lymphoma patients experience the worst high-grade toxicity when receiving CD19[-targeted] CAR T-cells.”
Are there better options? At the moment, “really, really early data” suggest benefits from molecular glues and degraders, novel inhibitors, antibody-drug conjugates, novel CAR T-cells, and bispecific antibodies, Dr. Patel said.
“All of these tools are in clinical trials, and hopefully some of them will help,” he said.
Disclosures were not provided. Dr. Wagner-Johnston recently disclosed advisory committee/board of directors’ relationships with ADC Therapeutics, Regeneron, Calibr, and Verastem. Dr. Patel recently disclosed ties with a long list of pharmaceutical companies, including AbbVie, AstraZeneca, BeiGene, Bristol Myers Squibb, Genentech, Janssen, Merck, and others.
A version of this article first appeared on Medscape.com.
In the frontline setting, findings suggest that regimens should differ significantly on the basis of whether patients are older or younger, whereas more data are needed to understand whether treatment can overcome poor prognoses in patients with TP53 mutations, lymphoma specialist Nina Wagner-Johnston, MD, of Johns Hopkins University School of Medicine, Baltimore, said in a presentation at the annual meeting of the Society of Hematologic Oncology (SOHO) 2024 in Houston, Texas.
On the relapsed/refractory front, patients need better options after treatment with Bruton tyrosine kinase inhibitors or chimeric antigen receptor (CAR) T-cell therapy, Krish Patel, MD, a lymphoma specialist with Swedish Cancer Institute in Seattle, said in an adjoining presentation. Fortunately, he said, some treatments are showing early promise.
Here’s a closer look at the presentations by Dr. Wagner-Johnston and Dr. Patel.
Frontline MCL: Age Helps Determine Best Approach
“For older and less fit patients, the standard approach has typically been bendamustine (Bendeka, Treanda) and rituximab (Rituxan), and the median progression-free survival is about 4 years, with overall survival not reached at a median 5 years of follow-up,” Dr. Wagner-Johnston said.
Low doses of the chemotherapy drug cytarabine have been added to the bendamustine-rituximab regimen, with encouraging results, she said. “Certainly there’s more toxicity associated even with lower doses, but those data look fairly promising.”
For younger and fit patients, “the standard of care approach has been to administer intensive chemoimmunotherapy that contains high-dose cytarabine, and then that’s typically followed with an autologous stem cell transplant,” she said. A 2016 study reported median progression-free survival of 8.5 years and median overall survival of 12.7 years.
Now, second-generation Bruton tyrosine kinase inhibitors “look very promising” in the frontline setting, Dr. Wagner-Johnston said.
The road has been rocky, however. The SHINE trial of more than 500 patients aged over 65 found that adding ibrutinib to bendamustine-rituximab improved progression-free survival. “However, progression-free survival did not [connect] to an overall survival benefit, and that’s likely due to the toxicity seen with ibrutinib,” she said.
“It’s not surprising to many of you that ibrutinib has been removed from the FDA label for mantle cell lymphoma,” she said. However, “second-generation [Bruton tyrosine kinase inhibitors] are known to be associated with less toxicity and potentially increased potency.”
What about Bruton tyrosine kinase inhibitors in younger and fitter patients? The TRIANGLE trial demonstrated their benefit, Dr. Wagner-Johnston said, linking ibrutinib to improvement in progression-free survival.
However, “it’s really too early to evaluate the statistical significance for overall survival.” And while the study looks at therapy without stem cell transplant, she believes it’s too early to know whether that’s a good option.
Dr. Wagner-Johnston tackled another topic: Can Bruton tyrosine kinase inhibitors overcome the poor prognosis seen with MCL with TP53 mutation? For now, the limitations of research makes it “hard to know,” she said, although early results of the BOVen trial are promising.
Relapsed/Refractory MCL: Better Options Are Still Needed
In his presentation, Dr. Patel spoke about therapy in patients with MCL and relapsed/refractory disease. “We know that outcomes for patients who progress on covalent [Bruton tyrosine kinase inhibitors] is really dismal,” he said. “This has been shown by multiple groups now across the globe.”
Noncovalent Bruton tyrosine kinase inhibitors are now an option, he noted. “We do understand that they work for some patients, and it can be quite useful, but even noncovalent [Bruton tyrosine kinase inhibitors] themselves are susceptible to resistance mutations. We’ve seen that in the [chronic lymphocytic leukemia] world.”
Dr. Patel asked the audience, “Why not just give everybody CAR T-cells, post-[Bruton tyrosine kinase inhibitors]? You get a CAR T-cell! You get a CAR T-cell! Everybody gets one.”
However, he noted, “Unfortunately, mantle cell lymphoma patients experience the worst high-grade toxicity when receiving CD19[-targeted] CAR T-cells.”
Are there better options? At the moment, “really, really early data” suggest benefits from molecular glues and degraders, novel inhibitors, antibody-drug conjugates, novel CAR T-cells, and bispecific antibodies, Dr. Patel said.
“All of these tools are in clinical trials, and hopefully some of them will help,” he said.
