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This book comprehensively describes the association between metabolic syndrome and pancreatic cancer progression, and the mechanism of action and target definition with a view to drug discovery. Metabolic syndrome, which includes adnominal obesity, hypertension, dyslipidemia, and hyperglycemia, has recently been shown to play an important role in the etiology and progression of various cancers. Further, obesity and diabetes have been associated with an increased incidence of gastric cancers. The book reviews the key biological mechanisms underlying the association between metabolic dysregulation, including obesity-associated enhancement of growth factor signaling, inflammation, and perturbation in pancreatic cancer cell growth and metastasis. It also illustrates the role of the inflammatory signaling pathway in metabolic diseases as well as tumor growth and explores the potential of these pathways as the rational targets for pancreatic cancer therapy. Lastly, the book offers a comprehensive description of the challenges associated with diabetes and pancreatic cancer therapy.
Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
Theranostic Approach for Pancreatic Cancer modulates the biologic properties of stroma in pancreatic cancer by targeting the several chemotherapy resistance mechanisms to impede their malignant property through introducing new strategies and drugs for tackling the disease. It brings information about ongoing research as well as clinical data about pancreatic cancer and provides detailed descriptions about diagnostic and therapeutic options for easy understanding. This book discusses several topics related to pancreatic cancer such as stem cells, drug resistance and pancreatic tumor microenvironment, the latest developments in chemotherapy for metastatic cancer and chemoprevention, and epigenome as a therapeutic strategy. Additionally, it encompasses a discussion on theranostic clinical applications for personalized treatment and management of pancreatic cancer. The book is a valuable resource for cancer researchers, oncologists, and several members of the biomedical field who need to understand more about the diagnosis and treatment of pancreatic cancer. Provides information on the roadblocks of chemotherapy in patients with newly diagnosed and metastatic pancreatic cancer Discusses treatment options available currently as well as prospective options for the future Focuses especially on stroma, tumor microenvironment, stem cells, stellate cells, transcription factors, growth factors, and important signaling pathways as already tested types of treatment
Breaking Tolerance to Pancreatic Cancer Unresponsiveness to Chemotherapy edited by Dr. Nagaraju, PhD., DSc. focuses on overriding the resistance from chemotherapeutic drugs with a broader range of treatment options. It particularly focuses on stroma, tumor microenvironment, stem cells, stellate cells, transcription factors, growth factors, and important signaling pathways. This volume discusses topics such as pancreatic cancer biology, current therapeutic options, EMT, chemotherapy resistance mechanisms, and genetic manipulations and natural products to enhance the sensitivity of pancreatic cancer to chemotherapy. Additionally, it discusses small targeted molecules and pancreatic cancer trials, and nanotechnology-based drug delivery. Breaking Tolerance to Pancreatic Cancer Unresponsiveness to Chemotherapy is a valuable source for researchers and advanced students in cancer and oncology as well as clinicians and medical students who are interested in learning more about ways to break pancreatic cancer resistance to chemotherapy. - Modulates the biologic properties of stroma in pancreatic cancer by targeting the several chemotherapy resistance mechanisms to impede their malignant property by introducing new strategies and drugs - Provides information about on-going research as well as clinical data on pancreatic cancer and detailed descriptions about therapeutic options for easy understanding - Utilizes full color figures to help the understanding of the content and tables for easy comparison of information as well as quick access to it
The MD Anderson Solid Tumor Oncology series presents cutting-edge surgical treatment and medical therapy for specific sites. This volume, Pancreatic Cancer, addresses epidemiology and molecular biology, inherited syndromes, staging, surgical techniques, multimodality therapy, and emerging therapies. The individual chapters focus on narrow, specific topics to produce a reference work of value to those interested in pancreatic cancer from a clinical and translational research perspective. A must-have for surgical oncologists and general surgeons.
