Replication stress links structural and numerical cancer chromosomal instability

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F13%3A33143744" target="_blank" >RIV/61989592:15110/13:33143744 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1038/nature11935" target="_blank" >http://dx.doi.org/10.1038/nature11935</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/nature11935" target="_blank" >10.1038/nature11935</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Replication stress links structural and numerical cancer chromosomal instability

Popis výsledku v původním jazyce

Cancer chromosomal instability (CIN) results in an increased rate of change of chromosome number and structure and generates intratumour heterogeneity(1,2). CIN is observed in most solid tumours and is associated with both poor prognosis and drug resistance(3,4). Understanding a mechanistic basis for CIN is therefore paramount. Here we find evidence for impaired replication fork progression and increased DNA replication stress in CIN+ colorectal cancer (CRC) cells relative to CIN- CRC cells, with structural chromosome abnormalities precipitating chromosome missegregation in mitosis. We identify three new CIN-suppressor genes (PIGN (also known as MCD4), MEX3C (RKHD2) and ZNF516 (KIAA0222)) encoded on chromosome 18q that are subject to frequent copy number loss in CIN+ CRC. Chromosome 18q loss was temporally associated with aneuploidy onset at the adenoma-carcinoma transition. CIN-suppressor gene silencing leads to DNA replication stress, structural chromosome abnormalities and chromosom

Název v anglickém jazyce

Replication stress links structural and numerical cancer chromosomal instability

Popis výsledku anglicky

Cancer chromosomal instability (CIN) results in an increased rate of change of chromosome number and structure and generates intratumour heterogeneity(1,2). CIN is observed in most solid tumours and is associated with both poor prognosis and drug resistance(3,4). Understanding a mechanistic basis for CIN is therefore paramount. Here we find evidence for impaired replication fork progression and increased DNA replication stress in CIN+ colorectal cancer (CRC) cells relative to CIN- CRC cells, with structural chromosome abnormalities precipitating chromosome missegregation in mitosis. We identify three new CIN-suppressor genes (PIGN (also known as MCD4), MEX3C (RKHD2) and ZNF516 (KIAA0222)) encoded on chromosome 18q that are subject to frequent copy number loss in CIN+ CRC. Chromosome 18q loss was temporally associated with aneuploidy onset at the adenoma-carcinoma transition. CIN-suppressor gene silencing leads to DNA replication stress, structural chromosome abnormalities and chromosom

Druh

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

CEP obor

FD - Onkologie a hematologie

OECD FORD obor

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Projekt

<a href="/cs/project/ED0030%2F01%2F01" target="_blank" >ED0030/01/01: Biomedicína pro regionální rozvoj a lidské zdroje</a><br>

Návaznosti

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

Rok uplatnění

2013

Kód důvěrnosti údajů

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

Název periodika

Nature

ISSN

0028-0836

e-ISSN

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Svazek periodika

494

Číslo periodika v rámci svazku

7438

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

5

Strana od-do

492-496

Kód UT WoS článku

000315661500042

EID výsledku v databázi Scopus

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