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Tumors can be induced by a variety of physical and chemical carcinogens. The resulting tumor cells are usually abnormal in their morphology and behavior and transmit their abnormalities to their daughter tumor cells. Most theories of the pathogenesis of tumors suggest that carcinogens in some way cause alterations either of the genomes or of inheritable patterns of gene expression in normal cells, which then cause morphological and behavioral changes. This volume presents a collection of articles aimed at the question by what genetic or epigenetic mechanisms carcinogens can cause morphological abnormalities of tumor cells. It includes reviews of cellular targets of known carcinogens, and presents varying viewpoints of how morphological abnormalities and the actions of carcinogens might be related. The volume will be of interest to all those who are involved in cancer research or in the prevention, diagnosis or management of tumors in humans or animals.
Many cancer biologists now believe that genomic instability not only initiates carcinogenesis, but also allows the tumour cell to become metastatic and evade drug toxicity. The loss of stability of the genome is becoming accepted as one of the most important aspects of carcinogenesis. One of the hallmarks of the cancer cell is the inherent instability of its genome. This book presents important research in this exciting field.
Holland-Frei Cancer Medicine, Ninth Edition, offers a balanced view of the most current knowledge of cancer science and clinical oncology practice. This all-new edition is the consummate reference source for medical oncologists, radiation oncologists, internists, surgical oncologists, and others who treat cancer patients. A translational perspective throughout, integrating cancer biology with cancer management providing an in depth understanding of the disease An emphasis on multidisciplinary, research-driven patient care to improve outcomes and optimal use of all appropriate therapies Cutting-edge coverage of personalized cancer care, including molecular diagnostics and therapeutics Concise, readable, clinically relevant text with algorithms, guidelines and insight into the use of both conventional and novel drugs Includes free access to the Wiley Digital Edition providing search across the book, the full reference list with web links, illustrations and photographs, and post-publication updates
Research over the past decades has firmly established the genetic basis of cancer. In particular, studies on animal tumour viruses and chromosome rearrangements in human tumours have concurred to identify so-called ‘proto-oncogenes’ and ‘tumour suppressor genes’, whose deregulation promotes carcinogenesis. These important findings not only explain the occurrence of certain hereditary tumours, but they also set the stage for the development of anti-cancer drugs that specifically target activated oncogenes. However, in spite of tremendous progress towards the elucidation of key signalling pathways involved in carcinogenesis, most cancers continue to elude currently available therapies. This stands as a reminder that “cancer” is an extraordinarily complex disease: although some cancers of the haematopoietic system show only a limited number of characteristic chromosomal aberrations, most solid tumours display a myriad of genetic changes and considerable genetic heterogeneity. This is thought to reflect a trait commonly referred to as ‘genome instability’, so that no two cancers are ever likely to display the exact same genetic alterations. Numerical and structural chromosome aberrations were recognised as a hallmark of human tumours for more than a century. Yet, the causes and consequences of these aberrations still remain to be fully understood. In particular, the question of how genome instability impacts on the development of human cancers continues to evoke intense debate.
Chromatin and DNA Repair in Cancer, Volume 364 in the International Review of Cell and Molecular Biology series reviews and details current advances in cell and molecular biology. Chapters in this new release cover Genomic Instability and metabolism in cancer, Histones variants and Histones modifications in cancer and Aging, DNA Double-stranded breaks Repair in Cancer, Reactive oxygen species and DNA damage response in cancer, Transcription-Associated DNA Breaks and Cancer: A Matter of DNA Topology, Mechanisms of Base Excision Repair: Its Significance to Human Health, and more. The IRCMB series has a worldwide readership, maintaining a high standard by publishing invited articles on important and timely topics that are authored by prominent cell and molecular biologists. The articles published in IRCMB have a high impact and an average cited half-life of 9 years. This great resource ranks high amongst scientific journals dealing with cell biology. Publishes only invited review articles on selected topics Authored by established and active cell and molecular biologists, drawn from international sources Offers a wide range of perspectives on specific subjects
Metastasis is the primary cause of mortality associated with cancer, and tumor genomic heterogeneity is a likely source for the cells that support cancer progression, resistance to therapy, and disease relapse. This book connects cancer metastasis with genomic instability in a comprehensive manner. Section 1 outlines the fundamental mechanisms responsible for these cellular and tissue phenotypes. Section 2 discusses in silico, in vitro, and in vivo models used for the experimental study of these processes. Section 3 reviews emerging themes (ex., microenvironment, mechanotransduction, and immunomodulation), and Section 4 highlights new therapeutic approaches to overcome the unique challenges presented by the heterogeneous and metastatic tumor. This book is intended for undergraduates and postgraduates with an interest in the areas of medicine, oncology, and cancer biology as well as for the content expert searching for thorough reviews of current knowledge in these areas.
This issue of Recent Results in Cancer Research presents a comprehensive review of current understanding of chromosomal instability in cancer and of strategies to use this information for better treatment of patients with cancer. Cancer is a disease of the chromosomes, and chromosomal instability in cancer disrupts gene function by either inactivating tumor suppressor genes or activating growth-promoting oncogenes. The chromosomal basis for these aberrations is either translocations, which change the integrity of genes, or abnormal numbers of chromosomes, a condition referred to as aneuploidy, which results in abnormal gene expression levels. Such structural or numerical chromosomal aberrations are specific for distinct tumor entities. The degree of chromosomal instability and the degree of intratumor heterogeneity have profound consequences for disease outcome and for therapeutic stratification.
Exploring the chromosomal imbalance (aneuploidy) theory of cancer, this volume describes how cancer is initiated and why progression takes years to decades. It clarifies why cancer cells often become drug resistant, provides objective, quantitative measures for detecting cancer and monitoring its progression, and suggests non-toxic strategies of ca