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Therapeutic Strategies to Overcome ALK Resistance in Cancer, Volume 13, presents current strategies to improve and prolong clinical benefit in ALK driven cancers. Most patients with ALK-driven cancer are sensitive to tyrosine kinase inhibitor (TKI) therapy, but resistance invariably develops. This book discusses topics such as structure and function of ALK, ALK rearranged lung cancer, resistance mechanisms to ALK TKI tumors, and novel therapeutic strategies to enhance crizotinib anti-tumor efficacy in ALCL. Additionally, it encompasses information on drug combinations to enhance ALK TKI anti-tumor efficacy in neuroblastoma and future perspectives in the field. This book is a valuable resource for cancer researchers, clinicians and several members of biomedical field who need to understand more about how to fight ALK resistance in cancer treatment.
New Targeting in The Reversal of Resistant Glioblastomas discusses alternative treatment strategies that not only target tumor cells but also target the tumor microenvironment, metabolic pathways and interaction of cytokines in tumor cells. The current treatment for primary and recurrent glioblastomas is failing because clinicians are not considering the effect of bone marrow derived cells to the development of resistance to clinically practiced therapies. This book helps readers rethink treatment strategies to successfully fight glioblastomas. It is a valuable resource for cancer researchers, clinicians, graduate students and other members of the biomedical field.
Glioblastoma Resistance to Chemotherapy: Molecular Mechanisms and Innovative Reversal Strategies brings current knowledge from an international team of experts on the science and clinical management of glioblastoma chemoresistance. The book discusses topics such as molecular mechanisms of chemoresistance, experimental models to study chemoresistance, chemoresistance to drugs other than Temozolomide, and specific strategies to reverse chemoresistance. Additionally, it encompasses information on how to mitigate chemoresistance by targeted enhancement of p53 function. This book is a valuable resource for cancer researchers, oncologists, neuro-oncologists and other members of the biomedical field. Glioblastoma (GBM) is the most invasive and malignant primary brain tumor in humans with poor survival after diagnosis, therefore it is imperative that molecular and cellular mechanisms behind therapy resistant GBM cells, as well as the therapeutic strategies available to counter the resistance are comprehensively understood.
Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC presents updated information on how EGFR mutant lung cancers evolve to evade EGFR inhibitors, clinical strategies that identify these mechanisms, and how to implement newer therapeutic strategies to combat resistance and improve patient survival. As resistance to EGFR inhibitors is often through re-activation of MEK/ERK and PI3K pathways, or through loss of cell death responses, there is much overlap with resistance to targeted therapies in other paradigms, such as BRAF inhibitors in BRAF mutant melanoma, and HER2 inhibitors in HER2 amplified breast cancer. This book is a valuable resource for cancer researchers, clinicians, graduate students and other members of the biomedical field who are interested in promising treatments for lung cancer.
Therapy Resistance in Prostate Cancer: Mechanisms and Insights, Volume 20highlights the main mechanisms that are responsible for therapy resistance in PCa allowing researchers and clinicians to have a synopsis of current options and therapies that can be proposed to overcome resistance. Understanding the mechanisms responsible for chemotherapy resistance helps researchers all over the world delve deeper into the pathways behind this resistance and potentially discover new therapeutic targets for PCa. Prostate cancer (PCa) is among the most diagnosed cancers in men worldwide, as well as one of the most common causes of cancer-related deaths. Despite the advances in treatment, the disease remains associated with poor survival and resistance to cytotoxic and targeted therapies.
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