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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 0555727 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, P. (CZ)
Anděra, Ladislav (UMG-J) RID
Opattova, A. (CZ)
Vodičková, L. (CZ)Number of authors 4 Article number 479 Source Title Cancers (Basel). - : MDPI
Roč. 13, č. 3 (2021)Number of pages 19 s. Publication form Online - E 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 Oncology Method of publishing Open access Institutional support UMG-J - RVO:68378050 UT WOS 000614962300001 DOI 10.3390/cancers13030479 Annotation 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 Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2022 Electronic address https://www.mdpi.com/2072-6694/13/3/479
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