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The Interactions of DNA Repair, Telomere Homeostasis, and p53 Mutational Status in Solid Cancers: Risk, Prognosis, and Prediction
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SYSNO ASEP 0552825 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title The Interactions of DNA Repair, Telomere Homeostasis, and p53 Mutational Status in Solid Cancers: Risk, Prognosis, and Prediction Author(s) Vodička, Pavel (UEM-P) RID
Anděra, Ladislav (BTO-N)
Opattová, Alena (UEM-P)
Vodičková, Ludmila (UEM-P) RIDArticle number 479 Source Title Cancers (Basel). - : MDPI
Roč. 13, č. 2 (2021)Number of pages 19 s. Language eng - English Country CH - Switzerland Keywords interactions ; DNA damage response ; telomere homeostasis ; TP53 mutational status ; cancer risk ; cancer progression ; cancer therapy Subject RIV EB - Genetics ; Molecular Biology OECD category Genetics and heredity (medical genetics to be 3) R&D Projects GA19-08772S GA ČR - Czech Science Foundation (CSF) GA19-10543S GA ČR - Czech Science Foundation (CSF) Method of publishing Open access Institutional support UEM-P - RVO:68378041 ; BTO-N - RVO:86652036 UT WOS 000614962300001 EID SCOPUS 85099793613 DOI 10.3390/cancers13030479 Annotation Simple Summary
p53 is a nuclear transcription factor with a pro-apoptotic function. Somatic mutations in this gene represent one of the most critical events in human carcinogenesis. The disruption of genomic integrity due to the accumulation of various kinds of DNA damage, deficient DNA repair capacity, and alteration of telomere homeostasis constitute the hallmarks of malignant diseases. The main aim of our review was to accentuate a complex comprehension of the interactions between fundamental players in carcinogenesis of solid malignancies such as DNA damage response, telomere homeostasis and TP53.
The disruption of genomic integrity due to the accumulation of various kinds of DNA damage, deficient DNA repair capacity, and telomere shortening constitute the hallmarks of malignant diseases. DNA damage response (DDR) is a signaling network to process DNA damage with importance for both cancer development and chemotherapy outcome. DDR represents the complex events that detect DNA lesions and activate signaling networks (cell cycle checkpoint induction, DNA repair, and induction of cell death). TP53, the guardian of the genome, governs the cell response, resulting in cell cycle arrest, DNA damage repair, apoptosis, and senescence. The mutational status of TP53 has an impact on DDR, and somatic mutations in this gene represent one of the critical events in human carcinogenesis. Telomere dysfunction in cells that lack p53-mediated surveillance of genomic integrity along with the involvement of DNA repair in telomeric DNA regions leads to genomic instability. While the role of individual players (DDR, telomere homeostasis, and TP53) in human cancers has attracted attention for some time, there is insufficient understanding of the interactions between these pathways. Since solid cancer is a complex and multifactorial disease with considerable inter- and intra-tumor heterogeneity, we mainly dedicated this review to the interactions of DNA repair, telomere homeostasis, and TP53 mutational status, in relation to (a) cancer risk, (b) cancer progression, and (c) cancer therapy.Workplace Institute of Experimental Medicine Contact Lenka Koželská, lenka.kozelska@iem.cas.cz, Tel.: 241 062 218, 296 442 218 Year of Publishing 2022 Electronic address https://www.mdpi.com/2072-6694/13/3/479
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