Last edited by Moogur
Friday, November 6, 2020 | History

5 edition of DNA REPAIR, GENETIC INSTABILITY, AND CANCER found in the catalog.

DNA REPAIR, GENETIC INSTABILITY, AND CANCER

  • 128 Want to read
  • 7 Currently reading

Published by World Scientific Publishing .
Written in English

    Subjects:
  • Medical genetics,
  • Oncology,
  • Medical,
  • Medical / Nursing,
  • Genetics,
  • Life Sciences - Biology - General,
  • Science,
  • Cancer,
  • DNA repair,
  • Genetic aspects,
  • Neoplasms,
  • etiology

  • Edition Notes

    ContributionsQingyi Wei (Editor), Lei Li (Editor), David J. Chen (Editor)
    The Physical Object
    FormatHardcover
    Number of Pages376
    ID Numbers
    Open LibraryOL9197988M
    ISBN 109812700145
    ISBN 109789812700148


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DNA REPAIR, GENETIC INSTABILITY, AND CANCER Download PDF EPUB FB2

One of the particular emphases of the book is the link between inherited DNA repair deficiencies and susceptibility to cancer in the general : Hardcover. Mechanisms have evolved to help protect our genetic material from endogenous and exogenous damage that are vital for an organism's survival.

This ability to recognize damaged DNA and simultaneously regulate cell cycle progression and DNA repair is critical for genomic stability, and defects in these pathways are hallmarks of cancer. title = "DNA repair, genetic instability, and cancer", abstract = "This volume describes the elaborate surveillance systems and various DNA repair mechanisms that ensure accurate passage of genetic information onto daughter by: Summary: Describes the elaborate surveillance systems and various DNA repair mechanisms that ensure accurate passage of genetic information onto daughter cells.

This book narrates how the cell cycle checkpoint and DNA repair machineries detect and restore DNA damages that are embedded in millions to billions of normal base pairs.

Thus, HR plays pivotal roles in maintaining genome stability and preventing tumorigenesis. Although HR is generally an error-free DNA repair process, hyper-recombination, hypo-recombination and altered HR outcomes can all lead to genomic instability. Thus HR can be mutagenic and contribute to genomic instability when it is not properly regulated.

Thus, deficiency in DNA repair causes genomic instability and genomic instability is the likely main underlying cause of the genetic alterations leading to tumorigenesis.

Deficient DNA repair permits the acquisition of a sufficient number of alterations in tumor suppressor genes and oncogenes to fuel by: Indeed, in inherited cancers, germ line mutations targeting DNA repair genes are present in every cell of the patient's body.

Thus, a single event, loss of the remaining wild type allele, would lead to genomic instability and drive tumor development, as predicted by Cited by:   However, evidence also supports the concept that hypoxia can drive and maintain genetic instability and a mutator phenotype. Genetic instability can arise as a function of hypoxia-mediated resistance to apoptosis and decreased DNA repair, leading to increased rates of mutagenesis and altered chromatin by: Cancer cells are characterized by genetic instability driven by deficiencies in DNA repair and/or DNA recombination genes.

This deficiency renders them vulnerable to agents whose effect is part of the synthetic lethal by: Genomic instability can initiate cancer, augment progression, and influence the overall prognosis of the affected patient.

Genomic instability arises from many different pathways, such as telomere damage, centrosome amplification, epigenetic modifications, and DNA damage from endogenous and exogenous sources, and can be perpetuating, or limiting, through the Cited by: The identification of the most frequent mutations that inactivate this gene will provide an important tool for the screening and diagnosis of cancer-prone individuals.

Human DNA repair and cancer associated diseases. A different cause for genetic instability is the frequent appearance of mismatches on the double helix of DNA. DNA damage causes cancer development when erroneous DNA repair leads to mutations of chromosomal aberration that activate oncogenes or inactivate tumor suppressors genes (red).

When DNA damage persists and interferes with replication or transcription, DNA damage checkpoints trigger cellular senescence or apoptosis that inactivate or eliminate Cited by: Humans with NER deficiencies suffer from the DNA repair syndrome, xeroderma pigmentosum (XP) with manifestations of both acute sunlight sensitivity and profoundly elevated occurrence of skin cancer.

