This book introduces readers to the molecules involved in apoptosis and genomal integrity and considers the gain or loss of the functions that lead to cancer.

Proceedings of the Eighth Annual Pezcoller Symposium held in Trento, Italy, June 17-19, 1996

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

The past five years have witnessed an explosion of research efforts in the study of how cells die. This book provides an up-to-date overview of our current knowledge of apoptosis and how discoveries in this area impact on our understanding of cancer. By synthesizing many of the recent developments in this area and placing them in perspective, it fulfills an important need. All the contributions are written by experts in their respective fields. The first two chapters give a basic introduction to the cell death machinery and its role in tumor development and progression; subsequent chapters cover current aspects of apoptosis research, including the involvement of cell cycle-related proteins (e.g. cyclin-dependent kinases) in apoptosis, the role of Bcl-2, Bcr-Abl, Rb, p53 and myc in the regulation of cell death, and apoptosis in the context of specific neoplasms such as cancer of the prostate, kidney, leukemia and neuroblastoma. It is also discussed how insights into the regulation of apoptosis may be exploited for designing new drugs aimed at eliminating malignant cells. Compiling the most recent research results on the relationship between apoptosis and cancer in one handy volume, this book will provide a valuable reference for scientists working in cancer research as well as newcomers to the field.

Intracellular checkpoint controls constitute a network of signal transd- tion pathways that protect cells from external stresses and internal errors. Ext- nal stresses can be generated by the continuous assault of DNA-damaging agents, such as environmental mutagens, ultraviolet (UV) light, ionizing radiation, or the reactive oxygen species that can arise during normal cellular metabolism. In response to any of these assaults on the integrity of the genome, the activation of the network of checkpoint control pathways can lead to diverse cellular responses, such as cell cycle arrest, DNA repair, or elimination of the cell by cell death (apoptosis) if the damage cannot be repaired. Moreover, internal errors can occur during the highly orchestrated replication of the cellular genome and its distribution into daughter cells. Here, the temporal order of these cell cycle events must be strictly enforced—for example, to ensure that DNA replication is c- plete and occurs only once before cell division, or to monitor mitotic spindle assembly, and to prevent exit from mitosis until chromosome segregation has been completed. Thus, well functioning checkpoint mechanisms are central to the maintenance of genomic integrity and the basic viability of cells and, the- fore, are essential for proper development and survival. The importance of proper functioning of checkpoints becomes plainly obvious under conditions in which this control network malfunctions and fails. Depending on the severity and timing, failure of this machinery can lead to embryonic lethality, genetic diseases, and cancer.

Provides insight into established practices and research into apoptosis and senescence by examining techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics which still hold mysteries for researchers. This book concludes with established cancer therapies.

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.