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Novel Treatment Shows Promise for Acute Lymphoblastic Leukemia
Thanks to gene-editing treatment, 2 babies who had leukemia have a longer lease on life. Researchers from University College London, Great Ormond Street Hospital National Health Service Trust, King’s College, and Sheffield Children’s Hospital, in the United Kingdom used genetically engineered white blood cells from healthy individuals to target the cancer cells.
Related: New Treatments for Chronic Lymphocytic Leukemia
One infant was 11 months old, and the second was 16 months old. Both had refractory relapsed B-cell acute lymphoblastic leukemia and had undergone multidrug treatments. Although the potential of the method has been demonstrated in autologous and human-leukocyte-antigen–matched allogeneic settings, the researchers say, “the infrastructure and expertise required to produce personalized cell products present challenges, and low T cell counts in heavily treated individuals may preclude autologous approaches.”
The treatment involves lymphodepleting chemotherapy and anti-CD52 serotherapy, followed by a single-dose infusion of universal CAR19 cells (autologous T cells engineered to express chimeric antigen receptor against the B-cell antigen CD19). This “bridge-to-transplantation strategy” demonstrates the therapeutic potential of gene-editing technology, the researchers say.
Related: Six Open Clinical Trials That Are Expanding Our Understanding of Immunotherapies
Just 28 days after the treatment, molecular markers showed remission in both infants. The treatments were well tolerated. The first infant had an immune reaction (cytopenia and graft-vs-host disease [GVHD] in skin and marrow) in the 2 months after the infusion and was treated with steroids and bone marrow transplantation. The other baby had no adverse reactions apart from mild skin GVHD that reversed “promptly” with topical steroids and an episode of “unexplained irritability” in the 3 weeks after infusion.
The first and second infant remained cancer free 18 and 12 months later.
Source:
Qasim W, Zhan H, Samarasinghe S, et al. Sci Transl Med. 2017;9(374):pii: eaaj2013.
doi: 10.1126/scitranslmed.aaj2013.
Thanks to gene-editing treatment, 2 babies who had leukemia have a longer lease on life. Researchers from University College London, Great Ormond Street Hospital National Health Service Trust, King’s College, and Sheffield Children’s Hospital, in the United Kingdom used genetically engineered white blood cells from healthy individuals to target the cancer cells.
Related: New Treatments for Chronic Lymphocytic Leukemia
One infant was 11 months old, and the second was 16 months old. Both had refractory relapsed B-cell acute lymphoblastic leukemia and had undergone multidrug treatments. Although the potential of the method has been demonstrated in autologous and human-leukocyte-antigen–matched allogeneic settings, the researchers say, “the infrastructure and expertise required to produce personalized cell products present challenges, and low T cell counts in heavily treated individuals may preclude autologous approaches.”
The treatment involves lymphodepleting chemotherapy and anti-CD52 serotherapy, followed by a single-dose infusion of universal CAR19 cells (autologous T cells engineered to express chimeric antigen receptor against the B-cell antigen CD19). This “bridge-to-transplantation strategy” demonstrates the therapeutic potential of gene-editing technology, the researchers say.
Related: Six Open Clinical Trials That Are Expanding Our Understanding of Immunotherapies
Just 28 days after the treatment, molecular markers showed remission in both infants. The treatments were well tolerated. The first infant had an immune reaction (cytopenia and graft-vs-host disease [GVHD] in skin and marrow) in the 2 months after the infusion and was treated with steroids and bone marrow transplantation. The other baby had no adverse reactions apart from mild skin GVHD that reversed “promptly” with topical steroids and an episode of “unexplained irritability” in the 3 weeks after infusion.
The first and second infant remained cancer free 18 and 12 months later.
Source:
Qasim W, Zhan H, Samarasinghe S, et al. Sci Transl Med. 2017;9(374):pii: eaaj2013.
doi: 10.1126/scitranslmed.aaj2013.
