title: CYP1A1 and GSTP1 polymorphisms in an oral cancer case-control study.
abstract: CYP1A1 and GSTP1 polymorphisms have been associated with a higher risk to develop several cancers, including oral squamous cell carcinoma (OSCC), which is closely related to tobacco and alcohol consumption. Both genes code for enzymes that have an important role in activating or detoxifying carcinogenic elements found in tobacco and other compounds, and polymorphic variants of these genes may result in alterations of the enzymatic activity. The CYP1A1 gene codes for the enzyme aryl hydrocarbon hydroxylase, which is responsible for the metabolism of polycyclic aromatic hydrocarbons. The investigated polymorphism, Ile/Val, seems to increase the activity of the enzyme in homozygous individuals, leading to an accumulation of carcinogens. The Ile/Val polymorphism occurs because of an A->G transition at exon 7, resulting in the CYP1A1*2B allele. The GSTP1*B variant shows an A->G transition at exon 5, changing the amino acid Ile to Val, with a reduced catalytic activity of the enzyme. Due to this reduction, the carriers of mutant alleles lost the capability to metabolize carcinogens, which could be responsible for a higher susceptibility to cancer. We conducted a case-control study in a group of 72 cases with newly diagnosed OSCC and 60 healthy controls matched for age, gender, smoking habits, and ethnicity. We used PCR methods to identify the allelic variants CYP1A1*2B and GSTP1*B. The data obtained showed no statistically significant association of allelic or genotypic variants of CYP1A1*2B (OR = 1.06; 95% CI = 0.49-2.29) and GSTP1*B (OR = 1.40; 95% CI = 0.70-2.79) with OSCC.
authors.affiliation: Laboratório de Citogenética Humana e Oncogenética, Departamento de Genética, Universidade Federal do Paraná, 81531-970 Curitiba, PR, Brazil. eribeiro@ufpr.br
authors.forename: A
authors.initials: A
authors.lastname: Leichsenring
authors.forename: R
authors.initials: R
authors.lastname: Losi-Guembarovski
authors.forename: M E
authors.initials: ME
authors.lastname: Maciel
authors.forename: A
authors.initials: A
authors.lastname: Losi-Guembarovski
authors.forename: B W
authors.initials: BW
authors.lastname: Oliveira
authors.forename: G
authors.initials: G
authors.lastname: Ramos
authors.forename: T C S
authors.initials: TC
authors.lastname: Cavalcanti
authors.forename: M G
authors.initials: MG
authors.lastname: Bicalho
authors.forename: I J
authors.initials: IJ
authors.lastname: Cavalli
authors.forename: I M S
authors.initials: IM
authors.lastname: Cólus
authors.forename: E M S F
authors.initials: EM
authors.lastname: Ribeiro
mesh_terms: D000483:Alleles; D016022:Case-Control Studies; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics*; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease; D051549:Glutathione S-Transferase pi / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000201:enzymology / Q000235:genetics*; D018307:Neoplasms, Squamous Cell / Q000201:enzymology / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D005819:Genetic Markers; D019363:Cytochrome P-450 CYP1A1; C496556:GSTP1 protein, human; D051549:Glutathione S-Transferase pi