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Research and Reviews for the Practicing Oncologist
Sizing up the costs and availability of drugs
It is ironic that as oncologists struggle to get the time-tested, “good old drugs,” which are less expensive but nevertheless essential for many standard chemotherapy regimens, some drug companies are coming out with extremely expensive new drugs. It seems that in their quest for conquering new markets and providing new drug indications, none is looking out for the interests of our patients. Oncologists are the strongest advocates for their patients, and it is important that we are proactive when it comes to addressing the extremely sensitive topic of drug shortages. New, prohibitively expensive drugs might make sense from a dollars-and-cents perspective, but not from the patient or oncologist perspective.
In a Commentary on page 277, my co-editor Debra Patt examines the causes of the drug shortages and offers some possible solutions for alleviating them...
*For a PDF of the full article, click on the link to the left of this introduction.
It is ironic that as oncologists struggle to get the time-tested, “good old drugs,” which are less expensive but nevertheless essential for many standard chemotherapy regimens, some drug companies are coming out with extremely expensive new drugs. It seems that in their quest for conquering new markets and providing new drug indications, none is looking out for the interests of our patients. Oncologists are the strongest advocates for their patients, and it is important that we are proactive when it comes to addressing the extremely sensitive topic of drug shortages. New, prohibitively expensive drugs might make sense from a dollars-and-cents perspective, but not from the patient or oncologist perspective.
In a Commentary on page 277, my co-editor Debra Patt examines the causes of the drug shortages and offers some possible solutions for alleviating them...
*For a PDF of the full article, click on the link to the left of this introduction.
It is ironic that as oncologists struggle to get the time-tested, “good old drugs,” which are less expensive but nevertheless essential for many standard chemotherapy regimens, some drug companies are coming out with extremely expensive new drugs. It seems that in their quest for conquering new markets and providing new drug indications, none is looking out for the interests of our patients. Oncologists are the strongest advocates for their patients, and it is important that we are proactive when it comes to addressing the extremely sensitive topic of drug shortages. New, prohibitively expensive drugs might make sense from a dollars-and-cents perspective, but not from the patient or oncologist perspective.
In a Commentary on page 277, my co-editor Debra Patt examines the causes of the drug shortages and offers some possible solutions for alleviating them...
*For a PDF of the full article, click on the link to the left of this introduction.
Navigating the drug shortages
In November 2010, pharmacists at Georgia Cancer Specialists, a private cancer practice with 27 offices, noticed our first instance of the latest wave of drug shortages. We had tried to place an order for doxorubicin, but our primary wholesaler was not able to fill it. We also discovered that our secondary wholesalers had little or no available doxorubicin, and that some suppliers had increased their prices for the drug to such an extent that it was out of our reach. We began to take inventory of the doxorubicin that we had in all of our offices. At that point, we realized we had a crisis on our hands...
*For a PDF of the full article and accompanying Commentary, click on the links to the left of this introduction.
In November 2010, pharmacists at Georgia Cancer Specialists, a private cancer practice with 27 offices, noticed our first instance of the latest wave of drug shortages. We had tried to place an order for doxorubicin, but our primary wholesaler was not able to fill it. We also discovered that our secondary wholesalers had little or no available doxorubicin, and that some suppliers had increased their prices for the drug to such an extent that it was out of our reach. We began to take inventory of the doxorubicin that we had in all of our offices. At that point, we realized we had a crisis on our hands...
*For a PDF of the full article and accompanying Commentary, click on the links to the left of this introduction.
In November 2010, pharmacists at Georgia Cancer Specialists, a private cancer practice with 27 offices, noticed our first instance of the latest wave of drug shortages. We had tried to place an order for doxorubicin, but our primary wholesaler was not able to fill it. We also discovered that our secondary wholesalers had little or no available doxorubicin, and that some suppliers had increased their prices for the drug to such an extent that it was out of our reach. We began to take inventory of the doxorubicin that we had in all of our offices. At that point, we realized we had a crisis on our hands...
*For a PDF of the full article and accompanying Commentary, click on the links to the left of this introduction.