Disclosures were not provided. Dr. Wagner-Johnston recently disclosed advisory committee/board of directors’ relationships with ADC Therapeutics, Regeneron, Calibr, and Verastem. Dr. Patel recently disclosed ties with a long list of pharmaceutical companies, including AbbVie, AstraZeneca, BeiGene, Bristol Myers Squibb, Genentech, Janssen, Merck, and others.
A version of this article first appeared on Medscape.com.
In the frontline setting, findings suggest that regimens should differ significantly on the basis of whether patients are older or younger, whereas more data are needed to understand whether treatment can overcome poor prognoses in patients with TP53 mutations, lymphoma specialist Nina Wagner-Johnston, MD, of Johns Hopkins University School of Medicine, Baltimore, said in a presentation at the annual meeting of the Society of Hematologic Oncology (SOHO) 2024 in Houston, Texas.
On the relapsed/refractory front, patients need better options after treatment with Bruton tyrosine kinase inhibitors or chimeric antigen receptor (CAR) T-cell therapy, Krish Patel, MD, a lymphoma specialist with Swedish Cancer Institute in Seattle, said in an adjoining presentation. Fortunately, he said, some treatments are showing early promise.
Here’s a closer look at the presentations by Dr. Wagner-Johnston and Dr. Patel.
Frontline MCL: Age Helps Determine Best Approach
“For older and less fit patients, the standard approach has typically been bendamustine (Bendeka, Treanda) and rituximab (Rituxan), and the median progression-free survival is about 4 years, with overall survival not reached at a median 5 years of follow-up,” Dr. Wagner-Johnston said.
Low doses of the chemotherapy drug cytarabine have been added to the bendamustine-rituximab regimen, with encouraging results, she said. “Certainly there’s more toxicity associated even with lower doses, but those data look fairly promising.”
For younger and fit patients, “the standard of care approach has been to administer intensive chemoimmunotherapy that contains high-dose cytarabine, and then that’s typically followed with an autologous stem cell transplant,” she said. A 2016 study reported median progression-free survival of 8.5 years and median overall survival of 12.7 years.
Now, second-generation Bruton tyrosine kinase inhibitors “look very promising” in the frontline setting, Dr. Wagner-Johnston said.
The road has been rocky, however. The SHINE trial of more than 500 patients aged over 65 found that adding ibrutinib to bendamustine-rituximab improved progression-free survival. “However, progression-free survival did not [connect] to an overall survival benefit, and that’s likely due to the toxicity seen with ibrutinib,” she said.
“It’s not surprising to many of you that ibrutinib has been removed from the FDA label for mantle cell lymphoma,” she said. However, “second-generation [Bruton tyrosine kinase inhibitors] are known to be associated with less toxicity and potentially increased potency.”
What about Bruton tyrosine kinase inhibitors in younger and fitter patients? The TRIANGLE trial demonstrated their benefit, Dr. Wagner-Johnston said, linking ibrutinib to improvement in progression-free survival.
However, “it’s really too early to evaluate the statistical significance for overall survival.” And while the study looks at therapy without stem cell transplant, she believes it’s too early to know whether that’s a good option.
Dr. Wagner-Johnston tackled another topic: Can Bruton tyrosine kinase inhibitors overcome the poor prognosis seen with MCL with TP53 mutation? For now, the limitations of research makes it “hard to know,” she said, although early results of the BOVen trial are promising.
Relapsed/Refractory MCL: Better Options Are Still Needed
In his presentation, Dr. Patel spoke about therapy in patients with MCL and relapsed/refractory disease. “We know that outcomes for patients who progress on covalent [Bruton tyrosine kinase inhibitors] is really dismal,” he said. “This has been shown by multiple groups now across the globe.”
Noncovalent Bruton tyrosine kinase inhibitors are now an option, he noted. “We do understand that they work for some patients, and it can be quite useful, but even noncovalent [Bruton tyrosine kinase inhibitors] themselves are susceptible to resistance mutations. We’ve seen that in the [chronic lymphocytic leukemia] world.”
Dr. Patel asked the audience, “Why not just give everybody CAR T-cells, post-[Bruton tyrosine kinase inhibitors]? You get a CAR T-cell! You get a CAR T-cell! Everybody gets one.”
However, he noted, “Unfortunately, mantle cell lymphoma patients experience the worst high-grade toxicity when receiving CD19[-targeted] CAR T-cells.”
Are there better options? At the moment, “really, really early data” suggest benefits from molecular glues and degraders, novel inhibitors, antibody-drug conjugates, novel CAR T-cells, and bispecific antibodies, Dr. Patel said.
“All of these tools are in clinical trials, and hopefully some of them will help,” he said.
Disclosures were not provided. Dr. Wagner-Johnston recently disclosed advisory committee/board of directors’ relationships with ADC Therapeutics, Regeneron, Calibr, and Verastem. Dr. Patel recently disclosed ties with a long list of pharmaceutical companies, including AbbVie, AstraZeneca, BeiGene, Bristol Myers Squibb, Genentech, Janssen, Merck, and others.
A version of this article first appeared on Medscape.com.
FROM SOHO 2024
Debate: Should Patients With CLL Take Breaks From Targeted Therapies?
