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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.
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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.
Genomic oncology: moving beyond the tip of the iceberg
In the 15 years since the first map of the human genome emerged, genetics has become an integral part of medical practice worldwide.1 Oncology is no exception; the genetic origins of cancer were suspected more than a century ago and it is now well understood that most cancers are driven by genetic alterations that disrupt key cellular pathways involved in tumor survival and progression.2
In the 15 years since the first map of the human genome emerged, genetics has become an integral part of medical practice worldwide.1 Oncology is no exception; the genetic origins of cancer were suspected more than a century ago and it is now well understood that most cancers are driven by genetic alterations that disrupt key cellular pathways involved in tumor survival and progression.2
In the 15 years since the first map of the human genome emerged, genetics has become an integral part of medical practice worldwide.1 Oncology is no exception; the genetic origins of cancer were suspected more than a century ago and it is now well understood that most cancers are driven by genetic alterations that disrupt key cellular pathways involved in tumor survival and progression.2
Oncogenic drivers and immunotherapy: staying one step ahead of lung cancer
The majority of newly diagnosed lung cancers are NSCLC, and about half of those are adenocarcinomas (Figure 1).2 Over the past decade there has been a significant evolution in the understanding and treatment of lung adenocarcinoma, mostly stemming from a greater appreciation of the distinct pathologies and unique molecular signatures of these tumors. Genomic characterization of the molecular signatures has led to the identification of numerous key genetic alterations that drive lung cancer. The dependency of lung tumors on these genetic drivers has enabled the pharmacological development of targeted therapies that exploit this vulnerability...
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The majority of newly diagnosed lung cancers are NSCLC, and about half of those are adenocarcinomas (Figure 1).2 Over the past decade there has been a significant evolution in the understanding and treatment of lung adenocarcinoma, mostly stemming from a greater appreciation of the distinct pathologies and unique molecular signatures of these tumors. Genomic characterization of the molecular signatures has led to the identification of numerous key genetic alterations that drive lung cancer. The dependency of lung tumors on these genetic drivers has enabled the pharmacological development of targeted therapies that exploit this vulnerability...
Click on the PDF icon at the top of this introduction to read the full article.
The majority of newly diagnosed lung cancers are NSCLC, and about half of those are adenocarcinomas (Figure 1).2 Over the past decade there has been a significant evolution in the understanding and treatment of lung adenocarcinoma, mostly stemming from a greater appreciation of the distinct pathologies and unique molecular signatures of these tumors. Genomic characterization of the molecular signatures has led to the identification of numerous key genetic alterations that drive lung cancer. The dependency of lung tumors on these genetic drivers has enabled the pharmacological development of targeted therapies that exploit this vulnerability...
Click on the PDF icon at the top of this introduction to read the full article.
Glioblastoma, bone sarcoma, and liver cancer: tough battles rage on for some tumors
osteosarcoma, chondrosarcoma, CS, Ewing sarcoma, ES, hepatocellular carcinoma, HCC
osteosarcoma, chondrosarcoma, CS, Ewing sarcoma, ES, hepatocellular carcinoma, HCC
osteosarcoma, chondrosarcoma, CS, Ewing sarcoma, ES, hepatocellular carcinoma, HCC
Rising to the therapeutic challenge of head and neck cancer
As a significant cause of cancer-related mortality, head and neck cancer presents an important therapeutic challenge that has proven relatively resistant to attempts to improve patient outcomes over the past several decades. In recent years, molecular profiling of head and neck cancers has provided greater insight into their significant genetic heterogeneity, creating potential opportunities for novel therapies. Here, we discuss the most promising advances.
Limited progress in HNSCC treatment
Cancers of the nasal cavity, sinuses, mouth, lips, salivary glands, throat, and larynx, collectively called head and neck cancers, are the sixth leading cause of cancer-related death worldwide. The majority of head and neck cancer arises in the epithelial cells that line the mucosal surfaces of the head and neck and is known as squamous cell carcinoma (HNSCC). If caught in the early stages, HNSCC has a high cure rate with single-modality treatment with either surgery or radiation therapy (RT).1 However, a substantial proportion of patients present with advanced disease that requires multimodality therapy and has significantly poorer outcomes. Locally advanced HNSCC is typically treated with various combinations of surgery, RT, and chemotherapy and survival rates for all patients at 5 years are 40%- 60%, compared with 70%-90% for patients with early-stage disease.1,3 Up to half of locally advanced tumors relapse within the first 2 years after treatment. For patients with recurrent/metastatic disease, various chemotherapeutic regimens are available but median survival is typically less than a year.3-5
Click on the PDF icon at the top of this introduction to read the full article.
As a significant cause of cancer-related mortality, head and neck cancer presents an important therapeutic challenge that has proven relatively resistant to attempts to improve patient outcomes over the past several decades. In recent years, molecular profiling of head and neck cancers has provided greater insight into their significant genetic heterogeneity, creating potential opportunities for novel therapies. Here, we discuss the most promising advances.
Limited progress in HNSCC treatment
Cancers of the nasal cavity, sinuses, mouth, lips, salivary glands, throat, and larynx, collectively called head and neck cancers, are the sixth leading cause of cancer-related death worldwide. The majority of head and neck cancer arises in the epithelial cells that line the mucosal surfaces of the head and neck and is known as squamous cell carcinoma (HNSCC). If caught in the early stages, HNSCC has a high cure rate with single-modality treatment with either surgery or radiation therapy (RT).1 However, a substantial proportion of patients present with advanced disease that requires multimodality therapy and has significantly poorer outcomes. Locally advanced HNSCC is typically treated with various combinations of surgery, RT, and chemotherapy and survival rates for all patients at 5 years are 40%- 60%, compared with 70%-90% for patients with early-stage disease.1,3 Up to half of locally advanced tumors relapse within the first 2 years after treatment. For patients with recurrent/metastatic disease, various chemotherapeutic regimens are available but median survival is typically less than a year.3-5
Click on the PDF icon at the top of this introduction to read the full article.