Intravenous iron in chemotherapy and cancer-related anemia
Recent guidance from the Centers for Medicare and Medicaid Services restricting erythropoiesis-stimulating agents (ESAs) in chemotherapy and cancer-related anemias has resulted in an increase in transfusions. Nine studies, without published contradictory evidence, have shown optimization of the response to ESAs by intravenous (IV) iron when the iron was added to the treatment of chemotherapy-induced anemia. The synergy observed, although greater in iron deficiency, was independent of pretreatment iron parameters. Three studies demonstrated decreased transfusions when IV iron is administered without ESAs. Discordant recommendations regarding IV iron currently exist among the American Society of Hematology/American Society of Clinical Oncology guidelines, the National Comprehensive Cancer Network, and the European Society of Medical Oncology. This discordance is at least partly the result of misconceptions about the clinical nature and incidence of adverse effects with IV iron. Other reasons for this discordance are presented in this review. Based on thousands of studied patients, we conclude that IV iron is safe and probably safer than most physicians realize. Education is needed relating to the interpretation of minor, subclinical infusion reactions that resolve without therapy. IV iron without ESAs may be an effective treatment for chemotherapy-induced anemia and warrants further study. We present evidence supporting the conclusion that baseline serum hepcidin levels may predict responses to IV iron, and we examine the published evidence supporting the conclusion that IV iron should be a standard addition to the management of chemotherapy and cancer-related anemia.
Click on the PDF icon at the top of this introduction to read the full article.
Recent guidance from the Centers for Medicare and Medicaid Services restricting erythropoiesis-stimulating agents (ESAs) in chemotherapy and cancer-related anemias has resulted in an increase in transfusions. Nine studies, without published contradictory evidence, have shown optimization of the response to ESAs by intravenous (IV) iron when the iron was added to the treatment of chemotherapy-induced anemia. The synergy observed, although greater in iron deficiency, was independent of pretreatment iron parameters. Three studies demonstrated decreased transfusions when IV iron is administered without ESAs. Discordant recommendations regarding IV iron currently exist among the American Society of Hematology/American Society of Clinical Oncology guidelines, the National Comprehensive Cancer Network, and the European Society of Medical Oncology. This discordance is at least partly the result of misconceptions about the clinical nature and incidence of adverse effects with IV iron. Other reasons for this discordance are presented in this review. Based on thousands of studied patients, we conclude that IV iron is safe and probably safer than most physicians realize. Education is needed relating to the interpretation of minor, subclinical infusion reactions that resolve without therapy. IV iron without ESAs may be an effective treatment for chemotherapy-induced anemia and warrants further study. We present evidence supporting the conclusion that baseline serum hepcidin levels may predict responses to IV iron, and we examine the published evidence supporting the conclusion that IV iron should be a standard addition to the management of chemotherapy and cancer-related anemia.
Click on the PDF icon at the top of this introduction to read the full article.
Recent guidance from the Centers for Medicare and Medicaid Services restricting erythropoiesis-stimulating agents (ESAs) in chemotherapy and cancer-related anemias has resulted in an increase in transfusions. Nine studies, without published contradictory evidence, have shown optimization of the response to ESAs by intravenous (IV) iron when the iron was added to the treatment of chemotherapy-induced anemia. The synergy observed, although greater in iron deficiency, was independent of pretreatment iron parameters. Three studies demonstrated decreased transfusions when IV iron is administered without ESAs. Discordant recommendations regarding IV iron currently exist among the American Society of Hematology/American Society of Clinical Oncology guidelines, the National Comprehensive Cancer Network, and the European Society of Medical Oncology. This discordance is at least partly the result of misconceptions about the clinical nature and incidence of adverse effects with IV iron. Other reasons for this discordance are presented in this review. Based on thousands of studied patients, we conclude that IV iron is safe and probably safer than most physicians realize. Education is needed relating to the interpretation of minor, subclinical infusion reactions that resolve without therapy. IV iron without ESAs may be an effective treatment for chemotherapy-induced anemia and warrants further study. We present evidence supporting the conclusion that baseline serum hepcidin levels may predict responses to IV iron, and we examine the published evidence supporting the conclusion that IV iron should be a standard addition to the management of chemotherapy and cancer-related anemia.
Click on the PDF icon at the top of this introduction to read the full article.
Community Oncology Podcast - Abiraterone in metastatic prostate cancer
Editor-in-chief Dr. David H. Henry takes you on an audio tour of the August issue of Community Oncology featuring a Community Translation: Abiraterone boosts survival in metastatic prostate cancer and a review on maintenance therapy in solid tumors.
Editor-in-chief Dr. David H. Henry takes you on an audio tour of the August issue of Community Oncology featuring a Community Translation: Abiraterone boosts survival in metastatic prostate cancer and a review on maintenance therapy in solid tumors.
