title: HIF-1α 1772 C/T and 1790 G/A polymorphisms are significantly associated with higher cancer risk: an updated meta-analysis from 34 case-control studies.
abstract: BACKGROUND
  HIF-1 activates various genes in cancer progression and metastasis. HIF-1α 1772 C/T and 1790 G/A polymorphisms are reportedly associated with cancer risk; however, the results are inconclusive.
  
  
  RESULTS
  A meta-analysis of 34 studies that involved 7522 cases and 9847 controls for 1772 C/T and 24 studies that involved 4884 cases and 8154 controls for 1790 G/A was conducted to identify the association of C/T and G/A polymorphisms with cancer risk. Odds ratio (OR) and 95% confidence intervals (95% CI) were used to assess the strength of association. HIF-1α 1772 C/T and 1790 G/A polymorphisms were associated with higher cancer risk in homozygote comparison (1772C/T: TT vs. CC: OR = 2.45, 95% CI: 1.52, 3.96; P heterogeneity = 0.028; 1790G/A: AA vs. GG: OR=4.74, 95% CI: 1.78, 12.6; P heterogeneity < 0.01), dominant model (1772C/T: TT/CT vs. CC: OR = 1.27, 95% CI: 1.04, 1.55; P heterogeneity < 0.01, 1790G/A: AA/GA vs. GG: OR = 1.65, 95% CI: 1.05, 2.60; P heterogeneity < 0.01), T allele versus C allele (T vs. C: OR = 1.42, 95% CI: 1.18, 1.70; P heterogeneity < 0.01), and A allele versus G allele (A vs. G: OR = 1.83, 95% CI: 1.13, 2.96; P heterogeneity < 0.01). On a subgroup analysis, the 1772 C/T polymorphism was significantly linked to higher risks for breast cancer, lung cancer, prostate cancer, and cervical cancer, whereas the 1790 G/A polymorphism was significantly linked to higher risks for lung cancer and prostate cancer. A significantly increased cancer risk was found in both Asians and Caucasians for 1772C/T polymorphism, whereas a significantly increased cancer risk was found in Caucasians in the heterozygote comparison and recessive model for 1790G/A polymorphism.
  
  
  CONCLUSIONS
  HIF-1α 1772 C/T and 1790 G/A polymorphisms are significantly associated with higher cancer risk.
authors.affiliation: Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Yang
authors.forename: Hong-Cheng
authors.initials: HC
authors.lastname: Zhu
authors.forename: Chi
authors.initials: C
authors.lastname: Zhang
authors.forename: Qin
authors.initials: Q
authors.lastname: Qin
authors.forename: Jia
authors.initials: J
authors.lastname: Liu
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Xu
authors.forename: Lian-Jun
authors.initials: LJ
authors.lastname: Zhao
authors.forename: Qu
authors.initials: Q
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Cai
authors.forename: Jian-Xin
authors.initials: JX
authors.lastname: Ma
authors.forename: Hong-Yan
authors.initials: HY
authors.lastname: Cheng
authors.forename: Xin-Chen
authors.initials: XC
authors.lastname: Sun
mesh_terms: D000483:Alleles; D016022:Case-Control Studies; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics*; D009369:Neoplasms / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012306:Risk
chemical_list: C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit