Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?

Chronic inflammation is a driving force for gastric carcinogenesis. Reactive oxygen species (ROS) generated during the inflammatory process generates DNA damage that is processed through the DNA repair pathways. In this study, we profiled key DNA repair proteins (single-strand-selective monofunction...

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Main Authors: Abdel-Fatah, Tarek, Arora, Arvind, Gorguc, Ipek, Abbotts, Rachel, Beebeejaun, Sarah, Storr, Sarah J., Mohan, Vivek, Hawkes, Claire, Soomro, Irshad N., Lobo, Dileep N., Parsons, Simon L., Madhusudan, Srinivasan
Format: Article
Published: Mary Ann Liebert 2013
Online Access:https://eprints.nottingham.ac.uk/2801/
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author Abdel-Fatah, Tarek
Arora, Arvind
Gorguc, Ipek
Abbotts, Rachel
Beebeejaun, Sarah
Storr, Sarah J.
Mohan, Vivek
Hawkes, Claire
Soomro, Irshad N.
Lobo, Dileep N.
Parsons, Simon L.
Madhusudan, Srinivasan
author_facet Abdel-Fatah, Tarek
Arora, Arvind
Gorguc, Ipek
Abbotts, Rachel
Beebeejaun, Sarah
Storr, Sarah J.
Mohan, Vivek
Hawkes, Claire
Soomro, Irshad N.
Lobo, Dileep N.
Parsons, Simon L.
Madhusudan, Srinivasan
author_sort Abdel-Fatah, Tarek
building Nottingham Research Data Repository
collection Online Access
description Chronic inflammation is a driving force for gastric carcinogenesis. Reactive oxygen species (ROS) generated during the inflammatory process generates DNA damage that is processed through the DNA repair pathways. In this study, we profiled key DNA repair proteins (single-strand-selective monofunctional uracil-DNA glycosylase 1 [SMUG1], Flap endonuclease 1 [FEN1], X-ray repair cross-complementing gene 1 [XRCC1], and Ataxia telangiectasia mutated [ATM]) involved in ROS-induced oxidative DNA damage repair in gastric cancer and correlated to clinicopathological outcomes. High expression of SMUG1, FEN1, and XRCC1 correlated to high T-stage (T3/T4) (p-values: 0.001, 0.005, and 0.02, respectively). High expression of XRCC1 and FEN1 also correlated to lymph node-positive disease (p-values: 0.009 and 0.02, respectively). High expression of XRCC1, FEN1, and SMUG1 correlated with poor disease-specific survival (DSS) (p-values: 0.001, 0.006, and 0.05, respectively) and poor disease-free survival (DFS) (p-values: 0.001, 0.001, and 0.02, respectively). Low expression of ATM correlated to lymph node positivity (p=0.03), vascular invasion (p=0.05), and perineural invasion (p=0.005) and poor DFS (p=0.001) and poor DSS (p=0.003). In the multivariate Cox model, high XRCC1 and low ATM were independently associated with poor survival (p=0.008 and 0.011, respectively). Our observation supports the hypothesis that DNA repair factors are promising biomarkers for personalized therapy in gastric cancer. Antioxid. Redox Signal. 18, 2392–2398.
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spelling nottingham-28012020-05-04T16:37:36Z https://eprints.nottingham.ac.uk/2801/ Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer? Abdel-Fatah, Tarek Arora, Arvind Gorguc, Ipek Abbotts, Rachel Beebeejaun, Sarah Storr, Sarah J. Mohan, Vivek Hawkes, Claire Soomro, Irshad N. Lobo, Dileep N. Parsons, Simon L. Madhusudan, Srinivasan Chronic inflammation is a driving force for gastric carcinogenesis. Reactive oxygen species (ROS) generated during the inflammatory process generates DNA damage that is processed through the DNA repair pathways. In this study, we profiled key DNA repair proteins (single-strand-selective monofunctional uracil-DNA glycosylase 1 [SMUG1], Flap endonuclease 1 [FEN1], X-ray repair cross-complementing gene 1 [XRCC1], and Ataxia telangiectasia mutated [ATM]) involved in ROS-induced oxidative DNA damage repair in gastric cancer and correlated to clinicopathological outcomes. High expression of SMUG1, FEN1, and XRCC1 correlated to high T-stage (T3/T4) (p-values: 0.001, 0.005, and 0.02, respectively). High expression of XRCC1 and FEN1 also correlated to lymph node-positive disease (p-values: 0.009 and 0.02, respectively). High expression of XRCC1, FEN1, and SMUG1 correlated with poor disease-specific survival (DSS) (p-values: 0.001, 0.006, and 0.05, respectively) and poor disease-free survival (DFS) (p-values: 0.001, 0.001, and 0.02, respectively). Low expression of ATM correlated to lymph node positivity (p=0.03), vascular invasion (p=0.05), and perineural invasion (p=0.005) and poor DFS (p=0.001) and poor DSS (p=0.003). In the multivariate Cox model, high XRCC1 and low ATM were independently associated with poor survival (p=0.008 and 0.011, respectively). Our observation supports the hypothesis that DNA repair factors are promising biomarkers for personalized therapy in gastric cancer. Antioxid. Redox Signal. 18, 2392–2398. Mary Ann Liebert 2013-06-03 Article PeerReviewed Abdel-Fatah, Tarek, Arora, Arvind, Gorguc, Ipek, Abbotts, Rachel, Beebeejaun, Sarah, Storr, Sarah J., Mohan, Vivek, Hawkes, Claire, Soomro, Irshad N., Lobo, Dileep N., Parsons, Simon L. and Madhusudan, Srinivasan (2013) Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer? Antioxidants & Redox Signaling, 18 (18). pp. 2392-2398. ISSN 1523-0864 http://online.liebertpub.com/doi/abs/10.1089/ars.2012.4873 doi:10.1089/ars.2012.4873 doi:10.1089/ars.2012.4873
spellingShingle Abdel-Fatah, Tarek
Arora, Arvind
Gorguc, Ipek
Abbotts, Rachel
Beebeejaun, Sarah
Storr, Sarah J.
Mohan, Vivek
Hawkes, Claire
Soomro, Irshad N.
Lobo, Dileep N.
Parsons, Simon L.
Madhusudan, Srinivasan
Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?
title Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?
title_full Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?
title_fullStr Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?
title_full_unstemmed Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?
title_short Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer?
title_sort are dna repair factors promising biomarkers for personalized therapy in gastric cancer?
url https://eprints.nottingham.ac.uk/2801/
https://eprints.nottingham.ac.uk/2801/
https://eprints.nottingham.ac.uk/2801/