title: Association of LEPR K109R polymorphisms with cancer risk: a systematic review and pooled analysis.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Shanghai Tenth People's Hospital , Tongji University, School of Medicine , Shanghai , China.
authors.forename: Hui
authors.initials: H
authors.lastname: Shi
authors.forename: Hexi
authors.initials: H
authors.lastname: Shu
authors.forename: Changjia
authors.initials: C
authors.lastname: Huang
authors.forename: Jinpeng
authors.initials: J
authors.lastname: Gong
authors.forename: Yunji
authors.initials: Y
authors.lastname: Yang
authors.forename: Run
authors.initials: R
authors.lastname: Liu
authors.forename: Yong
authors.initials: Y
authors.lastname: Yang
authors.forename: Pengcheng
authors.initials: P
authors.lastname: Liu
mesh_terms: D020022:Genetic Predisposition to Disease; D006801:Humans; D009369:Neoplasms / Q000209:etiology / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D017594:Publication Bias; D054411:Receptors, Leptin / Q000235:genetics*; D012306:Risk
chemical_list: C515448:LEPR protein, human; D054411:Receptors, Leptin