Thanks to gene-editing treatment, 2 babies who had leukemia have a longer lease on life. Researchers from University College London, Great Ormond Street Hospital National Health Service Trust, King’s College, and Sheffield Children’s Hospital, in the United Kingdom used genetically engineered white blood cells from healthy individuals to target the cancer cells.
Related: New Treatments for Chronic Lymphocytic Leukemia
One infant was 11 months old, and the second was 16 months old. Both had refractory relapsed B-cell acute lymphoblastic leukemia and had undergone multidrug treatments. Although the potential of the method has been demonstrated in autologous and human-leukocyte-antigen–matched allogeneic settings, the researchers say, “the infrastructure and expertise required to produce personalized cell products present challenges, and low T cell counts in heavily treated individuals may preclude autologous approaches.”
The treatment involves lymphodepleting chemotherapy and anti-CD52 serotherapy, followed by a single-dose infusion of universal CAR19 cells (autologous T cells engineered to express chimeric antigen receptor against the B-cell antigen CD19). This “bridge-to-transplantation strategy” demonstrates the therapeutic potential of gene-editing technology, the researchers say.
Related: Six Open Clinical Trials That Are Expanding Our Understanding of Immunotherapies
Just 28 days after the treatment, molecular markers showed remission in both infants. The treatments were well tolerated. The first infant had an immune reaction (cytopenia and graft-vs-host disease [GVHD] in skin and marrow) in the 2 months after the infusion and was treated with steroids and bone marrow transplantation. The other baby had no adverse reactions apart from mild skin GVHD that reversed “promptly” with topical steroids and an episode of “unexplained irritability” in the 3 weeks after infusion.
The first and second infant remained cancer free 18 and 12 months later.
Source:
Qasim W, Zhan H, Samarasinghe S, et al. Sci Transl Med. 2017;9(374):pii: eaaj2013.
doi: 10.1126/scitranslmed.aaj2013.
What Do Parasites Have to Do With Leukemia?
Parasites have been shown to have both pro- and antitumor effects. Malaria parasites (Plasmodium spp) are among those known to have this possible “bidirectional role” in carcinogenesis, say researchers from Aix-Marseille Université in France. They reviewed the current thinking on whether malaria—a worldwide killer—can be useful in cancer prevention and treatment.
Positive relationships between malaria and virus-associated cancers are relatively well documented, the researchers say. Evidence suggests that malaria can alter immune responses by modulating both humoral and cell-mediated immunity. Plasmodium-related cancers are primarily lymphoproliferative, vulnerable to virus reactivation. Epstein-Barr virus (EBV), for example, has been observed in lymphatic and hematologic tumors such as Hodgkin disease and T cell lymphoma, and malaria can reactivate EBV.
In animal studies, malarial infection with Plasmodium berghei (P berghei) increased the rate of spontaneous leukemia. In one study, concurrent infection with P berghei increased the incidence of malignant lymphoma in mice injected with Moloney leukemogenic virus.
On the other hand, Plasmodium spp also produces proteins that demonstrate certain anti-oncogenic effects, they note. The researchers suggest that using proteins in cancer treatment should be explored, adding that it’s a “safer approach than the inoculation of wild type Plasmodium.” Positive parasite-induced effects against cancers of the hematopoietic and lymphoid tissues are mentioned only for 2 species and those only in a decades-old study. Based on current knowledge, the researchers say, the antitumor effects observed are attributable to modifications to the host immune response. Thus, their characteristics and locations within the host can be highly diverse.
All in all, the researchers conclude, the growing evidence is opening intriguing pathways for using one ill to cure another.
Source:
Faure E. Parasitology. 2016;143(14):1811-1823.
Parasites have been shown to have both pro- and antitumor effects. Malaria parasites (Plasmodium spp) are among those known to have this possible “bidirectional role” in carcinogenesis, say researchers from Aix-Marseille Université in France. They reviewed the current thinking on whether malaria—a worldwide killer—can be useful in cancer prevention and treatment.