The book addresses controversies related to the origins of cancer and provides solutions to cancer management and prevention. It expands upon Otto Warburg's well-known theory that all cancer is a disease of energy metabolism. However, Warburg did not link his theory to the "hallmarks of cancer" and thus his theory was discredited. This book aims to provide evidence, through case studies, that cancer is primarily a metabolic disease requring metabolic solutions for its management and prevention. Support for this position is derived from critical assessment of current cancer theories. Brain cancer case studies are presented as a proof of principle for metabolic solutions to disease management, but similarities are drawn to other types of cancer, including breast and colon, due to the same cellular mutations that they demonstrate.
This textbook presents concise chapters written by internationally respected experts on various important aspects of cancer-associated metabolism, offering a comprehensive overview of the central features of this exciting research field. The discovery that tumor cells display characteristic alterations of metabolic pathways has significantly changed our understanding of cancer: while the first description of tumor-specific changes in cellular energetics was published more than 90 years ago, the causal significance of this observation for the pathogenesis of cancer was only discovered in the post-genome era. The first 10 years of the twenty-first century were characterized by rapid advances in our grasp of the functional role of cancer-specific metabolism as well as the underlying molecular pathways. Various unanticipated interrelations between metabolic alterations and cancer-driving pathways were identified and currently await translation into diagnostic and therapeutic applications. Yet the speed, quantity, and complexity of these new discoveries make it difficult for researchers to keep up to date with the latest developments, an issue this book helps to remedy.
The way a cell undergoes malignant transformation should meet their capacity of surviving in the microenvironment of the organ where the cancer will develop. Metabolic adaptation is for sure one of the criteria that must be accomplished, driven by metabolic plasticity that allows the adaptation of cancer cells to the availability of energy and biomass sources that will sustain cell survival and proliferation. Each human organ has a particular microenvironment which depends on several cell types and in some cases also on symbiotic microorganisms. These biological partners are constantly sharing organic compounds and signaling molecules that will control mitogenesis, cell death and differentiation, accounting for the organ's function. Nevertheless, cancer cells are capable of taking advantage of this metabolic and signaling microenvironmental dynamics. In this book, we intend to present the different components of the microenvironment driving the metabolic fitness of cancer cells. The metabolic changes required for establishing a tumor in a given microenvironment and how these metabolic changes limit the response to drugs will generally be the major items addressed. It is important to mention not only aspects of the microenvironment that stimulate metabolic changes and that select better adapted tumor cells, but also how this regulation of cell plasticity is made. Thus, the signaling pathways that orchestrate and are orchestrated throughout this panoply of metabolic rearrangements will also be addressed in this book. The subjects will be presented from the conceptual point of view of the cross-cancer mechanisms and also particularizing some models that can be examples and enlightening within the different areas.
This book reviews current immunotherapeutic strategies for gastrointestinal (GI) malignancies, including immune composition, immune checkpoint inhibitors, cell therapy, and peptide vaccines used to protect against esophageal, gastric, hepato-biliary, pancreatic and colorectal cancers. It also discusses the current challenges of using immunotherapy for the treatment of gastrointestinal malignancies. The book reviews highly sensitive and specific immunomarkers for the detection of GI malignancies, and examines therapeutic vaccines and the major cytokines involved in GI immunotherapy, as well as their basic biology and clinical applications. In closing, the book explores various aspects of computational biology for the detection and treatment of GI malignancies.
Gastrointestinal (GI) malignancies account for a large portion of cancers worldwide. Although incidence of esophageal, gastric, and colorectal cancers has decreased in recent years, pancreatic and liver cancer have increased. The mainstay of GI cancer therapy is chemoradiation and surgery. Despite significant medical advancements, diagnosis and therapy for GI cancers remain challenging due to tumor cell resistance to chemoradiotherapy. The tumor’s increased cell signalling due to excessive transcription factor activation and increased stellate cell activity leads to collagen deposition formation of a dense stroma around the tumor, which prevents drugs from reaching the malignant cells. This leads to tumor chemoresistance. To circumvent these difficulties, drug therapy targeting the tumor’s specific microenvironment and the additive anticancer effect of phytochemicals can allow for more effective treatment. This volume will be the first on the market on the topic of phytochemicals and their effect on the tumor microenvironment (TME). TME is an emerging area of research and the book will be a welcome introductory addition to the field.