Ribezzo, Flavia, Shiloh, Yosef and Schumacher, Bjoern (2016). Systemic DNA damage responses in aging and diseases. Semin. Cancer Biol., 37-38. S. 26 - 36. LONDON: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. ISSN 1096-3650

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Abstract

The genome is constantly attacked by a variety of genotoxic insults. The causal role for DNA damage in aging and cancer is exemplified by genetic defects in DNA repair that underlie a broad spectrum of acute and chronic human disorders that are characterized by developmental abnormalities, premature aging, and cancer predisposition. The disease symptoms are typically tissue-specific with uncertain genotype-phenotype correlation. The cellular DNA damage response (DDR) has been extensively investigated ever since yeast geneticists discovered DNA damage checkpoint mechanisms, several decades ago. In recent years, it has become apparent that not only cell-autonomous but also systemic DNA damage responses determine the outcome of genome instability in organisms. Understanding the mechanisms of non-cell-autonomous DNA damage responses will provide important new insights into the role of genome instability in human aging and a host of diseases including cancer and might better explain the complex phenotypes caused by genome instability. (C) 2016 Elsevier Ltd. All rights reserved.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Ribezzo, FlaviaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Shiloh, YosefUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schumacher, BjoernUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-274895
DOI: 10.1016/j.semcancer.2015.12.005
Journal or Publication Title: Semin. Cancer Biol.
Volume: 37-38
Page Range: S. 26 - 36
Date: 2016
Publisher: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Place of Publication: LONDON
ISSN: 1096-3650
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
ATM PROTEIN-KINASE; NF-KAPPA-B; NUCLEOTIDE EXCISION-REPAIR; NIJMEGEN BREAKAGE SYNDROME; FATAL NEOPLASTIC DISEASES; DOUBLE-STRAND BREAKS; ATAXIA-TELANGIECTASIA; SENESCENT CELLS; LIFE-SPAN; CELLULAR SENESCENCEMultiple languages
OncologyMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/27489

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