Positive relationships between malaria and virus-associated cancers are relatively well documented, the researchers say. Evidence suggests that malaria can alter immune responses by modulating both humoral and cell-mediated immunity. Plasmodium-related cancers are primarily lymphoproliferative, vulnerable to virus reactivation. Epstein-Barr virus (EBV), for example, has been observed in lymphatic and hematologic tumors such as Hodgkin disease and T cell lymphoma, and malaria can reactivate EBV.
In animal studies, malarial infection with Plasmodium berghei (P berghei) increased the rate of spontaneous leukemia. In one study, concurrent infection with P berghei increased the incidence of malignant lymphoma in mice injected with Moloney leukemogenic virus.
On the other hand, Plasmodium spp also produces proteins that demonstrate certain anti-oncogenic effects, they note. The researchers suggest that using proteins in cancer treatment should be explored, adding that it’s a “safer approach than the inoculation of wild type Plasmodium.” Positive parasite-induced effects against cancers of the hematopoietic and lymphoid tissues are mentioned only for 2 species and those only in a decades-old study. Based on current knowledge, the researchers say, the antitumor effects observed are attributable to modifications to the host immune response. Thus, their characteristics and locations within the host can be highly diverse.
All in all, the researchers conclude, the growing evidence is opening intriguing pathways for using one ill to cure another.
Source:
Faure E. Parasitology. 2016;143(14):1811-1823.
Parasites have been shown to have both pro- and antitumor effects. Malaria parasites (Plasmodium spp) are among those known to have this possible “bidirectional role” in carcinogenesis, say researchers from Aix-Marseille Université in France. They reviewed the current thinking on whether malaria—a worldwide killer—can be useful in cancer prevention and treatment.
Positive relationships between malaria and virus-associated cancers are relatively well documented, the researchers say. Evidence suggests that malaria can alter immune responses by modulating both humoral and cell-mediated immunity. Plasmodium-related cancers are primarily lymphoproliferative, vulnerable to virus reactivation. Epstein-Barr virus (EBV), for example, has been observed in lymphatic and hematologic tumors such as Hodgkin disease and T cell lymphoma, and malaria can reactivate EBV.
In animal studies, malarial infection with Plasmodium berghei (P berghei) increased the rate of spontaneous leukemia. In one study, concurrent infection with P berghei increased the incidence of malignant lymphoma in mice injected with Moloney leukemogenic virus.
On the other hand, Plasmodium spp also produces proteins that demonstrate certain anti-oncogenic effects, they note. The researchers suggest that using proteins in cancer treatment should be explored, adding that it’s a “safer approach than the inoculation of wild type Plasmodium.” Positive parasite-induced effects against cancers of the hematopoietic and lymphoid tissues are mentioned only for 2 species and those only in a decades-old study. Based on current knowledge, the researchers say, the antitumor effects observed are attributable to modifications to the host immune response. Thus, their characteristics and locations within the host can be highly diverse.
All in all, the researchers conclude, the growing evidence is opening intriguing pathways for using one ill to cure another.
Source:
Faure E. Parasitology. 2016;143(14):1811-1823.
Assessing Addiction From Multiple Perspectives
It’s time to change addiction assessment, and build on advances in neuroscience, say scientists at the National Institute on Alcohol Abuse and Alcoholism. They’ve proposed an assessment tool to diagnose addictive disorders that takes into account addiction-related behaviors, brain imaging, and genetic data. The Addictions Neuroclinical Assessment (ANA) could lead to more effective individualized treatments, they say.
Related: Who Overdoses at a VA Emergency Department?
“We currently approach addiction diagnosis as a ‘yes or no’ proposition,” said Laura Kwako, PhD, lead author of a review article on the subject. Addictive disorders are typically classified by the substance of abuse and the presence or absence of symptoms, such as difficulty controlling consumption. By “leveraging knowledge of the neuroscience” to identify a “package of assessments,” the researchers hope to more precisely identify different subtypes of addictive disorders. They compare the new assessment tool to those used to tailor cancer diagnoses, which combine cellular, genetic, molecular, and imaging information with clinical history.
