Polymorphisms of the XRCC1 DNA repair gene in head and neck cancer

2005 ◽  
Vol 11 (1) ◽  
pp. 22-25 ◽  
Author(s):  
Semra Demokan ◽  
Deniz Demir ◽  
Yusufhan Suoglu ◽  
Erkan Kiyak ◽  
Ugur Akar ◽  
...  
2013 ◽  
Vol 43 (3) ◽  
pp. 217-224 ◽  
Author(s):  
Rim Khlifi ◽  
Imen Kallel ◽  
Bouthaina Hammami ◽  
Amel Hamza-Chaffai ◽  
Ahmed Rebai

Oral Oncology ◽  
2017 ◽  
Vol 67 ◽  
pp. 70-76 ◽  
Author(s):  
D. Borchiellini ◽  
M.C. Etienne-Grimaldi ◽  
R.J. Bensadoun ◽  
K. Benezery ◽  
O. Dassonville ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74059 ◽  
Author(s):  
Yin Lou ◽  
Wen-jia Peng ◽  
Dong-sheng Cao ◽  
Juan Xie ◽  
Hong-hong Li ◽  
...  

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Shitong Xia ◽  
Sihai Wu ◽  
Minghao Wang

Background: Accumulated evidence shows that DNA repair gene X-ray repair cross complementing group 1 (XRCC1) may determine individual susceptibility to head and neck cancer (HNC) as a major DNA repair gene. However, the results from previous studies have been conflictive and inconsistent. In order to more accurately estimate and integrate the association between XRCC1 Arg399Gln polymorphism and HNC risk, we conducted a meta-analysis including 14586 subjects. Methods: In this meta-analysis, literatures were collected up until September 15, 2020 through multifarious retrieval strategies by searching through electronic databases of PubMed, Cochrane Library, EMBASE, Medline, Web of Science and CNKI. The association between the XRCC1 Arg399Gln polymorphism and HNC was analyzed through calculating summary odds ratios (OR) and 95% confidence intervals (CI). Results: Thirty-one studies consisting of 6025 cases and 8561 controls were identified and analyzed. No significant association between XRCC1 Arg399Gln polymorphisms and HNC risk was found under the allelic (OR = 0.94, 95% CI: 0.82-1.07, P = 0.35), homozygous (OR = 0.99, 95% CI: 0.81-1.21, P = 0.91), heterozygous (OR = 1.01, 95% CI: 0.90-1.13, P = 0.91), dominant (OR = 1.05, 95% CI: 0.85-1.29, P = 0.67) or recessive (OR = 0.93, 95% CI: 0.80-1.08, P = 0.35) genetic models in the overall comparison. In addition, subgroup analyses according to tumor site also displayed no significant association between XRCC1 Arg399Gln polymorphisms and HNC risk. However, subgroup analyses based on ethnicity indicated that HNC risk was significantly related to Arg399Gln genetic heterozygous model (OR = 1.21, 95%CI: 1.04-1.42, P = 0.02) and dominant model (OR = 1.27, 95%CI: 1.02-1.60, P = 0.04) in Caucasians populations. Conclusion: The results from this meta-analysis suggest that the XRCC1 Arg399Gln variants (Arg/Gln and Arg/Arg+Arg/Gln) may contribute to high HNC risk among Caucasians. Further well-designed studies and larger sample sizes are needed to validate our findings.


DNA Repair ◽  
2010 ◽  
Vol 9 (5) ◽  
pp. 558-566 ◽  
Author(s):  
Zhengdong Zhang ◽  
Luo Wang ◽  
Sheng Wei ◽  
Zhensheng Liu ◽  
Li-E. Wang ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2053
Author(s):  
Yu-Chu Wang ◽  
Jau-Ling Huang ◽  
Ka-Wo Lee ◽  
Hsing-Han Lu ◽  
Yuan-Jen Lin ◽  
...  

Arecoline is the principal alkaloid in the areca nut, a component of betel quids (BQs), which are carcinogenic to humans. Epidemiological studies indicate that BQ-chewing contributes to the occurrence of head and neck cancer (HNC). Previously, we have reported that arecoline (0.3 mM) is able to inhibit DNA repair in a p53-dependent pathway, but the underlying mechanism is unclear. Here we demonstrated that arecoline suppressed the expression of DDB2, which is transcriptionally regulated by p53 and is required for nucleotide excision repair (NER). Ectopic expression of DDB2 restored NER activity in arecoline-treated cells, suggesting that DDB2 downregulation was critical for arecoline-mediated NER inhibition. Mechanistically, arecoline inhibited p53-induced DDB2 promoter activity through the DNA-binding but not the transactivation domain of p53. Both NER and DDB2 promoter activities declined in the chronic arecoline-exposed cells, which were consistent with the downregulated DDB2 mRNA in BQ-associated HNC specimens, but not in those of The Cancer Genome Atlas (TCGA) cohort (no BQ exposure). Lower DDB2 mRNA expression was correlated with a poor outcome in HNC patients. These data uncover one of mechanisms underlying arecoline-mediated carcinogenicity through inhibiting p53-regulated DDB2 expression and DNA repair.


1999 ◽  
Vol 125 (2) ◽  
pp. 185 ◽  
Author(s):  
Erich M. Sturgis ◽  
Gary L. Clayman ◽  
Yongli Guan ◽  
Zhaozheng Guo ◽  
Qingyi Wei

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. e17025-e17025
Author(s):  
Beatriz Cirauqui ◽  
Vanesa Quiroga ◽  
Imane Chaib ◽  
Belen Sanchez ◽  
Niki Karachaliou ◽  
...  

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