Editor-in-chief Dr. David H. Henry takes you on an audio tour of the August issue of Community Oncology featuring a Community Translation: Abiraterone boosts survival in metastatic prostate cancer and a review on maintenance therapy in solid tumors.
Abiraterone increases survival in metastatic prostate cancer
Biosynthesis of extragonadal androgen may contribute to the progression of castration-resistant prostate cancer. Abiraterone acetate is a selective
inhibitor of androgen biosynthesis that acts by inhibiting cytochrome P450 c17, a critical enzyme in testosterone synthesis, and thereby inhibiting androgen synthesis by the adrenal glands and testis and within the prostate tumor. In 2011, abiraterone was approved by the Food and Drug Administration for use in combination with prednisone for the treatment of patients with metastatic castration-resistant prostate cancer who have received previous chemotherapy containing docetaxel.1,2
*For PDFs of the full Community Translations article and accompanying Commentary, click on the links to the left of this introduction.
Biosynthesis of extragonadal androgen may contribute to the progression of castration-resistant prostate cancer. Abiraterone acetate is a selective
inhibitor of androgen biosynthesis that acts by inhibiting cytochrome P450 c17, a critical enzyme in testosterone synthesis, and thereby inhibiting androgen synthesis by the adrenal glands and testis and within the prostate tumor. In 2011, abiraterone was approved by the Food and Drug Administration for use in combination with prednisone for the treatment of patients with metastatic castration-resistant prostate cancer who have received previous chemotherapy containing docetaxel.1,2
*For PDFs of the full Community Translations article and accompanying Commentary, click on the links to the left of this introduction.
Biosynthesis of extragonadal androgen may contribute to the progression of castration-resistant prostate cancer. Abiraterone acetate is a selective
inhibitor of androgen biosynthesis that acts by inhibiting cytochrome P450 c17, a critical enzyme in testosterone synthesis, and thereby inhibiting androgen synthesis by the adrenal glands and testis and within the prostate tumor. In 2011, abiraterone was approved by the Food and Drug Administration for use in combination with prednisone for the treatment of patients with metastatic castration-resistant prostate cancer who have received previous chemotherapy containing docetaxel.1,2
*For PDFs of the full Community Translations article and accompanying Commentary, click on the links to the left of this introduction.
Nutrition and exercise in cancer survivors
Obesity has reached epidemic proportions in the United States in the past 2 decades. According to a recent report, 36% of the adult population currently has a body mass index of more than 30 kg/m2, which is the diagnostic for obesity.1 If we focus only on the US adult cancer survivor population, then the magnitude of being overweight or obese is notably higher, ranging from 52% to 68%.2 In adult survivors of childhood cancer, several factors are associated with increased risk for obesity, such as hypothalamic or pituitary radiation, the use of certain antidepressants, and lifestyle factors.3
*For a PDF of the full article, click on the link to the left of this introduction.
Obesity has reached epidemic proportions in the United States in the past 2 decades. According to a recent report, 36% of the adult population currently has a body mass index of more than 30 kg/m2, which is the diagnostic for obesity.1 If we focus only on the US adult cancer survivor population, then the magnitude of being overweight or obese is notably higher, ranging from 52% to 68%.2 In adult survivors of childhood cancer, several factors are associated with increased risk for obesity, such as hypothalamic or pituitary radiation, the use of certain antidepressants, and lifestyle factors.3
*For a PDF of the full article, click on the link to the left of this introduction.
Obesity has reached epidemic proportions in the United States in the past 2 decades. According to a recent report, 36% of the adult population currently has a body mass index of more than 30 kg/m2, which is the diagnostic for obesity.1 If we focus only on the US adult cancer survivor population, then the magnitude of being overweight or obese is notably higher, ranging from 52% to 68%.2 In adult survivors of childhood cancer, several factors are associated with increased risk for obesity, such as hypothalamic or pituitary radiation, the use of certain antidepressants, and lifestyle factors.3
*For a PDF of the full article, click on the link to the left of this introduction.
Nasal septum perforation induced by bevacizumab therapy in patients with breast cancer
Bevacizumab is a recombinant monoclonal immunoglobulin G1 antibody that selectively binds to vascular endothelial growth factor (VEGF), thus preventing it from binding to the VEGF receptors, VEGFR-1 and VEGFR-2, which leads to the inhibition of angiogenesis.1 Numerous landmark clinical trials have shown overall and/or progression-free survival benefit with bevacizumab-based chemotherapy regimens for patients with metastatic colorectal,2,3 lung,4 breast,5 and renal cell6 carcinomas.