At the annual meeting of the Society of Hematologic Oncology, two hematologist-oncologists — Inhye Ahn, MD, of Dana-Farber Cancer Institute in Boston, Massachusetts, and Kerry A. Rogers, MD, of Ohio State University in Columbus — faced off in a debate. Ahn said the drugs can indeed be discontinued, while Rogers argued against stopping the medications.
“When I talk to my own patient about standard of care options in CLL, I use the analogy of a marathon and a sprint,” Dr. Ahn said. A marathon refers to continuous treatment with Bruton’s kinase inhibitors given daily for years, while the sprint refers to the combination of venetoclax with an anti-CD20 monoclonal antibody given over 12 cycles for the frontline regimen and 2 years for refractory CLL.
“I tell them these are both considered very efficacious regimens and well tolerated, one is by IV [the venetoclax regimen] and the other isn’t [Bruton’s kinase inhibitors], and they have different toxicity profile. I ask them what would you do? The most common question that I get from my patient is, ‘why would anyone do a marathon?’ ”
It’s not solely the length of treatment that’s important, Dr. Ahn said, as toxicities from the long-term use of Bruton’s kinase inhibitors build up over time and can lead to hypertension, arrhythmia, and sudden cardiac death.
In addition, she said, infections can occur, as well as hampered vaccine response, an important risk in the era of the COVID-19 pandemic. The cost of the drugs is high and adds up over time, and continuous use can boost resistance.
Is there a way to turn the marathon of Bruton’s kinase inhibitor use into a sprint without hurting patients? The answer is yes, through temporary discontinuation, Dr. Ahn said, although she cautioned that early cessation could lead to disease flare. “We dipped into our own database of 84 CLL patients treated with ibrutinib, and our conclusion was that temporary dose interruption or dose reduction did not impact progression-free survival”
Moving forward, she said, “more research is needed to define the optimal regimen that would lead to treatment cessation, the optimal patient population, who would benefit most from the cessation strategy, treatment duration, and how we define success.” For her part, Dr. Rogers argued that the continuous use of Bruton’s kinase inhibitors is “really the most effective treatment we have in CLL.”
It’s clear that “responses deepen with continued treatment,” Dr. Rogers said, noting that remission times grow over years of treatment. She highlighted a 2022 study of patients with CLL who took ibrutinib that found complete remission or complete remission with incomplete hematologic recovery was 7% at 12 months and 34% at 7 years. When patients quit taking the drugs, “you don’t get to maximize your patient’s response to this treatment.”
Dr. Rogers also noted that the RESONATE-2 trial found that ibrutinib is linked to the longest median progression-free survival of any CLL treatment at 8.9 years. “That really struck me a very effective initial therapy.”
Indeed, “when you’re offering someone initial therapy with a Bruton’s kinase inhibitor as a continuous treatment strategy, you can tell people that they can expect a normal lifespan with this approach. That’s extremely important when you’re talking to patients about whether they might want to alter their leukemia treatment.”
Finally, she noted that discontinuation of ibrutinib was linked to shorter survival in early research. “This was the first suggestion that discontinuation is not good.”
Dr. Rogers said that discontinuing the drugs is sometimes necessary because of adverse events, but patients can “certainly switch to a more tolerable Bruton’s kinase inhibitor. With the options available today, that should be a strategy that’s considered.”
Audience members at the debate were invited to respond to a live online survey about whether Bruton’s kinase inhibitors can be discontinued. Among 49 respondents, most (52.3%) said no, 42.8% said yes, and the rest were undecided/other.
Disclosures for the speakers were not provided. Dr. Ahn disclosed consulting for BeiGene and AstraZeneca. Dr. Rogers disclosed receiving research funding from Genentech, AbbVie, Janssen, and Novartis; consulting for AstraZeneca, BeiGene, Janssen, Pharmacyclics, AbbVie, Genentech, and LOXO@Lilly; and receiving travel funding from AstraZeneca.
A version of this article appeared on Medscape.com.
At the annual meeting of the Society of Hematologic Oncology, two hematologist-oncologists — Inhye Ahn, MD, of Dana-Farber Cancer Institute in Boston, Massachusetts, and Kerry A. Rogers, MD, of Ohio State University in Columbus — faced off in a debate. Ahn said the drugs can indeed be discontinued, while Rogers argued against stopping the medications.
“When I talk to my own patient about standard of care options in CLL, I use the analogy of a marathon and a sprint,” Dr. Ahn said. A marathon refers to continuous treatment with Bruton’s kinase inhibitors given daily for years, while the sprint refers to the combination of venetoclax with an anti-CD20 monoclonal antibody given over 12 cycles for the frontline regimen and 2 years for refractory CLL.
“I tell them these are both considered very efficacious regimens and well tolerated, one is by IV [the venetoclax regimen] and the other isn’t [Bruton’s kinase inhibitors], and they have different toxicity profile. I ask them what would you do? The most common question that I get from my patient is, ‘why would anyone do a marathon?’ ”
It’s not solely the length of treatment that’s important, Dr. Ahn said, as toxicities from the long-term use of Bruton’s kinase inhibitors build up over time and can lead to hypertension, arrhythmia, and sudden cardiac death.
In addition, she said, infections can occur, as well as hampered vaccine response, an important risk in the era of the COVID-19 pandemic. The cost of the drugs is high and adds up over time, and continuous use can boost resistance.
