Oncogenes And Carcinogenesis

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

Oncogenes are mutated and/or overexpressed at high levels in tumor cells. Tumors of the lung, breast, pancreas, and colon may display specific oncogenetic features. These tumors have been largely associated with exposure to environmental carcinogens and a variety of biological agents, including viruses. These carcinogens can induce specific genetic and epigenetic alterations in these tissues, leading to aberrant functioning of oncogenes and tumor suppressor genes. On the microRNAs (miRNAs) there are significant modifiers of both transcription and translation of oncogenes in carcinogenesis. In the last 50 years, several oncogenes and microRNAs related to these oncogenes have been identified in different types of human cancers. It is now clear that high expression of oncogenes, DNA damage response, and regulation of the cell cycle are related to the circadian clock. This book will mainly focus on the expressions of different oncogenes in breast, colon, and lung cancers. Moreover, readers will gain qualified scientific knowledge of the alterations in miRNAs in different types of cancers and the effects of the circadian clock on the expression of oncogenes in carcinogenesis.

"Cancer viruses" have played a paradoxical role in the history of cancer research. Discovered in 1911 by Peyton Rous (1) at the Rockefeller Institute, they were largely ignored for several decades. Witness his eventual recognition for a Nobel Prize, but not until 1966-setting an all time record for latency, and testimony to one more advantage of longevity. In the 1950s, another Rockefeller Nobelist, Wendell Stanley, spearheaded a campaign to focus attention on viruses as etiological agents in cancer, his plat form having been the chemical characterization of the tobacco mosaic virus as a pure protein-correction, ribonucleoprotein-in 1935 (2). This doctrine was a centerpiece of the U.S. National Cancer Crusade of 1971: if human cancers were caused by viruses, the central task was to isolate them and prepare vaccines for immunization. At that point, many observers felt that perhaps too much attention was being devoted to cancer viruses. It was problematic whether viruses played an etiological role in more than a handful of human cancers.

The first edition of Oncogenes (1989) focused on several of the better known transforming mechanisms and surveyed a spectrum of solid tumors and hematologic malignancies. Several of the nearly 50 known oncogenes most relevant to human disease were examined. In contrast, this volume presents a very different profile and balance of subject material that reflects the rapidly changing field of molecular oncology and its newly emerging concepts. Among the most important discoveries of the past 4 years are the identification of nearly a dozen different tumor suppressor genes and the finding of an entirely new class of cancer-causing gene (bcl-2) that acts by inhibiting cell death rather than stimulating cell proliferation. This edition begins by reviewing selected malignancies in which our earlier search for clinically relevant oncogenes has led to more focused studies on gain-of-function and loss-of-function genetic abnormalities, as well as autocrine and paracrine growth factor loops known to regulate tumor physiology and malignant cell behavior. Curiously, many of these genetic and functional abnormalities are shared by several different tumor types and are not uniformly present in all tumors of the same type. This observation brings up molecular questions about the tissue-specific determinants that underlie individual cancers and also gives added impetus to the suggestion that molecular abnormalities (referred to as tumor markers) be included among the histopathologic features used for clinical diagnosis and manage ment.

This volume brings together the latest studies on various aspects of molecular oncology. It emphasizes the current view that oncogenes and suppressor genes need to be discussed in the same context.

Providing the physician with a solid understanding of molecular biology and its applications for the diagnosis and treatment of cancer, this book reviews the basic molecular and other principles of cancer medicine, including controls of cell growth and senescence, carcinogenesis, tumorogenesis, and epidemiology. The second part of the book gives clinical examples to demonstrate the basic science principles, including chapters on leukaemia, colon cancer, and breast cancer. A chapter on molecular diagnostics and screening plus a chapter on new molecular anti-cancer therapies allow readers an insight into current therapies as well as the future of molecular cancer medicine. A useful glossary defines new terminology at-a-glance. Written in a user-friendly, conversational format, this text will be welcomed by all physicians eager to sharpen their own understanding of molecular cancer medicine as well as to help them provide patients with balanced information on the advances and limitations of current treatment options.