Association of LEPR K109R polymorphisms with cancer risk: a systematic review and pooled analysis
Hui Shi1, Hexi Shu, Changjia Huang
1Shanghai Tenth People's Hospital , Tongji University, School of Medicine , Shanghai , China.
Purpose:
This meta-analysis was conducted to evaluate the association between LEPR K109R (rs1137100) genetic polymorphism and cancer risk.
Methods:
To better understand the role of LEPR K109R(rs1137100) genetic polymorphism in global cancer, we conducted this comprehensive meta-analysis encompassing 5819 cases and 8068 controls.
Results:
Overall, the LEPR K109R(rs1137100) genetic polymorphism did not significantly affect the risk of cancer. In the stratified analysis, significant associations were found between the LEPR K109R(rs1137100) genetic polymorphism and breast cancer under additive genetic model (odds ratio/OR=0.67, 95% CI 0.61-0.73). For prostate cancer, there was no significant association of LEPR K109R(rs1137100) variant with this disease under any model. For lung cancer, there was significant association of LEPR K109R(rs1137100) variant with the disease under heterozygous co-dominant model (OR=0.72, 95% CI 0.55- 0.96), recessive genetic model (OR=0.76, 95% CI 0.61-0.94) and additive genetic model (OR=0.89, 95% CI 0.80-0.99). For gastric cancer, significant association was found in the 3 genetic models (AG vs GG, AA/AG vs GG and A vs G), the ORS (95%CI) being 2.93 (1.25-6.86), 2.93 (1.25-6.86) and 2.25 (1.07-4.72), respectively. Moreover, no significant cancer risk was found in any genetic model among Caucasian and Asian populations. When stratified by study design, no significantly elevated susceptibility to cancer was found among any studies. No significant differences in the genotype method and sample size in cases were found among genotypes.
Conclusion:
These findings suggested that the LEPR K109R(rs1137100) genetic polymorphism may decrease the susceptibility in breast cancer, especially in the additive genetic model. The findings also indicate that single nucleotide polymorphism (SNP) functions as a recessive mutation, which needs to be verified or linked with functional studies.
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