Is there a way to turn the marathon of Bruton’s kinase inhibitor use into a sprint without hurting patients? The answer is yes, through temporary discontinuation, Dr. Ahn said, although she cautioned that early cessation could lead to disease flare. “We dipped into our own database of 84 CLL patients treated with ibrutinib, and our conclusion was that temporary dose interruption or dose reduction did not impact progression-free survival”
Moving forward, she said, “more research is needed to define the optimal regimen that would lead to treatment cessation, the optimal patient population, who would benefit most from the cessation strategy, treatment duration, and how we define success.” For her part, Dr. Rogers argued that the continuous use of Bruton’s kinase inhibitors is “really the most effective treatment we have in CLL.”
It’s clear that “responses deepen with continued treatment,” Dr. Rogers said, noting that remission times grow over years of treatment. She highlighted a 2022 study of patients with CLL who took ibrutinib that found complete remission or complete remission with incomplete hematologic recovery was 7% at 12 months and 34% at 7 years. When patients quit taking the drugs, “you don’t get to maximize your patient’s response to this treatment.”
Dr. Rogers also noted that the RESONATE-2 trial found that ibrutinib is linked to the longest median progression-free survival of any CLL treatment at 8.9 years. “That really struck me a very effective initial therapy.”
Indeed, “when you’re offering someone initial therapy with a Bruton’s kinase inhibitor as a continuous treatment strategy, you can tell people that they can expect a normal lifespan with this approach. That’s extremely important when you’re talking to patients about whether they might want to alter their leukemia treatment.”
Finally, she noted that discontinuation of ibrutinib was linked to shorter survival in early research. “This was the first suggestion that discontinuation is not good.”
Dr. Rogers said that discontinuing the drugs is sometimes necessary because of adverse events, but patients can “certainly switch to a more tolerable Bruton’s kinase inhibitor. With the options available today, that should be a strategy that’s considered.”
Audience members at the debate were invited to respond to a live online survey about whether Bruton’s kinase inhibitors can be discontinued. Among 49 respondents, most (52.3%) said no, 42.8% said yes, and the rest were undecided/other.
Disclosures for the speakers were not provided. Dr. Ahn disclosed consulting for BeiGene and AstraZeneca. Dr. Rogers disclosed receiving research funding from Genentech, AbbVie, Janssen, and Novartis; consulting for AstraZeneca, BeiGene, Janssen, Pharmacyclics, AbbVie, Genentech, and LOXO@Lilly; and receiving travel funding from AstraZeneca.
A version of this article appeared on Medscape.com.
At the annual meeting of the Society of Hematologic Oncology, two hematologist-oncologists — Inhye Ahn, MD, of Dana-Farber Cancer Institute in Boston, Massachusetts, and Kerry A. Rogers, MD, of Ohio State University in Columbus — faced off in a debate. Ahn said the drugs can indeed be discontinued, while Rogers argued against stopping the medications.
“When I talk to my own patient about standard of care options in CLL, I use the analogy of a marathon and a sprint,” Dr. Ahn said. A marathon refers to continuous treatment with Bruton’s kinase inhibitors given daily for years, while the sprint refers to the combination of venetoclax with an anti-CD20 monoclonal antibody given over 12 cycles for the frontline regimen and 2 years for refractory CLL.
“I tell them these are both considered very efficacious regimens and well tolerated, one is by IV [the venetoclax regimen] and the other isn’t [Bruton’s kinase inhibitors], and they have different toxicity profile. I ask them what would you do? The most common question that I get from my patient is, ‘why would anyone do a marathon?’ ”
It’s not solely the length of treatment that’s important, Dr. Ahn said, as toxicities from the long-term use of Bruton’s kinase inhibitors build up over time and can lead to hypertension, arrhythmia, and sudden cardiac death.
In addition, she said, infections can occur, as well as hampered vaccine response, an important risk in the era of the COVID-19 pandemic. The cost of the drugs is high and adds up over time, and continuous use can boost resistance.
Is there a way to turn the marathon of Bruton’s kinase inhibitor use into a sprint without hurting patients? The answer is yes, through temporary discontinuation, Dr. Ahn said, although she cautioned that early cessation could lead to disease flare. “We dipped into our own database of 84 CLL patients treated with ibrutinib, and our conclusion was that temporary dose interruption or dose reduction did not impact progression-free survival”
Moving forward, she said, “more research is needed to define the optimal regimen that would lead to treatment cessation, the optimal patient population, who would benefit most from the cessation strategy, treatment duration, and how we define success.” For her part, Dr. Rogers argued that the continuous use of Bruton’s kinase inhibitors is “really the most effective treatment we have in CLL.”
It’s clear that “responses deepen with continued treatment,” Dr. Rogers said, noting that remission times grow over years of treatment. She highlighted a 2022 study of patients with CLL who took ibrutinib that found complete remission or complete remission with incomplete hematologic recovery was 7% at 12 months and 34% at 7 years. When patients quit taking the drugs, “you don’t get to maximize your patient’s response to this treatment.”
Dr. Rogers also noted that the RESONATE-2 trial found that ibrutinib is linked to the longest median progression-free survival of any CLL treatment at 8.9 years. “That really struck me a very effective initial therapy.”
