New Research on Genomic InstabilityNew Research on Genomic Instability



One of the hallmarks of the cancer cell is the inherent instability of its genome. This book presents important research in this exciting field.

Author: Eleanor J. Gloscow

Publisher: Nova Publishers

ISBN: 1600213200

Category:

Page: 302

View: 779

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.

Genome Stability and Human DiseasesGenome Stability and Human Diseases



This book is written by international leading scientists in the field of genome stability.

Author: Heinz-Peter Nasheuer

Publisher: Springer Science & Business Media

ISBN: 9048134714

Category:

Page: 340

View: 437

Since the establishment of the DNA structure researchers have been highly interested in the molecular basis of the inheritance of genes and of genetic disorders. Scientific investigations of the last two decades have shown that, in addition to oncogenic viruses and signalling pathways alterations, genomic instability is important in the development of cancer. This view is supported by the findings that aneuploidy, which results from chromosome instability, is one of the hallmarks of cancer cells. Chromosomal instability also underpins our fundamental principles of understanding tumourigenesis: It thought that cancer arises from the sequential acquisition of genetic alterations in specific genes. In this hypothesis, these rare genetic events represent rate-limiting ‘bottlenecks’ in the clonal evolution of a cancer, and pre-cancerous cells can evolve into neoplastic cells through the acquisition of somatic mutations. This book is written by international leading scientists in the field of genome stability. Chapters are devoted to genome stability and anti-cancer drug targets, histone modifications, chromatin factors, DNA repair, apoptosis and many other key areas of research. The chapters give insights into the newest development of the genome stability and human diseases and bring the current understanding of the mechanisms leading to chromosome instability and their potential for clinical impact to the reader.

Genome Instability in Cancer DevelopmentGenome Instability in Cancer Development



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.

Author: Erich A. Nigg

Publisher: Springer Science & Business Media

ISBN: 9781402037641

Category:

Page: 512

View: 478

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 Genomic Instability in CancerChromatin and Genomic Instability in Cancer



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.

Author:

Publisher: Academic Press

ISBN: 9780323855624

Category:

Page: 284

View: 799

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

Genome StabilityGenome Stability



This volume is an essential resource for geneticists, epigeneticists, and molecular biologists who are looking to gain a deeper understanding of this rapidly expanding field, and can also be of great use to advanced students who are looking ...

Author: Igor Kovalchuk

Publisher: Academic Press

ISBN: 9780323856805

Category:

Page: 760

View: 119

Genome Stability: From Virus to Human Application, Second Edition, a volume in the Translational Epigenetics series, explores how various species maintain genome stability and genome diversification in response to environmental factors. Here, across thirty-eight chapters, leading researchers provide a deep analysis of genome stability in DNA/RNA viruses, prokaryotes, single cell eukaryotes, lower multicellular eukaryotes, and mammals, examining how epigenetic factors contribute to genome stability and how these species pass memories of encounters to progeny. Topics also include major DNA repair mechanisms, the role of chromatin in genome stability, human diseases associated with genome instability, and genome stability in response to aging. This second edition has been fully revised to address evolving research trends, including CRISPRs/Cas9 genome editing; conventional versus transgenic genome instability; breeding and genetic diseases associated with abnormal DNA repair; RNA and extrachromosomal DNA; cloning, stem cells, and embryo development; programmed genome instability; and conserved and divergent features of repair. This volume is an essential resource for geneticists, epigeneticists, and molecular biologists who are looking to gain a deeper understanding of this rapidly expanding field, and can also be of great use to advanced students who are looking to gain additional expertise in genome stability. A deep analysis of genome stability research from various kingdoms, including epigenetics and transgenerational effects Provides comprehensive coverage of mechanisms utilized by different organisms to maintain genomic stability Contains applications of genome instability research and outcomes for human disease Features all-new chapters on evolving areas of genome stability research, including CRISPRs/Cas9 genome editing, RNA and extrachromosomal DNA, programmed genome instability, and conserved and divergent features of repair

Genomic Instability and Cancer MetastasisGenomic Instability and Cancer Metastasis



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.

