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Post-treatment recovery of suboptimal DNA repair capacity and gene expression levels in colorectal cancer patients
J. Slyskova, F. Cordero, B. Pardini, V. Korenkova, V. Vymetalkova, L. Bielik, L. Vodickova, P. Pitule, V. Liska, VM. Matejka, M. Levy, T. Buchler, M. Kubista, A. Naccarati, P. Vodicka,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NT14329
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
Odkazy
PubMed
24585457
DOI
10.1002/mc.22141
Knihovny.cz E-zdroje
- MeSH
- antitumorózní látky terapeutické užití MeSH
- kolon účinky léků metabolismus MeSH
- kolorektální nádory krev farmakoterapie genetika MeSH
- lidé středního věku MeSH
- lidé MeSH
- následné studie MeSH
- oprava DNA * účinky léků MeSH
- regulace genové exprese u nádorů účinky léků MeSH
- rektum účinky léků metabolismus MeSH
- senioři MeSH
- studie případů a kontrol MeSH
- zlomy DNA účinky léků MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
DNA repair in blood cells was observed to be suboptimal in cancer patients at diagnosis, including colorectal cancer (CRC). To explore the causality of this phenomenon, we studied the dynamics of DNA repair from diagnosis to 1 yr follow-up, and with respect to CRC treatment. Systemic CRC therapy is targeted to DNA damage induction and DNA repair is thus of interest. 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 excision repair (NER), and by levels of DNA strand breaks (SBs). NER and base excision repair genes were significantly under-expressed (P < 0.016) in patients at diagnosis compared to controls, in accordance with reduced NER function (P = 0.008) and increased SBs (P = 0.015). 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. In conclusion, our results support a model in which DNA repair is altered as a result of cancer.
Biomedical Centre Medical School Pilsen Charles University Prague Pilsen Czech Republic
Human Genetics Foundation Torino Italy
Institute of Biotechnology ASCR Prague Czech Republic
Institute of Biotechnology ASCR Prague Czech Republic TATAA Biocenter Goteborg Sweden
Institute of Experimental Medicine ASCR Prague Czech Republic Human Genetics Foundation Torino Italy
Thomayer Hospital and 1st Faculty of Medicine Charles University Prague Czech Republic
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