The behavioral assessment would include 3 functional processes most relevant to addiction: altered perception of an object or event, or “incentive salience” (where drug-taking makes something seem more attractive or important); negative emotionality (increased negative responses when drugs are no longer available); and executive functioning (e.g., deficits in organizing behavior toward goals).
Related: Coordinating Better Care for Opioid-Addicted Women and Their Children
“The assessment framework that we describe recognizes the great advances that continue to be made in our understanding of the neuroscience of addiction,” said NIAAA director George Koob, PhD, a coauthor of the review. “These advances underscore how much we know about the core neurobiologcal manifestations of addiction in people.”
It’s time to change addiction assessment, and build on advances in neuroscience, say scientists at the National Institute on Alcohol Abuse and Alcoholism. They’ve proposed an assessment tool to diagnose addictive disorders that takes into account addiction-related behaviors, brain imaging, and genetic data. The Addictions Neuroclinical Assessment (ANA) could lead to more effective individualized treatments, they say.
Related: Who Overdoses at a VA Emergency Department?
“We currently approach addiction diagnosis as a ‘yes or no’ proposition,” said Laura Kwako, PhD, lead author of a review article on the subject. Addictive disorders are typically classified by the substance of abuse and the presence or absence of symptoms, such as difficulty controlling consumption. By “leveraging knowledge of the neuroscience” to identify a “package of assessments,” the researchers hope to more precisely identify different subtypes of addictive disorders. They compare the new assessment tool to those used to tailor cancer diagnoses, which combine cellular, genetic, molecular, and imaging information with clinical history.
The behavioral assessment would include 3 functional processes most relevant to addiction: altered perception of an object or event, or “incentive salience” (where drug-taking makes something seem more attractive or important); negative emotionality (increased negative responses when drugs are no longer available); and executive functioning (e.g., deficits in organizing behavior toward goals).
Related: Coordinating Better Care for Opioid-Addicted Women and Their Children
“The assessment framework that we describe recognizes the great advances that continue to be made in our understanding of the neuroscience of addiction,” said NIAAA director George Koob, PhD, a coauthor of the review. “These advances underscore how much we know about the core neurobiologcal manifestations of addiction in people.”
It’s time to change addiction assessment, and build on advances in neuroscience, say scientists at the National Institute on Alcohol Abuse and Alcoholism. They’ve proposed an assessment tool to diagnose addictive disorders that takes into account addiction-related behaviors, brain imaging, and genetic data. The Addictions Neuroclinical Assessment (ANA) could lead to more effective individualized treatments, they say.
Related: Who Overdoses at a VA Emergency Department?
“We currently approach addiction diagnosis as a ‘yes or no’ proposition,” said Laura Kwako, PhD, lead author of a review article on the subject. Addictive disorders are typically classified by the substance of abuse and the presence or absence of symptoms, such as difficulty controlling consumption. By “leveraging knowledge of the neuroscience” to identify a “package of assessments,” the researchers hope to more precisely identify different subtypes of addictive disorders. They compare the new assessment tool to those used to tailor cancer diagnoses, which combine cellular, genetic, molecular, and imaging information with clinical history.
The behavioral assessment would include 3 functional processes most relevant to addiction: altered perception of an object or event, or “incentive salience” (where drug-taking makes something seem more attractive or important); negative emotionality (increased negative responses when drugs are no longer available); and executive functioning (e.g., deficits in organizing behavior toward goals).
Related: Coordinating Better Care for Opioid-Addicted Women and Their Children
“The assessment framework that we describe recognizes the great advances that continue to be made in our understanding of the neuroscience of addiction,” said NIAAA director George Koob, PhD, a coauthor of the review. “These advances underscore how much we know about the core neurobiologcal manifestations of addiction in people.”