As a significant cause of cancer-related mortality, head and neck cancer presents an important therapeutic challenge that has proven relatively resistant to attempts to improve patient outcomes over the past several decades. In recent years, molecular profiling of head and neck cancers has provided greater insight into their significant genetic heterogeneity, creating potential opportunities for novel therapies. Here, we discuss the most promising advances.
Limited progress in HNSCC treatment
Cancers of the nasal cavity, sinuses, mouth, lips, salivary glands, throat, and larynx, collectively called head and neck cancers, are the sixth leading cause of cancer-related death worldwide. The majority of head and neck cancer arises in the epithelial cells that line the mucosal surfaces of the head and neck and is known as squamous cell carcinoma (HNSCC). If caught in the early stages, HNSCC has a high cure rate with single-modality treatment with either surgery or radiation therapy (RT).1 However, a substantial proportion of patients present with advanced disease that requires multimodality therapy and has significantly poorer outcomes. Locally advanced HNSCC is typically treated with various combinations of surgery, RT, and chemotherapy and survival rates for all patients at 5 years are 40%- 60%, compared with 70%-90% for patients with early-stage disease.1,3 Up to half of locally advanced tumors relapse within the first 2 years after treatment. For patients with recurrent/metastatic disease, various chemotherapeutic regimens are available but median survival is typically less than a year.3-5
Click on the PDF icon at the top of this introduction to read the full article.
Small victories add up to paradigm shifts for hard-to-treat tumors
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Delivering on the promise of cancer biomarkers in the clinic
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JCSO 2014;12:381-388
Moving beyond the one-size-fits-all formula for breast cancer treatments
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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.
Targeting B-cell signaling pathways: a central role for Bruton’s tyrosine kinase
B-cell cancers constitute a large group of diseases with diverse clinical and pathological characteristics that arise from the B (bursal- or bone marrow-derived) lymphocytes of the immune system. B cells are involved in humoral immunity as part of the adaptive immune response. They display a unique B-cell receptor (BCR) on their surface which binds to a specific antigen. Antigen- binding activates the process of clonal expansion, during which the B cell reproduces to form an army of clones that secrete the same antibody. These antibodies then bind to the target antigen on foreign cells and initiate a range of immune responses that ultimately lead to the destruction of that cell.
Click on the PDF icon at the top of this introduction to read the full article.
B-cell cancers constitute a large group of diseases with diverse clinical and pathological characteristics that arise from the B (bursal- or bone marrow-derived) lymphocytes of the immune system. B cells are involved in humoral immunity as part of the adaptive immune response. They display a unique B-cell receptor (BCR) on their surface which binds to a specific antigen. Antigen- binding activates the process of clonal expansion, during which the B cell reproduces to form an army of clones that secrete the same antibody. These antibodies then bind to the target antigen on foreign cells and initiate a range of immune responses that ultimately lead to the destruction of that cell.
Click on the PDF icon at the top of this introduction to read the full article.
B-cell cancers constitute a large group of diseases with diverse clinical and pathological characteristics that arise from the B (bursal- or bone marrow-derived) lymphocytes of the immune system. B cells are involved in humoral immunity as part of the adaptive immune response. They display a unique B-cell receptor (BCR) on their surface which binds to a specific antigen. Antigen- binding activates the process of clonal expansion, during which the B cell reproduces to form an army of clones that secrete the same antibody. These antibodies then bind to the target antigen on foreign cells and initiate a range of immune responses that ultimately lead to the destruction of that cell.
Click on the PDF icon at the top of this introduction to read the full article.
Synthetic lethality: beating cancer at its own game
The primary focus for targeted cancer agents has typically been to counteract the oncogenic signaling that results from genetic defects. A new strategy is emerging that actually seeks to exploit the oncogenic features of tumor cells rather than overcome them. Synthetic lethality (SL) is a situation in which 2 nonlethal mutations become lethal to a cell when they are present simultaneously. If SL were to be exploited for anticancer therapy, it could lead to the development of highly selective, less toxic drugs, while expanding therapeutic targets to include those that have, until now, proven pharmaceutically intractable. Here, we discuss the idea of SL and how it can be applied to cancer therapy.
Click on the PDF icon at the top of this introduction to read the full article.
The primary focus for targeted cancer agents has typically been to counteract the oncogenic signaling that results from genetic defects. A new strategy is emerging that actually seeks to exploit the oncogenic features of tumor cells rather than overcome them. Synthetic lethality (SL) is a situation in which 2 nonlethal mutations become lethal to a cell when they are present simultaneously. If SL were to be exploited for anticancer therapy, it could lead to the development of highly selective, less toxic drugs, while expanding therapeutic targets to include those that have, until now, proven pharmaceutically intractable. Here, we discuss the idea of SL and how it can be applied to cancer therapy.
Click on the PDF icon at the top of this introduction to read the full article.
The primary focus for targeted cancer agents has typically been to counteract the oncogenic signaling that results from genetic defects. A new strategy is emerging that actually seeks to exploit the oncogenic features of tumor cells rather than overcome them. Synthetic lethality (SL) is a situation in which 2 nonlethal mutations become lethal to a cell when they are present simultaneously. If SL were to be exploited for anticancer therapy, it could lead to the development of highly selective, less toxic drugs, while expanding therapeutic targets to include those that have, until now, proven pharmaceutically intractable. Here, we discuss the idea of SL and how it can be applied to cancer therapy.
Click on the PDF icon at the top of this introduction to read the full article.