Indeed, “when you’re offering someone initial therapy with a Bruton’s kinase inhibitor as a continuous treatment strategy, you can tell people that they can expect a normal lifespan with this approach. That’s extremely important when you’re talking to patients about whether they might want to alter their leukemia treatment.”
Finally, she noted that discontinuation of ibrutinib was linked to shorter survival in early research. “This was the first suggestion that discontinuation is not good.”
Dr. Rogers said that discontinuing the drugs is sometimes necessary because of adverse events, but patients can “certainly switch to a more tolerable Bruton’s kinase inhibitor. With the options available today, that should be a strategy that’s considered.”
Audience members at the debate were invited to respond to a live online survey about whether Bruton’s kinase inhibitors can be discontinued. Among 49 respondents, most (52.3%) said no, 42.8% said yes, and the rest were undecided/other.
Disclosures for the speakers were not provided. Dr. Ahn disclosed consulting for BeiGene and AstraZeneca. Dr. Rogers disclosed receiving research funding from Genentech, AbbVie, Janssen, and Novartis; consulting for AstraZeneca, BeiGene, Janssen, Pharmacyclics, AbbVie, Genentech, and LOXO@Lilly; and receiving travel funding from AstraZeneca.
A version of this article appeared on Medscape.com.
FROM SOHO 2024
Could Aspirin Avert Bad Outcomes in Leukemia?
A new analysis hints that there may be a benefit from aspirin for hospitalized patients with leukemia. In a preliminary study, researchers found that aspirin users had much lower odds of intracranial bleeding, deep vein thrombosis, in-hospital mortality, and septic stroke.
Aspirin users also spent less time in the hospital and had less costly care.
No one is suggesting that clinicians give aspirin to hospitalized patients with leukemia when the drug is not otherwise indicated. However, the findings, released at the Society of Hematologic Oncology (SOHO 2024) meeting in Houston, do indicate that more research is warranted, study lead author Jayalekshmi Jayakumar, MD, of the Brooklyn Hospital Center in New York City, said in a presentation.
“We hope our study can act as background for further prospective and experimental studies to explore this association,” she said. “If we can establish causation, then aspirin has a potential to be a thromboprophylactic agent to enhance outcomes and reduce resource utilization among leukemia hospitalizations.”
Dr. Jayakumar noted that previous research has suggested aspirin may help prevent deep vein thrombosis in patients with breast and pancreatic cancer. And in blood cancer, animal research has suggested that aspirin may “promote apoptosis in leukemia cells and decrease the spread of leukemia cells through platelet inhibition,” she said.
However, “we do not have any prospective or retrospective studies to establish causation or to see if this actually has some value within the clinical practice,” she noted.
Dr. Jayakumar stated that new study aims to detect whether aspirin may be beneficial in leukemia. She and her colleagues retrospectively tracked 1,663,149 US hospitalizations of patients with leukemia from 2016 to 2020 via the National Inpatient Sample. Of those patients, 11.2% used aspirin, although the data didn’t say whether they started it during hospitalization, and dosages were not reported. Aspirin users were older (mean age, 74.53 years vs 64.83 years in nonusers).
After adjustment for confounders, aspirin users had lower odds of several conditions than nonusers:
- Epistaxis (odds ratio [OR], 0.63; 95% CI, 0.55-0.72; P < .001)
- Hemoptysis (OR, 0.71; 95% CI, 0.61-0.82; P < .001)
- Intracranial bleed (OR, 0.74; 95% CI, 0.64-0.85; P < .001)
- Deep vein thrombosis (OR, 0.72; 95% CI, 0.66-0.78; P < .001)
- In-hospital mortality (OR, 0.54; 95% CI, 0.50-0.58; P < .001)
- Sepsis (OR, 0.71; 95% CI, 0.68-0.75; P < .001)
- Septic shock (OR, 0.55; 95% CI, 0.50-0.60; P < .001)
There was no association reported for gastrointestinal bleeding, a possible side effect of aspirin use, or tumor lysis syndrome. Aspirin users also had a shorter typical stay (−2.8 days) and lower typical hospital charges ($40,719).
“We also found that aspirin users had a slightly reduced risk of minor bleeding and infection compared to non–aspirin users,” Dr. Jayakumar said.
In an interview, Dr. Jayakumar noted that the study is retrospective and declined to speculate on why aspirin may have benefits or why it may have the seemingly contradictory effect of reducing both blood clots and bleeding.
Aspirin is one of the least expensive drugs in existence.
In an interview, Richard M. Stone, MD, oncologist at Dana-Farber Cancer Institute in Boston, who’s familiar with the study findings but didn’t take part in the research, said the findings are “totally counterintuitive.”
“It doesn’t mean they should be rejected, but they should be highly scrutinized,” he said.
Dr. Stone added that bleeding is a major risk in leukemia due to low platelet counts, although platelet transplants can be helpful, and patients rarely die of bleeding. Thrombosis is also a problem in leukemia, he said, and it’s being increasingly recognized as a risk in acute myeloid leukemia.
No funding was reported. Dr. Jayakumar and Dr. Stone had no disclosures.
A version of this article appeared on Medscape.com.