New Device Helps Reduce Risk of Second Stroke
The FDA has approved the Amplatzer PFO Occluder (St. Jude Medical Inc), a nonsurgical method to close a patent foramen ovale (PFO) in patients who have had a stroke.
About 25% to 30% of patients have a PFO, which typically does not require treatment. However, patients with an unidentified cause of stroke and a PFO may have a higher risk of a second stroke.
The Amplatzer PFO Occluder is inserted through a catheter placed in a leg vein and advanced to the heart. It is then implanted close to the hole in the heart between the right and left atria.
Related: Standard vs Intensive Emergency Stroke Treatment
Researchers evaluated 499 patients treated with the Amplatzer PFO Occluder plus blood-thinning medication, and 481 patients treated with blood-thinners alone. The rate of new strokes in both groups was very low, but the group treated with the device had a 50% lower rate.
The device had been on the market more than 10 years ago with a humanitarian device exemption. It was withdrawn when the FDA concluded that the target population was greater than 4,000 patients and the device no longer qualified for the exemption. No FDA-approved heart occluder devices with this indication have been on the market in the years since. Now, in approving the device—again—the FDA says it has demonstrated a “reasonable assurance of safety and effectiveness.”
Related: Development of a Multidisciplinary Stroke Program
The FDA advises that patients should be evaluated carefully by a neurologist and cardiologist to rule out other known causes of stroke, to ensure that PFO closure is likely to help reduce the risk of recurrent stroke.
The FDA has approved the Amplatzer PFO Occluder (St. Jude Medical Inc), a nonsurgical method to close a patent foramen ovale (PFO) in patients who have had a stroke.
About 25% to 30% of patients have a PFO, which typically does not require treatment. However, patients with an unidentified cause of stroke and a PFO may have a higher risk of a second stroke.
The Amplatzer PFO Occluder is inserted through a catheter placed in a leg vein and advanced to the heart. It is then implanted close to the hole in the heart between the right and left atria.
Related: Standard vs Intensive Emergency Stroke Treatment
Researchers evaluated 499 patients treated with the Amplatzer PFO Occluder plus blood-thinning medication, and 481 patients treated with blood-thinners alone. The rate of new strokes in both groups was very low, but the group treated with the device had a 50% lower rate.
The device had been on the market more than 10 years ago with a humanitarian device exemption. It was withdrawn when the FDA concluded that the target population was greater than 4,000 patients and the device no longer qualified for the exemption. No FDA-approved heart occluder devices with this indication have been on the market in the years since. Now, in approving the device—again—the FDA says it has demonstrated a “reasonable assurance of safety and effectiveness.”
Related: Development of a Multidisciplinary Stroke Program
The FDA advises that patients should be evaluated carefully by a neurologist and cardiologist to rule out other known causes of stroke, to ensure that PFO closure is likely to help reduce the risk of recurrent stroke.
The FDA has approved the Amplatzer PFO Occluder (St. Jude Medical Inc), a nonsurgical method to close a patent foramen ovale (PFO) in patients who have had a stroke.
About 25% to 30% of patients have a PFO, which typically does not require treatment. However, patients with an unidentified cause of stroke and a PFO may have a higher risk of a second stroke.
The Amplatzer PFO Occluder is inserted through a catheter placed in a leg vein and advanced to the heart. It is then implanted close to the hole in the heart between the right and left atria.
Related: Standard vs Intensive Emergency Stroke Treatment
Researchers evaluated 499 patients treated with the Amplatzer PFO Occluder plus blood-thinning medication, and 481 patients treated with blood-thinners alone. The rate of new strokes in both groups was very low, but the group treated with the device had a 50% lower rate.
The device had been on the market more than 10 years ago with a humanitarian device exemption. It was withdrawn when the FDA concluded that the target population was greater than 4,000 patients and the device no longer qualified for the exemption. No FDA-approved heart occluder devices with this indication have been on the market in the years since. Now, in approving the device—again—the FDA says it has demonstrated a “reasonable assurance of safety and effectiveness.”
