title: Angiotensinogen polymorphism is associated with risk for malignancy but not for oral cancer.
abstract: BACKGROUND
  In light of the recently found contribution of angiogenic and inflammation-related factors to malignancies, this study investigated the possible association of the angiotensinogen gene (AGT) with increased risk of oral cancer.
  
  
  METHODS
  The M235T polymorphism, which influences AGT gene expression, was evaluated by restriction fragment length polymorphism analysis in the DNA samples of 163 German and Greek patients with oral squamous cell carcinoma (OSCC) and 124 healthy controls of equivalent gender, ethnicity and age.
  
  
  RESULTS
  No significant difference of the mutant (235T) allele, which results in higher AGT gene expression, was observed in the whole patient group in comparison with the normal controls. Similarly, compared to the controls no significant difference of either allele or carrier frequency was detected in almost every subgroup of patients. Only in the subgroup of patients with a positive family history of cancer was a significant increase of mutant T allele and carrier frequencies observed, compared to the controls (50% vs. 36.7% and 79.3% vs. 61.3%, respectively, p < 0.05 in both cases). In this particular subgroup of patients the odds ratio for OSCC of TT homozygotes was 3.57 (CI 95% 1.2-10.62), while for the MT heterozygotes it was 2.41 (CI 95% 1.06-5.49).
  
  
  CONCLUSIONS
  This study did not reveal an association of the AGT M235T polymorphism with oral oncogenesis, but certainly suggested a possible association of this specific polymorphism with other types of cancer. The present findings support a previous suggestion that the pathway of oral oncogenesis is probably based on angiotensin-converting enzyme and bradykinin interaction and not on AGT and angiotensin peptides.
authors.affiliation: Department of Oral and Maxillofacial Surgery, University of Athens Medical School, Athens, Greece. lvairakt@med.uoa.gr
authors.forename: Eleftherios
authors.initials: E
authors.lastname: Vairaktaris
authors.forename: Christos
authors.initials: C
authors.lastname: Yapijakis
authors.forename: Antonis
authors.initials: A
authors.lastname: Vylliotis
authors.forename: Spyridoula
authors.initials: S
authors.lastname: Derka
authors.forename: Stavros
authors.initials: S
authors.lastname: Vassiliou
authors.forename: Emeka
authors.initials: E
authors.lastname: Nkenke
authors.forename: Zoe
authors.initials: Z
authors.lastname: Serefoglou
authors.forename: Vasileios
authors.initials: V
authors.lastname: Ragos
authors.forename: Elena
authors.initials: E
authors.lastname: Critselis
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Avgoustidis
authors.forename: Friedrich
authors.initials: F
authors.lastname: Neukam
authors.forename: Efstratios
authors.initials: E
authors.lastname: Patsouris
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D000808:Angiotensinogen / Q000096:biosynthesis / Q000235:genetics*; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000378:metabolism; D004273:DNA, Neoplasm / Q000235:genetics; D015870:Gene Expression; D020022:Genetic Predisposition to Disease; D006801:Humans; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length
chemical_list: D004273:DNA, Neoplasm; D000808:Angiotensinogen