Universität zu Köln

Jachimowicz, Ron D., Goergens, Jonas and Reinhardt, H. Christian (2019). DNA double-strand break repair pathway choice-from basic biology to clinical exploitation. Cell Cycle, 18 (13). S. 1423 - 1435. PHILADELPHIA: TAYLOR & FRANCIS INC. ISSN 1551-4005

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Abstract

Mutations in genes encoding components of the DNA damage response (DDR) are among the most frequent aberrations in human tumors. Moreover, a large array of human syndromes is caused by mutations in genes involved in DDR pathways. Among others, homologous recombination repair (HR) of DNA double-strand breaks (DSB) is frequently affected by disabling mutations. While impaired HR is clearly promoting tumorigenesis, it is also associated with an actionable sensitivity against PARP inhibitors. PARP inhibitors have recently received FDA approval for the treatment of breast- and ovarian cancer. However, as with all molecularly targeted agents, acquired resistance limits its use. Both pharmaco-genomic approaches and the study of human genome instability syndromes have led to a profound understanding of PARP inhibitor resistance. These experiments have revealed new insights into the molecular mechanisms that drive mammalian DSB repair. Here, we review recent discoveries in the field and provide a clinical perspective.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Jachimowicz, Ron D. UNSPECIFIED UNSPECIFIED UNSPECIFIED Goergens, Jonas UNSPECIFIED UNSPECIFIED UNSPECIFIED Reinhardt, H. Christian UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-147906
DOI:	10.1080/15384101.2019.1618542
Journal or Publication Title:	Cell Cycle
Volume:	18
Number:	13
Page Range:	S. 1423 - 1435
Date:	2019
Publisher:	TAYLOR & FRANCIS INC
Place of Publication:	PHILADELPHIA
ISSN:	1551-4005
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language HOMOLOGOUS RECOMBINATION; END RESECTION; DAMAGE RESPONSE; SYNTHETIC LETHALITY; ATM DEFICIENCY; FANCONI-ANEMIA; CANCER; MUTATIONS; INHIBITOR; SENSITIVITY Multiple languages Cell Biology Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/14790