Related: Development of a Multidisciplinary Stroke Program
The FDA advises that patients should be evaluated carefully by a neurologist and cardiologist to rule out other known causes of stroke, to ensure that PFO closure is likely to help reduce the risk of recurrent stroke.
Pancreatic cancer: a therapeutic challenge yet to be met
Although there are numerous hard-to-treat tumor types, pancreatic cancer, which most commonly presents as pancreatic ductal adenocarcinoma (PDA) is particularly notorious and arguably the most challenging and deadly of all cancers. It is currently ranked as the fourth most common cause of cancer-related mortality, and looks set to move up to the number 2 slot within the next 15 years.1 Here, we discuss the evolution of much-needed novel treatment strategies.
Click on the PDF icon at the top of this introduction to read the full article.
Although there are numerous hard-to-treat tumor types, pancreatic cancer, which most commonly presents as pancreatic ductal adenocarcinoma (PDA) is particularly notorious and arguably the most challenging and deadly of all cancers. It is currently ranked as the fourth most common cause of cancer-related mortality, and looks set to move up to the number 2 slot within the next 15 years.1 Here, we discuss the evolution of much-needed novel treatment strategies.
Click on the PDF icon at the top of this introduction to read the full article.
Although there are numerous hard-to-treat tumor types, pancreatic cancer, which most commonly presents as pancreatic ductal adenocarcinoma (PDA) is particularly notorious and arguably the most challenging and deadly of all cancers. It is currently ranked as the fourth most common cause of cancer-related mortality, and looks set to move up to the number 2 slot within the next 15 years.1 Here, we discuss the evolution of much-needed novel treatment strategies.
Click on the PDF icon at the top of this introduction to read the full article.
Expanding treatment options and ongoing challenges for urologic cancers
Urologic cancers are those that form in organs of the urinary and male reproductive systems, the most significant among them being cancers of the bladder, kidney, prostate, and testicles. Collectively, they are diagnosed in close to 400,000 Americans each year and are responsible for almost 60,000 deaths annually.1 Here, we describe the most recent developments in treating these malignancies.
Update/related article
Atezolizumab approval marks first new treatment option for bladder cancer in more than 3 decades
Click on the PDF icon at the top of this introduction to read the full article.
Urologic cancers are those that form in organs of the urinary and male reproductive systems, the most significant among them being cancers of the bladder, kidney, prostate, and testicles. Collectively, they are diagnosed in close to 400,000 Americans each year and are responsible for almost 60,000 deaths annually.1 Here, we describe the most recent developments in treating these malignancies.
Update/related article
Atezolizumab approval marks first new treatment option for bladder cancer in more than 3 decades
Click on the PDF icon at the top of this introduction to read the full article.
Urologic cancers are those that form in organs of the urinary and male reproductive systems, the most significant among them being cancers of the bladder, kidney, prostate, and testicles. Collectively, they are diagnosed in close to 400,000 Americans each year and are responsible for almost 60,000 deaths annually.1 Here, we describe the most recent developments in treating these malignancies.
Update/related article
Atezolizumab approval marks first new treatment option for bladder cancer in more than 3 decades
Click on the PDF icon at the top of this introduction to read the full article.
Evolving therapeutic strategies maintain clinical momentum in melanoma
The past 5 years have witnessed a watershed moment in the management of metastatic melanoma. The successes of molecularly targeted and immune-based therapies have transformed it from an aggressively lethal malignancy into one that is readily treatable. Here, we discuss continued efforts to find new therapies and broaden the clinical impact of existing options to maintain the unprecedented momentum of improving patient outcomes.
Click on the PDF icon at the top of this introduction to read the full article.
The past 5 years have witnessed a watershed moment in the management of metastatic melanoma. The successes of molecularly targeted and immune-based therapies have transformed it from an aggressively lethal malignancy into one that is readily treatable. Here, we discuss continued efforts to find new therapies and broaden the clinical impact of existing options to maintain the unprecedented momentum of improving patient outcomes.