Author: Chris Maxwell

Publisher: Springer

ISBN: 9783319121369

Category:

Page: 247

View: 357

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.

New Research on DNA RepairNew Research on DNA Repair



Abnormalities in these processes have been implicated in cancer and ageing. This book presents leading-edge research from around the world in this frontal field.

Author: Breehn R. Landseer

Publisher: Nova Publishers

ISBN: 1600213855

Category:

Page: 393

View: 306

As a major defence against environmental damage to cells DNA repair is present in all organisms including bacteria, yeast, drosophila, fish, amphibians, rodents and humans. DNA repair is involved in processes that minimise cell killing, mutations, replication errors, persistence of DNA damage and genomic instability. Abnormalities in these processes have been implicated in cancer and ageing. This book presents leading-edge research from around the world in this frontal field.

Aging of the GenomeAging of the Genome



This is particularly important in a time when we are urgently trying to unravel the genetic component of aging-related diseases.

Author: Jan Vijg

Publisher: OUP Oxford

ISBN: 9780191524585

Category:

Page: 384

View: 405

Aging has long since been ascribed to the gradual accumulation of DNA mutations in the genome of somatic cells. However, it is only recently that the necessary sophisticated technology has been developed to begin testing this theory and its consequences. Vijg critically reviews the concept of genomic instability as a possible universal cause of aging in the context of a new, holistic understanding of genome functioning in complex organisms resulting from recent advances in functional genomics and systems biology. It provides an up-to-date synthesis of current research, as well as a look ahead to the design of strategies to retard or reverse the deleterious effects of aging. This is particularly important in a time when we are urgently trying to unravel the genetic component of aging-related diseases. Moreover, there is a growing public recognition of the imperative of understanding more about the underlying biology of aging, driven by continuing demographic change.

Cancer Cell Structures Carcinogens and Genomic InstabilityCancer Cell Structures Carcinogens and Genomic Instability



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.

Author: Leon P. Bignold

Publisher: Springer Science & Business Media

ISBN: 3764371560

Category:

Page: 375

View: 830

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.

Checkpoint Kinase Dependent Regulation of DNA Repair and Genome Instability in Breast CancerCheckpoint Kinase Dependent Regulation of DNA Repair and Genome Instability in Breast Cancer



The DNA damage response (DDR) functions as a tumorigenesis barrier. It is activated in precancerous lesions, potentially as a consequence of aberrant DNA replication.

Author:

Publisher:

ISBN: OCLC:495783637

Category:

Page: 29

View: 325

The DNA damage response (DDR) functions as a tumorigenesis barrier. It is activated in precancerous lesions, potentially as a consequence of aberrant DNA replication. The genetic alterations that create this genomic instability are poorly defined. Using a functional genomic screen in human cells we identified seventy-four genes that when silenced by RNAi activate the DDR. Using a series of secondary assays we determined that many have DNA replication-associated genome maintenance activities. In particular, we identified DDB1 as a genome maintenance gene, and further demonstrated that the replicationdependent genome maintenance activity of DDB1 involves the ubiquitin-mediated degradation of the replication protein CDT1. Our RNAi screen also identified CDK2-interacting protein (CINP) as a genome maintenance gene. Further characterization of CINP revealed this protein is a novel regulator of the ATR-mediated DDR pathway. CINP binds ATR through the ATRinteracting protein (ATRIP), and regulates ATR-dependent CHK1 phosphorylation and maintenance of the G2 checkpoint. Approximately seventeen of the seventy-four genome maintenance genes are known or putative tumor suppressors, including six that were identified as being mutated in breast and colorectal cancers by a cancer genome sequencing effort. Our results suggest that loss of these gene functions may promote tumorigenesis by causing genomic instability.