*For a PDF of the full article, click on the link to the left of this introduction.
Bevacizumab is a recombinant monoclonal immunoglobulin G1 antibody that selectively binds to vascular endothelial growth factor (VEGF), thus preventing it from binding to the VEGF receptors, VEGFR-1 and VEGFR-2, which leads to the inhibition of angiogenesis.1 Numerous landmark clinical trials have shown overall and/or progression-free survival benefit with bevacizumab-based chemotherapy regimens for patients with metastatic colorectal,2,3 lung,4 breast,5 and renal cell6 carcinomas.
*For a PDF of the full article, click on the link to the left of this introduction.
Bevacizumab is a recombinant monoclonal immunoglobulin G1 antibody that selectively binds to vascular endothelial growth factor (VEGF), thus preventing it from binding to the VEGF receptors, VEGFR-1 and VEGFR-2, which leads to the inhibition of angiogenesis.1 Numerous landmark clinical trials have shown overall and/or progression-free survival benefit with bevacizumab-based chemotherapy regimens for patients with metastatic colorectal,2,3 lung,4 breast,5 and renal cell6 carcinomas.
*For a PDF of the full article, click on the link to the left of this introduction.
PCA3 permutation increases the prostate biopsy yield
Background: A direct correlation between the preoperative prostate cancer antigen 3 (PCA3) gene and total tumor volume in postprostatectomy specimens has recently been reported. This suggests that the PCA3 score could serve as a surrogate for tumor burden in patients with prostate cancer. Accordingly, the PCA3 density (that is, the ratio of the PCA3 score to prostate volume) is representative of the degree of prostate volume occupied by tumor.
Objective: To show that the PCA3 density would be directly related to the likelihood of finding cancer on prostate biopsy, given that larger tumors in smaller glands would be more likely to be detected through prostate biopsy.
Methods: We identified 288 men referred for prostate biopsy for an elevated prostate-specific antigen (PSA) level, high PSA velocity, low free- to total-PSA ratio, or suspicious digital rectal exam. All of the patients had had a urinary PCA3 test performed no more than 4 weeks before biopsy, and prostate volume was recorded by transrectal ultrasound determination at the time of biopsy. The diagnostic yield of PSA level, PSA density (PSAD), PCA3 score, and PCA3 density in detecting cancer was evaluated using a receiver operating characteristic (ROC) curve.
Results: Of the 288 patients included for analysis, 183 (63.5%) underwent an initial prostate biopsy and 105 (36.5%) had at least 1 previous negative biopsy. Cancer was detected in 74 (25.7%) patients. The area under the curve was 0.486 for PSA level, 0.590 for PSAD, 0.687 for PCA3 score, and 0.717 for PCA3 density.
Conclusion: PCA3 density is strongly correlated with cancer detection and may be useful in selecting patients for biopsy.
*For a PDF of the full article, click on the link to the left of this introduction.
Background: A direct correlation between the preoperative prostate cancer antigen 3 (PCA3) gene and total tumor volume in postprostatectomy specimens has recently been reported. This suggests that the PCA3 score could serve as a surrogate for tumor burden in patients with prostate cancer. Accordingly, the PCA3 density (that is, the ratio of the PCA3 score to prostate volume) is representative of the degree of prostate volume occupied by tumor.
Objective: To show that the PCA3 density would be directly related to the likelihood of finding cancer on prostate biopsy, given that larger tumors in smaller glands would be more likely to be detected through prostate biopsy.
Methods: We identified 288 men referred for prostate biopsy for an elevated prostate-specific antigen (PSA) level, high PSA velocity, low free- to total-PSA ratio, or suspicious digital rectal exam. All of the patients had had a urinary PCA3 test performed no more than 4 weeks before biopsy, and prostate volume was recorded by transrectal ultrasound determination at the time of biopsy. The diagnostic yield of PSA level, PSA density (PSAD), PCA3 score, and PCA3 density in detecting cancer was evaluated using a receiver operating characteristic (ROC) curve.
Results: Of the 288 patients included for analysis, 183 (63.5%) underwent an initial prostate biopsy and 105 (36.5%) had at least 1 previous negative biopsy. Cancer was detected in 74 (25.7%) patients. The area under the curve was 0.486 for PSA level, 0.590 for PSAD, 0.687 for PCA3 score, and 0.717 for PCA3 density.