Click on the PDF icon at the top of this introduction to read the full article.
The past 5 years have witnessed a watershed moment in the management of metastatic melanoma. The successes of molecularly targeted and immune-based therapies have transformed it from an aggressively lethal malignancy into one that is readily treatable. Here, we discuss continued efforts to find new therapies and broaden the clinical impact of existing options to maintain the unprecedented momentum of improving patient outcomes.
Click on the PDF icon at the top of this introduction to read the full article.
Multiple myeloma: newly approved drugs forge paradigm shift toward chronic disease
The pace of drug development for multiple myeloma was dizzying in 2015, with 5 regulatory approvals for the treatment of relapsed/refractory disease, 3 in a single month. As we stand on the brink of another paradigm shift in the management of this disease, we discuss the new classes of drugs and how they are shaping standard of care with the potential to make multiple myeloma a chronic disease.
Click on the PDF icon at the top of this introduction to read the full article.
The pace of drug development for multiple myeloma was dizzying in 2015, with 5 regulatory approvals for the treatment of relapsed/refractory disease, 3 in a single month. As we stand on the brink of another paradigm shift in the management of this disease, we discuss the new classes of drugs and how they are shaping standard of care with the potential to make multiple myeloma a chronic disease.
Click on the PDF icon at the top of this introduction to read the full article.
The pace of drug development for multiple myeloma was dizzying in 2015, with 5 regulatory approvals for the treatment of relapsed/refractory disease, 3 in a single month. As we stand on the brink of another paradigm shift in the management of this disease, we discuss the new classes of drugs and how they are shaping standard of care with the potential to make multiple myeloma a chronic disease.
Click on the PDF icon at the top of this introduction to read the full article.
New GI therapies bring hope after much frustration
Click on the PDF icon at the top of this introduction to read the full article.
Click on the PDF icon at the top of this introduction to read the full article.
Click on the PDF icon at the top of this introduction to read the full article.
Entering an era of intelligent combination therapy in cancer
The past few decades have witnessed unprecedented advances in our understanding of the molecular underpinnings of cancer. Although indiscriminately cytotoxic therapies like chemo- and radiation therapy remain standard of care for many cancer types, more precise targeted therapies and immune-boosting immunotherapies have added to our arsenal and afforded considerable survival gains. Despite those advances, we are still no closer to a cure, particularly for the most aggressive and insidious cancers that progress rapidly or go undiagnosed until advanced stages of disease. The substantial genetic diversity of tumors and universal nature of drug resistance present the most formidable and enduring challenges to effective cancer treatment.
Click on the PDF icon at the top of this introduction to read the full article.
The past few decades have witnessed unprecedented advances in our understanding of the molecular underpinnings of cancer. Although indiscriminately cytotoxic therapies like chemo- and radiation therapy remain standard of care for many cancer types, more precise targeted therapies and immune-boosting immunotherapies have added to our arsenal and afforded considerable survival gains. Despite those advances, we are still no closer to a cure, particularly for the most aggressive and insidious cancers that progress rapidly or go undiagnosed until advanced stages of disease. The substantial genetic diversity of tumors and universal nature of drug resistance present the most formidable and enduring challenges to effective cancer treatment.
Click on the PDF icon at the top of this introduction to read the full article.
The past few decades have witnessed unprecedented advances in our understanding of the molecular underpinnings of cancer. Although indiscriminately cytotoxic therapies like chemo- and radiation therapy remain standard of care for many cancer types, more precise targeted therapies and immune-boosting immunotherapies have added to our arsenal and afforded considerable survival gains. Despite those advances, we are still no closer to a cure, particularly for the most aggressive and insidious cancers that progress rapidly or go undiagnosed until advanced stages of disease. The substantial genetic diversity of tumors and universal nature of drug resistance present the most formidable and enduring challenges to effective cancer treatment.
Click on the PDF icon at the top of this introduction to read the full article.