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Peer-reviewedCC BY-NC-ND 4.0Cancer Genomics & Proteomics

RAD51 Genetic Variants and Oral Cancer Susceptibility: Gene-Environment Interactions with Smoking and Alcohol Consumption in a Taiwanese Population

  • LIANG-CHUN SHIH1,2,3
  • CHE-LUN HSU2,3,4
  • JIE-LONG HE5
  • JAW-CHYUN CHEN6
  • AI-CHIA TUNG7
7 affiliations
  1. 1Department of Otorhinolaryngology-Head and Neck Surgery, China Medical University Hospital, Taichung, Taiwan, R.O.C.
  2. 2Department of Otorhinolaryngology-Head and Neck Surgery, Asia University Hospital, Taichung, Taiwan, R.O.C.
  3. 3School of Medicine, China Medical University, Taichung, Taiwan, R.O.C.
  4. 4Terry Fox Cancer Research Laboratory, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, R.O.C.
  5. 5Department of Post-Baccalaureate Veterinary Medicine, Asia University, Taichung, Taiwan, R.O.C.
  6. 6Department of Medicinal Botanicals and Foods on Health Applications, Da-Yeh University, Changhua, Taiwan, R.O.C.
  7. 7International Department, Mingdao High School, Taichung, Taiwan, R.O.C.
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Abstract

Background/Aim: Oral cancer is a major health burden in Taiwan, with tobacco, alcohol, and betel quid use as major environmental risk factors. RAD51 is essential for homologous recombination repair and may influence cancer susceptibility through gene-environment interactions. This study evaluated associations of RAD51 rs2619679, rs5030789, and rs1801320 with oral cancer risk and environmental exposures in Taiwanese individuals.

Materials and Methods: A total of 958 patients with histologically confirmed oral cancer and 958 cancer-free controls were genotyped via PCR-restriction fragment length polymorphism methods with blinded duplicate analysis showing 100% concordance. Genotype distributions, allelic frequencies, and stratified associations were evaluated using odds ratios (ORs), 95% confidence intervals (CIs), and multivariable logistic regression. The control genotypic distributions conformed well to Hardy-Weinberg equilibrium for rs2619679, rs5030789, and rs1801320 (p=0.3244, 0.3077, and 0.1422, respectively).

Results: None of the three RAD51 polymorphisms showed a significant overall association with oral cancer susceptibility. For rs1801320, the CG and CC genotypes yielded ORs of 1.09 (95% CI=0.88-1.34, p=0.4684) and 1.44 (95% CI=0.86-2.44, p=0.2107), respectively. However, exposure-stratified analyses revealed marked associations. Among smokers, rs5030789 AG and AA were associated with increased oral cancer risk [adjusted OR (aOR)=1.43, 95% CI=1.08-1.94, p=0.0241; aOR=2.76, 95% CI=1.05-6.78, p=0.0424]. Likewise, smokers carrying rs1801320 CG or CC had elevated risks (aOR=1.50, 95% CI=1.17-1.94, p=0.0026; aOR=2.08, 95% CI=1.23-3.56, p=0.0112). In contrast, rs1801320 CG was protective among nonsmokers (aOR=0.43, 95% CI=0.28-0.68, p=0.0001). Among alcohol drinkers, rs1801320 CG and CC were associated with increased susceptibility (aOR=1.31, p=0.0491; aOR=2.01, 95% CI=1.06-3.58, p=0.0330), whereas no significant associations were detected after stratification by betel quid chewing.

Conclusion: RAD51 variants showed limited independent effects on oral cancer susceptibility but may act as exposure-dependent modifiers, particularly with smoking and alcohol consumption, supporting a role for gene-environment interactions in oral carcinogenesis.

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Cite

BibTeXRIS
BibTeX
@article{shih2026rad51,
  title = {{RAD51 Genetic Variants and Oral Cancer Susceptibility: Gene-Environment Interactions with Smoking and Alcohol Consumption in a Taiwanese Population}},
  author = {LIANG-CHUN SHIH and CHE-LUN HSU and JIE-LONG HE and JAW-CHYUN CHEN and AI-CHIA TUNG},
  journal = {Cancer Genomics \& Proteomics},
  year = {2026},
  month = oct,
  doi = {10.21873/cgp.20618},
  url = {https://doi.org/10.21873/cgp.20618},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - RAD51 Genetic Variants and Oral Cancer Susceptibility: Gene-Environment Interactions with Smoking and Alcohol Consumption in a Taiwanese Population
AU  - LIANG-CHUN SHIH
AU  - CHE-LUN HSU
AU  - JIE-LONG HE
AU  - JAW-CHYUN CHEN
AU  - AI-CHIA TUNG
PY  - 2026
DA  - 2026/10/31
JO  - Cancer Genomics & Proteomics
DO  - 10.21873/cgp.20618
UR  - https://doi.org/10.21873/cgp.20618
AB  - Background/Aim: Oral cancer is a major health burden in Taiwan, with tobacco, alcohol, and betel quid use as major environmental risk factors. RAD51 is essential for homologous recombination repair and may influence cancer susceptibility through gene-environment interactions. This study evaluated associations of RAD51 rs2619679, rs5030789, and rs1801320 with oral cancer risk and environmental exposures in Taiwanese individuals.  Materials and Methods: A total of 958 patients with histologically confirmed oral cancer and 958 cancer-free controls were genotyped via PCR-restriction fragment length polymorphism methods with blinded duplicate analysis showing 100% concordance. Genotype distributions, allelic frequencies, and stratified associations were evaluated using odds ratios (ORs), 95% confidence intervals (CIs), and multivariable logistic regression. The control genotypic distributions conformed well to Hardy-Weinberg equilibrium for rs2619679, rs5030789, and rs1801320 (p=0.3244, 0.3077, and 0.1422, respectively).  Results: None of the three RAD51 polymorphisms showed a significant overall association with oral cancer susceptibility. For rs1801320, the CG and CC genotypes yielded ORs of 1.09 (95% CI=0.88-1.34, p=0.4684) and 1.44 (95% CI=0.86-2.44, p=0.2107), respectively. However, exposure-stratified analyses revealed marked associations. Among smokers, rs5030789 AG and AA were associated with increased oral cancer risk [adjusted OR (aOR)=1.43, 95% CI=1.08-1.94, p=0.0241; aOR=2.76, 95% CI=1.05-6.78, p=0.0424]. Likewise, smokers carrying rs1801320 CG or CC had elevated risks (aOR=1.50, 95% CI=1.17-1.94, p=0.0026; aOR=2.08, 95% CI=1.23-3.56, p=0.0112). In contrast, rs1801320 CG was protective among nonsmokers (aOR=0.43, 95% CI=0.28-0.68, p=0.0001). Among alcohol drinkers, rs1801320 CG and CC were associated with increased susceptibility (aOR=1.31, p=0.0491; aOR=2.01, 95% CI=1.06-3.58, p=0.0330), whereas no significant associations were detected after stratification by betel quid chewing.  Conclusion: RAD51 variants showed limited independent effects on oral cancer susceptibility but may act as exposure-dependent modifiers, particularly with smoking and alcohol consumption, supporting a role for gene-environment interactions in oral carcinogenesis.
SN  - 1109-6535
SN  - 1790-6245
ER  -