XP is a classical example of the direct relationship between genomic instability and cancer development. Genre/Form: Libros electronicos Electronic books Electronic book: Additional Physical Format: Print version: DNA repair, genetic instability, and cancer.

Normal cells are often capable of withstanding mutational assault because they have checkpoints and "DNA repair" mechanisms in place. When such mechanisms fail, "cancer" may be a result. Through "mutation", such protective mechanisms are compromised in cancer cells.

Homologous recombination (HR) is a molecular pathway involved in a multitude of processes, from the generation of genetic diversity to DNA repair and replication. HR provides a mechanism for the accurate repair of DNA double-strand breaks, protecting cells from chromosomal aberrations such as those seen in cancer.

Get this from a library. DNA repair, genetic instability, and cancer. [Qingyi Wei; Lei Li, Dr.; David Chen, Dr.;] -- This volume describes the elaborate surveillance systems and various DNA repair mechanisms that ensure accurate passage of genetic information onto daughter cells.

In particular, it narrates how the. Microsatellite instability has been encountered in many forms of human cancer and its possible involvement in their growth, invasive, and metastatic behaviors is well recognized. p53 abnormalities are not associated with the RER phenotype and microsatellite instability, and mismatch repair also has no influence on it.

In particular, GIAD publishes novel data regarding the regulatory mechanisms of genome stability, including epigenetic and post-translational modifications, and the DNA damage response and its association with the inheritance of mutations that contribute to genetic disorders, neurodegenerative diseases, cancer, and ageing.

Excessive genomic instability usually leads to cell death, a factor in the utility of MLN as an anticancer agent. However, because of the many redundant pathways for preventing overreplication or for repair, it is rare for mutations (or epigenetic silencing) affecting single pathways to create so much genomic instability as to cause cell by: Base excision repair (BER) is the major repair mechanism that removes oxidized, alkylated, deaminated bases as well as apurinic/apyrimidinic (AP) sites.

BER is initiated by specific and versatile DNA glycosylases, many of which have redundant functions. Genomic instability is one of the most pervasive characteristics of tumour cells and is probably the combined effect of DNA damage, tumour-specific DNA repair defects, and Author: Ana Rita Carlos.

Among several factors involved in determining the hypermutated status, such as inactivating mutations in the DNA polymerases as well as exposure to external (cigarette smoke, UV radiation, chemicals) and endogenous (reactive oxygen species) mutagens, a defective DNA mismatch repair system may give rise to genetic instability and, particularly Author: Giuseppe Palmieri, Milena Casula, Antonella Manca, Grazia Palomba, Maria Cristina Sini, Valentina Do.

DNA repair, genome stability and cancer: a historical DNA repair, genome stability and cancer – a historical perspective. have been shown to arise from genetic defects in DNA repair systems, as have subsets of familial breast, ovarian, prostate and pancreatic cancersCited by: Eukaryotic cells from yeast to humans have a pathway known as DNA post-replication repair (PRR) or DNA damage tolerance (DDT), which employs one of two means to bypass the replication-blocking lesion instead of removing it.

One method is translesion DNA synthesis (TLS), which utilizes a panel of specialized DNA polymerases. Introduction --DNA synthesis errors, mutators and cancer --DNA polymerase and the control of DNA damage induced mutagenesis in eukaryotes --Patterns of mutation in cancer cells --Mismatch repair and cancer --Genomic instability and tolerance to alkylating agents --The relationship of DNA methylation to cancer --Neoplastic transformation: the.

This book reviews our current level of understanding of the role of genetic instability in human tumorigenesis. In this most rapidly moving field, discoveries in recent years have elucidated a number of important gene products which control cellular responses to DNA damaging agents, e.g., DNA repair and cell cycle by: DNA Repair and Genetic Instability: Medicine & Health Science Books @ Genetic Instability Xeroderma Pigmentosum Nijmegen Breakage Syndrome Bloom Syndrome Fanconi Anemia Patient These keywords were added by machine and not by the authors.