Conclusion: PCA3 density is strongly correlated with cancer detection and may be useful in selecting patients for biopsy.
*For a PDF of the full article, click on the link to the left of this introduction.
Background: A direct correlation between the preoperative prostate cancer antigen 3 (PCA3) gene and total tumor volume in postprostatectomy specimens has recently been reported. This suggests that the PCA3 score could serve as a surrogate for tumor burden in patients with prostate cancer. Accordingly, the PCA3 density (that is, the ratio of the PCA3 score to prostate volume) is representative of the degree of prostate volume occupied by tumor.
Objective: To show that the PCA3 density would be directly related to the likelihood of finding cancer on prostate biopsy, given that larger tumors in smaller glands would be more likely to be detected through prostate biopsy.
Methods: We identified 288 men referred for prostate biopsy for an elevated prostate-specific antigen (PSA) level, high PSA velocity, low free- to total-PSA ratio, or suspicious digital rectal exam. All of the patients had had a urinary PCA3 test performed no more than 4 weeks before biopsy, and prostate volume was recorded by transrectal ultrasound determination at the time of biopsy. The diagnostic yield of PSA level, PSA density (PSAD), PCA3 score, and PCA3 density in detecting cancer was evaluated using a receiver operating characteristic (ROC) curve.
Results: Of the 288 patients included for analysis, 183 (63.5%) underwent an initial prostate biopsy and 105 (36.5%) had at least 1 previous negative biopsy. Cancer was detected in 74 (25.7%) patients. The area under the curve was 0.486 for PSA level, 0.590 for PSAD, 0.687 for PCA3 score, and 0.717 for PCA3 density.
Conclusion: PCA3 density is strongly correlated with cancer detection and may be useful in selecting patients for biopsy.
*For a PDF of the full article, click on the link to the left of this introduction.
Maintenance therapy in solid tumors
The concept of maintenance therapy has been well studied in hematologic malignancies, and now, an increasing number of clinical trials explore the role of maintenance therapy in solid cancers. Both biological and lower-intensity chemotherapeutic agents are currently being evaluated as maintenance therapy. However, despite the increase in research in this area, there has not been consensus about the definition and timing of maintenance therapy. In this review, we will focus on continuation maintenance therapy and switch maintenance therapy in patients with metastatic solid tumors who have achieved stable disease, partial response, or complete response after first-line treatment.
*For a PDF of the full article, click on the link to the left of this introduction.
The concept of maintenance therapy has been well studied in hematologic malignancies, and now, an increasing number of clinical trials explore the role of maintenance therapy in solid cancers. Both biological and lower-intensity chemotherapeutic agents are currently being evaluated as maintenance therapy. However, despite the increase in research in this area, there has not been consensus about the definition and timing of maintenance therapy. In this review, we will focus on continuation maintenance therapy and switch maintenance therapy in patients with metastatic solid tumors who have achieved stable disease, partial response, or complete response after first-line treatment.
*For a PDF of the full article, click on the link to the left of this introduction.
The concept of maintenance therapy has been well studied in hematologic malignancies, and now, an increasing number of clinical trials explore the role of maintenance therapy in solid cancers. Both biological and lower-intensity chemotherapeutic agents are currently being evaluated as maintenance therapy. However, despite the increase in research in this area, there has not been consensus about the definition and timing of maintenance therapy. In this review, we will focus on continuation maintenance therapy and switch maintenance therapy in patients with metastatic solid tumors who have achieved stable disease, partial response, or complete response after first-line treatment.
*For a PDF of the full article, click on the link to the left of this introduction.
Community Oncology Podcast - Axitinib and sorafenib in advanced renal cell carcinoma.
Editor-in-Chief Dr. David H. Henry takes you on an audio tour of the July issue including discussions of an original research report on the impact of depression on cancer comorbidity and this month's Community Translation: Axitinib and sorafenib in second-line treatment of advanced renal cell carcinoma.
Editor-in-Chief Dr. David H. Henry takes you on an audio tour of the July issue including discussions of an original research report on the impact of depression on cancer comorbidity and this month's Community Translation: Axitinib and sorafenib in second-line treatment of advanced renal cell carcinoma.
Editor-in-Chief Dr. David H. Henry takes you on an audio tour of the July issue including discussions of an original research report on the impact of depression on cancer comorbidity and this month's Community Translation: Axitinib and sorafenib in second-line treatment of advanced renal cell carcinoma.