Shi Hui, Shu Hexi, Huang Changjia, Gong Jinpeng, Yang Yunji, Liu Run, Yang Yong, Liu Pengcheng
Shanghai Tenth People's Hospital , Tongji University, School of Medicine , Shanghai , China.
J BUON. 2014 Jul-Sep;19(3):847-54.
This meta-analysis was conducted to evaluate the association between LEPR K109R (rs1137100) genetic polymorphism and cancer risk.
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.
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.
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.
本荟萃分析旨在评估LEPR K109R(rs1137100)基因多态性与癌症风险之间的关联。
为了更好地理解LEPR K109R(rs1137100)基因多态性在全球癌症中的作用,我们进行了这项综合荟萃分析,纳入了5819例病例和8068例对照。
总体而言,LEPR K109R(rs1137100)基因多态性并未显著影响癌症风险。在分层分析中,在加性遗传模型下发现LEPR K109R(rs1137100)基因多态性与乳腺癌之间存在显著关联(比值比/OR = 0.67,95%置信区间0.61 - 0.73)。对于前列腺癌,在任何模型下LEPR K109R(rs1137100)变异与该疾病均无显著关联。对于肺癌,在杂合共显性模型(OR = 0.72,95%置信区间0.55 - 0.96)、隐性遗传模型(OR = 0.76,95%置信区间0.61 - 0.94)和加性遗传模型(OR = 0.89,95%置信区间0.80 - 0.99)下,LEPR K109R(rs1137100)变异与该疾病存在显著关联。对于胃癌,在3种遗传模型(AG与GG、AA/AG与GG以及A与G)中均发现显著关联,OR值(95%置信区间)分别为2.93(1.25 - 6.86)、2.93(1.25 - 6.86)和2.25(1.07 - 4.72)。此外,在白种人和亚洲人群的任何遗传模型中均未发现显著的癌症风险。按研究设计分层时,在任何研究中均未发现对癌症易感性显著升高。在各基因型之间,病例的基因型方法和样本量未发现显著差异。
这些发现表明,LEPR K109R(rs1137100)基因多态性可能会降低乳腺癌的易感性,尤其是在加性遗传模型中。这些发现还表明单核苷酸多态性(SNP)起隐性突变的作用,这需要通过功能研究进行验证或关联。