A new analysis hints that there may be a benefit from aspirin for hospitalized patients with leukemia. In a preliminary study, researchers found that aspirin users had much lower odds of intracranial bleeding, deep vein thrombosis, in-hospital mortality, and septic stroke.
Aspirin users also spent less time in the hospital and had less costly care.
No one is suggesting that clinicians give aspirin to hospitalized patients with leukemia when the drug is not otherwise indicated. However, the findings, released at the Society of Hematologic Oncology (SOHO 2024) meeting in Houston, do indicate that more research is warranted, study lead author Jayalekshmi Jayakumar, MD, of the Brooklyn Hospital Center in New York City, said in a presentation.
“We hope our study can act as background for further prospective and experimental studies to explore this association,” she said. “If we can establish causation, then aspirin has a potential to be a thromboprophylactic agent to enhance outcomes and reduce resource utilization among leukemia hospitalizations.”
Dr. Jayakumar noted that previous research has suggested aspirin may help prevent deep vein thrombosis in patients with breast and pancreatic cancer. And in blood cancer, animal research has suggested that aspirin may “promote apoptosis in leukemia cells and decrease the spread of leukemia cells through platelet inhibition,” she said.
However, “we do not have any prospective or retrospective studies to establish causation or to see if this actually has some value within the clinical practice,” she noted.
Dr. Jayakumar stated that new study aims to detect whether aspirin may be beneficial in leukemia. She and her colleagues retrospectively tracked 1,663,149 US hospitalizations of patients with leukemia from 2016 to 2020 via the National Inpatient Sample. Of those patients, 11.2% used aspirin, although the data didn’t say whether they started it during hospitalization, and dosages were not reported. Aspirin users were older (mean age, 74.53 years vs 64.83 years in nonusers).
After adjustment for confounders, aspirin users had lower odds of several conditions than nonusers:
- Epistaxis (odds ratio [OR], 0.63; 95% CI, 0.55-0.72; P < .001)
- Hemoptysis (OR, 0.71; 95% CI, 0.61-0.82; P < .001)
- Intracranial bleed (OR, 0.74; 95% CI, 0.64-0.85; P < .001)
- Deep vein thrombosis (OR, 0.72; 95% CI, 0.66-0.78; P < .001)
- In-hospital mortality (OR, 0.54; 95% CI, 0.50-0.58; P < .001)
- Sepsis (OR, 0.71; 95% CI, 0.68-0.75; P < .001)
- Septic shock (OR, 0.55; 95% CI, 0.50-0.60; P < .001)
There was no association reported for gastrointestinal bleeding, a possible side effect of aspirin use, or tumor lysis syndrome. Aspirin users also had a shorter typical stay (−2.8 days) and lower typical hospital charges ($40,719).
“We also found that aspirin users had a slightly reduced risk of minor bleeding and infection compared to non–aspirin users,” Dr. Jayakumar said.
In an interview, Dr. Jayakumar noted that the study is retrospective and declined to speculate on why aspirin may have benefits or why it may have the seemingly contradictory effect of reducing both blood clots and bleeding.
Aspirin is one of the least expensive drugs in existence.
In an interview, Richard M. Stone, MD, oncologist at Dana-Farber Cancer Institute in Boston, who’s familiar with the study findings but didn’t take part in the research, said the findings are “totally counterintuitive.”
“It doesn’t mean they should be rejected, but they should be highly scrutinized,” he said.
Dr. Stone added that bleeding is a major risk in leukemia due to low platelet counts, although platelet transplants can be helpful, and patients rarely die of bleeding. Thrombosis is also a problem in leukemia, he said, and it’s being increasingly recognized as a risk in acute myeloid leukemia.
No funding was reported. Dr. Jayakumar and Dr. Stone had no disclosures.
A version of this article appeared on Medscape.com.
A new analysis hints that there may be a benefit from aspirin for hospitalized patients with leukemia. In a preliminary study, researchers found that aspirin users had much lower odds of intracranial bleeding, deep vein thrombosis, in-hospital mortality, and septic stroke.
Aspirin users also spent less time in the hospital and had less costly care.
No one is suggesting that clinicians give aspirin to hospitalized patients with leukemia when the drug is not otherwise indicated. However, the findings, released at the Society of Hematologic Oncology (SOHO 2024) meeting in Houston, do indicate that more research is warranted, study lead author Jayalekshmi Jayakumar, MD, of the Brooklyn Hospital Center in New York City, said in a presentation.
“We hope our study can act as background for further prospective and experimental studies to explore this association,” she said. “If we can establish causation, then aspirin has a potential to be a thromboprophylactic agent to enhance outcomes and reduce resource utilization among leukemia hospitalizations.”
Dr. Jayakumar noted that previous research has suggested aspirin may help prevent deep vein thrombosis in patients with breast and pancreatic cancer. And in blood cancer, animal research has suggested that aspirin may “promote apoptosis in leukemia cells and decrease the spread of leukemia cells through platelet inhibition,” she said.
However, “we do not have any prospective or retrospective studies to establish causation or to see if this actually has some value within the clinical practice,” she noted.
