title: Hypoxia-inducible factor 1α polymorphisms and early-stage cervical cancer.
abstract: BACKGROUND
  Human papillomavirus can stabilize and induce hypoxia-inducible factor 1α (HIF-1α) protein, which is associated with diminished response to treatment and poor prognosis for cervical cancer. Hypoxia-inducible factor 1α polymorphisms (1772C>T and 1790G>A) in the N-terminal transactivation domain generate significantly increased transcriptional activity and have been linked to poor outcome in various malignancies.
  
  
  OBJECTIVE
  The aim of this study was to analyze the possible influence of HIF-1α genetic polymorphisms on cancer susceptibility, tumor aggressiveness, and survival of patients with early-stage cervical cancer.
  
  
  METHODS
  One hundred ninety-nine patients with early-stage cervical cancer who were treated with surgical resection were retrospectively investigated. Hypoxia-inducible factor 1α 1772C>T and 1790G>A genetic polymorphisms were compared with 205 healthy subjects and correlated with the clinical outcome of patients with early-stage cervical cancer.
  
  
  RESULTS
  The risk of cervical cancer was not affected by HIF-1α 1772C>T and 1790G>A polymorphisms. However, lymph node metastasis was significantly increased in patients who had the 1790 variant (adjusted odds ratio, 5.01; 95% confidence interval, 1.05-23.88; P = 0.043). In survival analysis, HIF-1α 1772C>T and 1790G>A polymorphisms were not related to disease-free survival and overall survival.
  
  
  CONCLUSIONS
  Although HIF-1α genetic polymorphisms had little association with cervical cancer risk and prognosis, individual variance of HIF-1α gene may be associated with cervical cancer invasiveness.
authors.affiliation: Departments of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors.forename: Yun Hwan
authors.initials: YH
authors.lastname: Kim
authors.forename: In-Ae
authors.initials: IA
authors.lastname: Park
authors.forename: Woong-Yang
authors.initials: WY
authors.lastname: Park
authors.forename: Jae Weon
authors.initials: JW
authors.lastname: Kim
authors.forename: Seung Cheol
authors.initials: SC
authors.lastname: Kim
authors.forename: Noh-Hyun
authors.initials: NH
authors.lastname: Park
authors.forename: Yong-Sang
authors.initials: YS
authors.lastname: Song
authors.forename: Soon-Beom
authors.initials: SB
authors.lastname: Kang
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D000328:Adult; D000368:Aged; D000483:Alleles; D018288:Carcinoma, Small Cell / Q000235:genetics* / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology; D018450:Disease Progression; D018572:Disease-Free Survival; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D053208:Kaplan-Meier Estimate; D008207:Lymphatic Metastasis; D008875:Middle Aged; D006899:Mixed Function Oxygenases; D011110:Polymorphism, Genetic; D012097:Repressor Proteins / Q000235:genetics*; D012189:Retrospective Studies; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000473:pathology
chemical_list: D012097:Repressor Proteins; D006899:Mixed Function Oxygenases; C439790:HIF1AN protein, human