This process is experimental and the keywords may be updated as the learning algorithm improves. Two biological processes, DNA polymerase proofreading and DNA mismatch repair (DMR), are known to affect spontaneous mutation rates dramatically in both prokaryotes and eukaryotes (83,98).

Keywords Mismatch Repair Microsatellite Instability HNPCC Patient MutS Homolog Hereditary Nonpolyposis Colon CancerCited by: 2. 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. In many instances, accumulation of DNA damage has been linked to cancer, and genetic deficiencies in specific DNA repair genes are associated with tumor-prone phenotypes.

In addition to mutations, which can be either inherited or somatically acquired, epigenetic silencing of DNA repair genes may promote by:   Vafa, O.

et al. c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability. Mol. Cell 9, – ().Cited by: The clinical implications that polymorphisms in DNA repair genes may modify levels of CAG instability are far reaching: such polymorphisms may explain the variable levels of disease age-of-onset, disease progression and severity, which may be driven by the highly variable levels of repeat instability between individuals.

To this degree, the Cited by: Microsatellite Instability and Progression of Cancer: Microsatellite Instability is raised in Gallbladder Cancer [Singh, Rachana, Shukla, Hari Shankar, Pandey, Haushla Prasad] on *FREE* shipping on qualifying offers.

Microsatellite Instability and Progression of Cancer: Microsatellite Instability is raised in Gallbladder CancerAuthor: Rachana Singh, Hari Shankar Shukla, Haushla Prasad Pandey.

Instability underlies vast majority of genomic events. Such events could involve chromosome alterations, telomere dysfunction, DNA damage and irregular repair etc. During tumourigenesis, telomerase is up-regulated facilitating immortal nature of cancer cells.

Increased rates of damage may arise from either external or internal published: 01 Jun,   Accumulating evidence showed that common mutations or polymorphisms in DNA repair genes involved in altering protein function and capacity to repair damaged DNA, thus deficits in repair capacity which lead to genetic instability, pathogenesis and carcinogenesis, however, the results were inconsistent in distinct cancers, and need further to be elucidated Author: Huizhe Wu, Shanqiong Li, Xiaoyun Hu, Wenyan Qin, Yilin Wang, Tong Sun, Zhikun Wu, Xiufang Wang, Senx.

Failure of these repair mechanisms, leading to genomic instability, is common in cancer, and has even been suggested to be a universal characteristic of malignancy. This chapter outlines these cellular processes and reviews the both the mechanisms and consequences of their dysregulation in human cancer.

Genetic instability is one of the common characteristics of colorectal cancer. Three major types of genetic instability have been reported in colorectal cancer [7–10].Microsatellite instability occurs due to variations in DNA mismatch repair genes, while chromosomal instability (CIN) is distinguished by major chromosomal alterations occurring at cell division and usually involves Author: Narasimha Reddy Parine, Reddy Sri Varsha, Mohammad SaudAlanazi.

Research on DNA and chromosome aberrations focuses on cancer genetics and epigenetics. Topics include regulation of gene expression; DNA damage from exposure to chemical, physical, and endogenous agents; mechanisms of DNA damage signaling and DNA repair; and genomic instability and related molecular, cytogenetic, and chromosomal effects during tumor.

Gene amplification mechanisms \/ Michelle Debatisse and Bernard Malfoy. DNA methylation and cancer-associated genetic instability \/ Melanie Ehrlich. Deregulation of the centrosome cycle and the origin of chromosomal instability in cancer \/ Wilma L.

Lingle, Kara Lukaswiewicz and Jeffrey L. Salisbury -- Genome integrity checkpoints.DNA DSBs represent the most serious DNA damage, which, if not repaired accurately, can result in genomic instability, including chromosome rearrangements or gene mutations, and finally can lead to cancer defects in the genes encoding ATM, NBN (NBS1), BRCA1, FANCD2, BLM, TP53, CDS1/CHK2, and others, can cause.An exciting finding was the identification of mrt-2, a gene responsible for germline immortality (Ahmed and Hodgkin, ).

mrt-2 mutants exhibit progressive telomere shortening and accumulate end-to-end chromosome fusions. In addition, mrt-2 mutants are defective in DNA damage-induced mitotic arrest and apoptosis in the germline (Gartner et al., ).