Nucleases in homologous recombination as targets for cancer therapy

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F14%3A00061104" target="_blank" >RIV/00159816:_____/14:00061104 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14110/14:00073831

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.febslet.2014.06.010" target="_blank" >http://dx.doi.org/10.1016/j.febslet.2014.06.010</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.febslet.2014.06.010" target="_blank" >10.1016/j.febslet.2014.06.010</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Nucleases in homologous recombination as targets for cancer therapy

Popis výsledku v původním jazyce

Genomic DNA is constantly challenged from endogenous as well as exogenous sources. The DNA damage response (DDR) mechanism has evolved to combat these challenges and ensure genomic integrity. In this review, we will focus on repair of DNA double-strand breaks (DSB) by homologous recombination and the role of several nucleases and other recombination factors as suitable targets for cancer therapy. Their inactivation as well as overexpression have been shown to sensitize cancer cells by increasing toxicity to DNA-damaging agents and radiation or to be responsible for resistance of cancer cells. These factors can also be used in targeted cancer therapy by taking advantage of specific genetic abnormalities of cancer cells that are not present in normal cells and that result in cancer cell lethality.

Název v anglickém jazyce

Nucleases in homologous recombination as targets for cancer therapy

Popis výsledku anglicky

Genomic DNA is constantly challenged from endogenous as well as exogenous sources. The DNA damage response (DDR) mechanism has evolved to combat these challenges and ensure genomic integrity. In this review, we will focus on repair of DNA double-strand breaks (DSB) by homologous recombination and the role of several nucleases and other recombination factors as suitable targets for cancer therapy. Their inactivation as well as overexpression have been shown to sensitize cancer cells by increasing toxicity to DNA-damaging agents and radiation or to be responsible for resistance of cancer cells. These factors can also be used in targeted cancer therapy by taking advantage of specific genetic abnormalities of cancer cells that are not present in normal cells and that result in cancer cell lethality.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

FEBS Letters

ISSN

0014-5793

e-ISSN

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Svazek periodika

588

Číslo periodika v rámci svazku

15

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

11

Strana od-do

2446-2456

Kód UT WoS článku

000339535200013

EID výsledku v databázi Scopus

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