title: Tooth agenesis association with self-reported family history of cancer.
abstract: It has been proposed that tooth agenesis and cancer development share common molecular pathways. We performed a cross-sectional study to investigate the epidemiological and molecular association between tooth agenesis and self-reported family history of cancer. Eighty-two individuals with tooth agenesis and 328 individuals with no birth defect were recruited from the same institution. Tooth agenesis was assessed in permanent teeth and was defined based on the age of the participants and when initial tooth formation should be radiographically visible. We also investigated the role of genes involved in dental development that have been implicated in tumorigenesis, and 14 markers in AXIN2, FGF3, FGF10, and FGFR2 were genotyped. Individuals with tooth agenesis had an increased risk of having a family history of cancer (p = 0.00006; OR = 2.7; 95% C.I., 1.6-4.4). There were associations between AXIN2, FGF3, FGF10, and FGFR2 with tooth agenesis [i.e., individuals who carried the polymorphic allele of FGFR2 (rs1219648) presented higher risk for having premolar agenesis (p = 0.02; OR = 1.8; 95% C.I., 1.1-3.0)]. In conclusion, tooth agenesis was associated with positive self-reported family history of cancer and with variants in AXIN2, FGF3, FGF10, and FGFR2. Prospective studies are needed to confirm if tooth agenesis can be used as a risk marker for cancer.
authors.affiliation: Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, 3501 Terrace Street, Pittsburgh, PA 15261, USA.
authors.forename: E C
authors.initials: EC
authors.lastname: Küchler
authors.forename: A
authors.initials: A
authors.lastname: Lips
authors.forename: P N
authors.initials: PN
authors.lastname: Tannure
authors.forename: B
authors.initials: B
authors.lastname: Ho
authors.forename: M C
authors.initials: MC
authors.lastname: Costa
authors.forename: J M
authors.initials: JM
authors.lastname: Granjeiro
authors.forename: A R
authors.initials: AR
authors.lastname: Vieira
mesh_terms: D000483:Alleles; D000848:Anodontia / Q000453:epidemiology / Q000235:genetics*; D060466:Axin Protein / Q000235:genetics; D001641:Bicuspid / Q000002:abnormalities; D001938:Brazil / Q000453:epidemiology; D001943:Breast Neoplasms / Q000453:epidemiology / Q000235:genetics; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D016021:Epidemiologic Studies; D005260:Female; D051526:Fibroblast Growth Factor 10 / Q000235:genetics; D051518:Fibroblast Growth Factor 3 / Q000235:genetics; D014644:Genetic Variation / Q000235:genetics; D005838:Genotype; D006801:Humans; D007180:Incisor / Q000002:abnormalities; D008297:Male; D017720:Molecular Epidemiology; D009369:Neoplasms / Q000453:epidemiology / Q000235:genetics*; D009805:Odontogenesis / Q000235:genetics; D011110:Polymorphism, Genetic / Q000235:genetics; D011471:Prostatic Neoplasms / Q000453:epidemiology / Q000235:genetics; D051497:Receptor, Fibroblast Growth Factor, Type 2 / Q000235:genetics; D012307:Risk Factors; D057566:Self Report
chemical_list: C491761:AXIN2 protein, human; D060466:Axin Protein; C496463:FGF10 protein, human; C496444:FGF3 protein, human; D051526:Fibroblast Growth Factor 10; D051518:Fibroblast Growth Factor 3; C496353:FGFR2 protein, human; D051497:Receptor, Fibroblast Growth Factor, Type 2