DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F20%3A00539304" target="_blank" >RIV/68378041:_____/20:00539304 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11140/20:10412352 RIV/75010330:_____/20:00013321 RIV/00216208:11110/20:10412352 RIV/00216208:11120/20:43920273
Výsledek na webu
<a href="https://www.mdpi.com/2072-6694/12/7/1713" target="_blank" >https://www.mdpi.com/2072-6694/12/7/1713</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/cancers12071713" target="_blank" >10.3390/cancers12071713</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome
Popis výsledku v původním jazyce
There is ample evidence for the essential involvement of DNA repair and DNA damage response in the onset of solid malignancies, including ovarian cancer. Indeed, high-penetrance germline mutations in DNA repair genes are important players in familial cancers:BRCA1,BRCA2mutations or mismatch repair, and polymerase deficiency in colorectal, breast, and ovarian cancers. Recently, some molecular hallmarks (e.g.,TP53,KRAS,BRAF,RAD51C/DorPTENmutations) of ovarian carcinomas were identified. The manuscript overviews the role of DNA repair machinery in ovarian cancer, its risk, prognosis, and therapy outcome. We have attempted to expose molecular hallmarks of ovarian cancer with a focus on DNA repair system and scrutinized genetic, epigenetic, functional, and protein alterations in individual DNA repair pathways (homologous recombination, non-homologous end-joining, DNA mismatch repair, base- and nucleotide-excision repair, and direct repair). We suggest that lack of knowledge particularly in non-homologous end joining repair pathway and the interplay between DNA repair pathways needs to be confronted. The most important genes of the DNA repair system are emphasized and their targeting in ovarian cancer will deserve further attention. The function of those genes, as well as the functional status of the entire DNA repair pathways, should be investigated in detail in the near future.
Název v anglickém jazyce
DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome
Popis výsledku anglicky
There is ample evidence for the essential involvement of DNA repair and DNA damage response in the onset of solid malignancies, including ovarian cancer. Indeed, high-penetrance germline mutations in DNA repair genes are important players in familial cancers:BRCA1,BRCA2mutations or mismatch repair, and polymerase deficiency in colorectal, breast, and ovarian cancers. Recently, some molecular hallmarks (e.g.,TP53,KRAS,BRAF,RAD51C/DorPTENmutations) of ovarian carcinomas were identified. The manuscript overviews the role of DNA repair machinery in ovarian cancer, its risk, prognosis, and therapy outcome. We have attempted to expose molecular hallmarks of ovarian cancer with a focus on DNA repair system and scrutinized genetic, epigenetic, functional, and protein alterations in individual DNA repair pathways (homologous recombination, non-homologous end-joining, DNA mismatch repair, base- and nucleotide-excision repair, and direct repair). We suggest that lack of knowledge particularly in non-homologous end joining repair pathway and the interplay between DNA repair pathways needs to be confronted. The most important genes of the DNA repair system are emphasized and their targeting in ovarian cancer will deserve further attention. The function of those genes, as well as the functional status of the entire DNA repair pathways, should be investigated in detail in the near future.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30101 - Human genetics
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2020
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Cancers (Basel)
ISSN
2072-6694
e-ISSN
—
Svazek periodika
12
Číslo periodika v rámci svazku
7
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
37
Strana od-do
1713
Kód UT WoS článku
000556366400001
EID výsledku v databázi Scopus
2-s2.0-85086923920