Dr. Jayakumar stated that new study aims to detect whether aspirin may be beneficial in leukemia. She and her colleagues retrospectively tracked 1,663,149 US hospitalizations of patients with leukemia from 2016 to 2020 via the National Inpatient Sample. Of those patients, 11.2% used aspirin, although the data didn’t say whether they started it during hospitalization, and dosages were not reported. Aspirin users were older (mean age, 74.53 years vs 64.83 years in nonusers).
After adjustment for confounders, aspirin users had lower odds of several conditions than nonusers:
- Epistaxis (odds ratio [OR], 0.63; 95% CI, 0.55-0.72; P < .001)
- Hemoptysis (OR, 0.71; 95% CI, 0.61-0.82; P < .001)
- Intracranial bleed (OR, 0.74; 95% CI, 0.64-0.85; P < .001)
- Deep vein thrombosis (OR, 0.72; 95% CI, 0.66-0.78; P < .001)
- In-hospital mortality (OR, 0.54; 95% CI, 0.50-0.58; P < .001)
- Sepsis (OR, 0.71; 95% CI, 0.68-0.75; P < .001)
- Septic shock (OR, 0.55; 95% CI, 0.50-0.60; P < .001)
There was no association reported for gastrointestinal bleeding, a possible side effect of aspirin use, or tumor lysis syndrome. Aspirin users also had a shorter typical stay (−2.8 days) and lower typical hospital charges ($40,719).
“We also found that aspirin users had a slightly reduced risk of minor bleeding and infection compared to non–aspirin users,” Dr. Jayakumar said.
In an interview, Dr. Jayakumar noted that the study is retrospective and declined to speculate on why aspirin may have benefits or why it may have the seemingly contradictory effect of reducing both blood clots and bleeding.
Aspirin is one of the least expensive drugs in existence.
In an interview, Richard M. Stone, MD, oncologist at Dana-Farber Cancer Institute in Boston, who’s familiar with the study findings but didn’t take part in the research, said the findings are “totally counterintuitive.”
“It doesn’t mean they should be rejected, but they should be highly scrutinized,” he said.
Dr. Stone added that bleeding is a major risk in leukemia due to low platelet counts, although platelet transplants can be helpful, and patients rarely die of bleeding. Thrombosis is also a problem in leukemia, he said, and it’s being increasingly recognized as a risk in acute myeloid leukemia.
No funding was reported. Dr. Jayakumar and Dr. Stone had no disclosures.
A version of this article appeared on Medscape.com.
FROM SOHO 2024
To Choose the Best First-line Drug for CML, Consider Efficacy and Cost
When it comes to selecting a cost-effective, first-line tyrosine kinase inhibitor (TKI) for the treatment of chronic myeloid leukemia (CML), consider the treatment goal.
For survival, generic imatinib remains the gold standard, Elias Jabbour, MD, said during a session at the annual meeting of the Society of Hematologic Oncology in Houston.
For treatment-free remission, generic dasatinib or another generic second-generation TKI is needed, but not yet available in the United States, so generic imatinib is the best current choice, said Dr. Jabbour, a professor of medicine in the Department of Leukemia at the University of Texas MD Anderson Cancer Center, Houston.
Prior to the availability of generic imatinib, that wasn’t the case, he noted, explaining that second-generation TKIs met the cost-efficacy criteria, but now — at about $35 per month or about $400 per year — imatinib is far less expensive than the approximately $250,000 per year that brand-name second- and third-generation TKIs can currently cost.
To have treatment value, any new TKI should cost $40,000-$50,000 per quality-adjusted life-year, which is defined as the quality and duration of life after a novel TKI vs with the existing standard of care, Dr. Jabbour said.
And to qualify as a frontline therapy for CML, any new TKI should show efficacy superior to second-generation TKIs, in addition to meeting the cost-effectiveness criteria.
“It is hard to show survival benefit anymore, but we need to improve on the rate of durable deep molecular remission,” he said.
An equivalent or better long-term safety profile over at least 7-8 years is also needed.
Based on the current literature, none of the TKIs currently being evaluated has met that standard, although some trials are ongoing.
In a recent editorial, Dr. Jabbour and colleagues outlined treatment recommendations based on the currently available data. They suggested using lower-than-approved doses of TKIs in both frontline and later therapies to reduce toxicity, improve treatment compliance, and reduce costs.
They also suggested that the absence of an early molecular response might not warrant changing the TKI, especially when a second-generation TKI was used first line.
When treatment-free remission is not a therapeutic goal or is unlikely, changing the TKI to improve the depth of molecular response, which has been shown to improve the likelihood of treatment-free remission, could do more harm than good, they argued.
Instead, consider reducing the dose to manage reversible side effects, they suggested, noting that generic imatinib, and eventually generic dasatinib and possibly other generic second-generation TKIs, will likely offer 90% of patients with CML an effective, safe, and affordable treatment that normalizes life expectancy and leads to treatment-free remission in 30%-50% of patients over time.
Dr. Jabbour disclosed ties with AbbVie, Almoosa Specialist Hospital, Amgen, Ascentage Pharma, Biologix FZ, Hikma Pharmaceuticals, Kite, Takeda, and Terns.
A version of this article first appeared on Medscape.com.
When it comes to selecting a cost-effective, first-line tyrosine kinase inhibitor (TKI) for the treatment of chronic myeloid leukemia (CML), consider the treatment goal.
