Post-treatment recovery of suboptimal DNA repair capacity and gene expression levels in colorectal cancer patients

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F14%3A00432485" target="_blank" >RIV/68378041:_____/14:00432485 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/86652036:_____/14:00432485 RIV/00064190:_____/15:#0001046 RIV/00216208:11310/15:10285710 RIV/00216208:11110/15:10285710 a 2 dalších

Výsledek na webu

<a href="http://dx.doi.org/10.1002/mc.22141" target="_blank" >http://dx.doi.org/10.1002/mc.22141</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/mc.22141" target="_blank" >10.1002/mc.22141</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Post-treatment recovery of suboptimal DNA repair capacity and gene expression levels in colorectal cancer patients

Popis výsledku v původním jazyce

DNA repair in blood cells was observed to be suboptimal in cancer patiens at diagnosis, including colorectal cancer (CRC). We studied the dynamics of DNA repair from diagnosis to 1 yr follow-up, and with respect to CRC treatment. CRC patients were blood-sampled three times in 6-mo intervals, starting at the diagnosis, and compared to healthy controls. DNA repair was characterized by mRNA levels of 40 repair genes, by capacity of nucleotide exciton repair (NER), and by levels of DNA strand breaks (SBs). NER and base excision repair genes were significantly under-expressed (P<0.02) in patients at diagnosis compared to controls, in accordance with reduced NER function (P<0.031) and increased SBs (P<0.013). Six months later, there was an increase of NER capacity, but not of gene expression levels, in treated patients only. A year from diagnosis, gene expression profiles and NER capacity were significantly modified in all patients and were no longer different from those measured in controls. All patients were free of relapse at the last sampling, so we were unable to clarify the impact of DNA repair parameters on treatment response. However, we identified a panel of blood DNA repair-related markers discerning acute stage of the disease from the remission period.

Název v anglickém jazyce

Post-treatment recovery of suboptimal DNA repair capacity and gene expression levels in colorectal cancer patients

Popis výsledku anglicky

DNA repair in blood cells was observed to be suboptimal in cancer patiens at diagnosis, including colorectal cancer (CRC). We studied the dynamics of DNA repair from diagnosis to 1 yr follow-up, and with respect to CRC treatment. CRC patients were blood-sampled three times in 6-mo intervals, starting at the diagnosis, and compared to healthy controls. DNA repair was characterized by mRNA levels of 40 repair genes, by capacity of nucleotide exciton repair (NER), and by levels of DNA strand breaks (SBs). NER and base excision repair genes were significantly under-expressed (P<0.02) in patients at diagnosis compared to controls, in accordance with reduced NER function (P<0.031) and increased SBs (P<0.013). Six months later, there was an increase of NER capacity, but not of gene expression levels, in treated patients only. A year from diagnosis, gene expression profiles and NER capacity were significantly modified in all patients and were no longer different from those measured in controls. All patients were free of relapse at the last sampling, so we were unable to clarify the impact of DNA repair parameters on treatment response. However, we identified a panel of blood DNA repair-related markers discerning acute stage of the disease from the remission period.

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

2015

Kód důvěrnosti údajů

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

Název periodika

Molecular Carcinogenesis

ISSN

0899-1987

e-ISSN

—

Svazek periodika

54

Číslo periodika v rámci svazku

9

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

769-778

Kód UT WoS článku

000359710600011

EID výsledku v databázi Scopus

2-s2.0-84894676129