The Molecular Basis of Cancer E-Book 4th Edition
Research in molecular genetics and cancer biology and advances in analytical technologies have revolutionized our understanding of cancer. Over the past three decades, there has been a massive acceleration in discoveries and observations that explains the genetic basis of cancer, a disease that until recently was thought about primarily in purely descriptive terms. Conversely, the study of malignancy has transformed our understanding of the molecular and genetic processes that govern the growth and proliferation of normal cells.
By 1995, our knowledge had expanded to the point that we felt it worthwhile to write a textbook describing the molecular basis of cancer for students, researchers, and providers of clinical care from a variety of disciplines. The aim in this fourth edition of the textbook continues to explain, rather than to merely recount. Five editors, selected for their diverse expertise and their reputations as educators, met to design a sequence of sections and chapters that would lead the reader from the basic genetic and molecular mechanisms of carcinogenesis, to the molecular and biological features of cancer cell growth and metastasis, then to advances in sequencing technologies and bioinformatics that enable personalized risk assessment and diagnostics, followed by a description of molecular and genetic abnormalities that drive the common types of cancer, and finally to the molecular basis for new, targeted approaches to cancer therapy.
A purpose of this textbook is to describe the scientific underpinnings that will enable clinicians and other professionals who manage cancer patients to better understand the disease and its therapy. This book will be of equal, or possibly greater, interest to laboratory and clinical investigators in biomedical research and to advanced students and trainees, who need to understand the molecular mechanisms that govern the functioning and malfunctioning of malignant cells. Although the chapters follow a sequence that moves from pathogenesis to therapy, each chapter stands alone in its treatment of the subject matter.
Cancer arises as a result of genetic and epigenetic alterations that either enhance or diminish the activities of critical pathways that mediate normal cellular activities. Impaired capacity to repair genetic alterations can contribute to the likelihood that cells accumulate these genetic abnormalities, leading to malignant transformation. The disease is not merely a disorder of individual transformed cells. These cells grow into tumor masses and attract a blood supply, and they invade through surrounding tissues and metastasize. Molecular influences from the environment around the cancer cells contribute importantly to the capacity of genetically altered cells to produce malignant tumors.
A remarkable lesson gained from cancer research is that the strategies utilized by widely divergent cell lineages to regulate growth and differentiation share common molecular pathways. The accumulation of mutations and altered expression of genes critical for these pathways is a recurrent theme observed in many different types of cancer. Cancers also appear to select for genetic abnormalities that may be most advantageous for escape from normal regulatory mechanisms in their particular microenvironments.
What is most exciting today is the active dialogue between clinical investigators and laboratory scientists who share an interest
in applying the new knowledge of genetics and molecular biology to the early diagnosis, targeted treatment, and improved prevention of disease. Today we have the opportunity to select treatments for clinical administration from among hundreds of new biological and chemical anticancer agents targeting pathways altered by specific molecular irregularities that result from aberrant genes. It is only recently that we can detect the genetic aberrations in cancer specimens from individual patients in a reasonable time frame and at a reasonable cost. This means that genomic assays can be used to select therapies that target the products of the aberrant genes in a patient’s cancer and are more likely to provide benefit for that patient. The knowledge we present in this textbook should supply a basis upon which these new approaches to cancer therapy can be evaluated and implemented by those interested in understanding and critically assessing the many new products of the biotechnology revolution.
The editors are delighted that we were able to recruit as contributing authors outstanding investigators who are excited about the challenge of presenting their areas of expertise in a textbook format. In many cases this has required more time and effort than they initially anticipated, and we are grateful for their dedication.
We hope that we have come at least part of the way toward achieving what we set out to do. We have been assisted and encouraged by the professionals at Elsevier, as well as the patient and everessential help of the secretaries in our offices.
John Mendelsohn, MD
Joe W. Gray, PhD
Peter M. Howley, MD
Mark A. Israel, MD
Craig B. Thompson, MD
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|December 22, 2017|
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