For survival, generic imatinib remains the gold standard, Elias Jabbour, MD, said during a session at the annual meeting of the Society of Hematologic Oncology in Houston.
For treatment-free remission, generic dasatinib or another generic second-generation TKI is needed, but not yet available in the United States, so generic imatinib is the best current choice, said Dr. Jabbour, a professor of medicine in the Department of Leukemia at the University of Texas MD Anderson Cancer Center, Houston.
Prior to the availability of generic imatinib, that wasn’t the case, he noted, explaining that second-generation TKIs met the cost-efficacy criteria, but now — at about $35 per month or about $400 per year — imatinib is far less expensive than the approximately $250,000 per year that brand-name second- and third-generation TKIs can currently cost.
To have treatment value, any new TKI should cost $40,000-$50,000 per quality-adjusted life-year, which is defined as the quality and duration of life after a novel TKI vs with the existing standard of care, Dr. Jabbour said.
And to qualify as a frontline therapy for CML, any new TKI should show efficacy superior to second-generation TKIs, in addition to meeting the cost-effectiveness criteria.
“It is hard to show survival benefit anymore, but we need to improve on the rate of durable deep molecular remission,” he said.
An equivalent or better long-term safety profile over at least 7-8 years is also needed.
Based on the current literature, none of the TKIs currently being evaluated has met that standard, although some trials are ongoing.
In a recent editorial, Dr. Jabbour and colleagues outlined treatment recommendations based on the currently available data. They suggested using lower-than-approved doses of TKIs in both frontline and later therapies to reduce toxicity, improve treatment compliance, and reduce costs.
They also suggested that the absence of an early molecular response might not warrant changing the TKI, especially when a second-generation TKI was used first line.
When treatment-free remission is not a therapeutic goal or is unlikely, changing the TKI to improve the depth of molecular response, which has been shown to improve the likelihood of treatment-free remission, could do more harm than good, they argued.
Instead, consider reducing the dose to manage reversible side effects, they suggested, noting that generic imatinib, and eventually generic dasatinib and possibly other generic second-generation TKIs, will likely offer 90% of patients with CML an effective, safe, and affordable treatment that normalizes life expectancy and leads to treatment-free remission in 30%-50% of patients over time.
Dr. Jabbour disclosed ties with AbbVie, Almoosa Specialist Hospital, Amgen, Ascentage Pharma, Biologix FZ, Hikma Pharmaceuticals, Kite, Takeda, and Terns.
A version of this article first appeared on Medscape.com.
When it comes to selecting a cost-effective, first-line tyrosine kinase inhibitor (TKI) for the treatment of chronic myeloid leukemia (CML), consider the treatment goal.
For survival, generic imatinib remains the gold standard, Elias Jabbour, MD, said during a session at the annual meeting of the Society of Hematologic Oncology in Houston.
For treatment-free remission, generic dasatinib or another generic second-generation TKI is needed, but not yet available in the United States, so generic imatinib is the best current choice, said Dr. Jabbour, a professor of medicine in the Department of Leukemia at the University of Texas MD Anderson Cancer Center, Houston.
Prior to the availability of generic imatinib, that wasn’t the case, he noted, explaining that second-generation TKIs met the cost-efficacy criteria, but now — at about $35 per month or about $400 per year — imatinib is far less expensive than the approximately $250,000 per year that brand-name second- and third-generation TKIs can currently cost.
To have treatment value, any new TKI should cost $40,000-$50,000 per quality-adjusted life-year, which is defined as the quality and duration of life after a novel TKI vs with the existing standard of care, Dr. Jabbour said.
And to qualify as a frontline therapy for CML, any new TKI should show efficacy superior to second-generation TKIs, in addition to meeting the cost-effectiveness criteria.
“It is hard to show survival benefit anymore, but we need to improve on the rate of durable deep molecular remission,” he said.
An equivalent or better long-term safety profile over at least 7-8 years is also needed.
Based on the current literature, none of the TKIs currently being evaluated has met that standard, although some trials are ongoing.
In a recent editorial, Dr. Jabbour and colleagues outlined treatment recommendations based on the currently available data. They suggested using lower-than-approved doses of TKIs in both frontline and later therapies to reduce toxicity, improve treatment compliance, and reduce costs.
They also suggested that the absence of an early molecular response might not warrant changing the TKI, especially when a second-generation TKI was used first line.
When treatment-free remission is not a therapeutic goal or is unlikely, changing the TKI to improve the depth of molecular response, which has been shown to improve the likelihood of treatment-free remission, could do more harm than good, they argued.
Instead, consider reducing the dose to manage reversible side effects, they suggested, noting that generic imatinib, and eventually generic dasatinib and possibly other generic second-generation TKIs, will likely offer 90% of patients with CML an effective, safe, and affordable treatment that normalizes life expectancy and leads to treatment-free remission in 30%-50% of patients over time.
Dr. Jabbour disclosed ties with AbbVie, Almoosa Specialist Hospital, Amgen, Ascentage Pharma, Biologix FZ, Hikma Pharmaceuticals, Kite, Takeda, and Terns.
A version of this article first appeared on Medscape.com.
FROM SOHO 2024