The role of double‐strand break repair, translesion synthesis, and interstrand crosslinks in colorectal cancer progression—clinicopathological data and survival

Background and Objectives DNA repair is a new and important pathway that explains colorectal carcinogenesis. This study will evaluate the prognostic value of molecular modulation of double‐strand break repair (XRCC2 and XRCC5); DNA damage tolerance/translesion synthesis (POLH, POLK, and POLQ), and i...

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Bibliographic Details
Published in:Journal of surgical oncology 2020-04, Vol.121 (5), p.906-916
Main Authors: Laporte, Gustavo A., Leguisamo, Natália M., Gloria, Helena de Castro e, Azambuja, Daniel B., Kalil, Antonio N., Saffi, Jenifer
Format: Article
Language:English
Subjects:
Aged
Biomarkers - metabolism
Case-Control Studies
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Colorectal cancer
Colorectal Neoplasms - genetics
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
CpG Islands
Disease-Free Survival
DNA Breaks, Double-Stranded
DNA Damage
DNA damage response
DNA Methylation
DNA Polymerase theta
DNA Repair
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
DNA-Directed DNA Polymerase - genetics
DNA-Directed DNA Polymerase - metabolism
Exodeoxyribonucleases - genetics
Exodeoxyribonucleases - metabolism
Female
Gene Expression
Humans
Ku Autoantigen - genetics
Ku Autoantigen - metabolism
Male
MutL Protein Homolog 1 - genetics
MutL Protein Homolog 1 - metabolism
MutS Homolog 2 Protein - genetics
MutS Homolog 2 Protein - metabolism
Neoplasm Metastasis - genetics
Prognosis
prognostic biomarkers
Reverse Transcriptase Polymerase Chain Reaction
Tumors
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Summary:Background and Objectives DNA repair is a new and important pathway that explains colorectal carcinogenesis. This study will evaluate the prognostic value of molecular modulation of double‐strand break repair (XRCC2 and XRCC5); DNA damage tolerance/translesion synthesis (POLH, POLK, and POLQ), and interstrand crosslink repair (DCLRE1A) in sporadic colorectal cancer (CRC). Methods Tumor specimens and matched healthy mucosal tissues from 47 patients with CRC who underwent surgery were assessed for gene expression of XRCC2, XRCC5, POLH, POLK, POLQ, and DCLRE1A; protein expression of Polk, Ku80, p53, Ki67, and mismatch repair MLH1 and MSH2 components; CpG island promoter methylation of XRCC5, POLH, POLK, POLQ, and DCLRE1A was performed. Results Neoplastic tissues exhibited induction of POLK (P 
ISSN:0022-4790
1096-9098
DOI:10.1002/jso.25737