title: Shorter telomere length is associated with increased ovarian cancer risk in both familial and sporadic cases.
abstract: BACKGROUND
  Alterations in telomere maintenance mechanisms leading to short telomeres underlie different genetic disorders of ageing and cancer predisposition syndromes. It is known that short telomeres and subsequent genomic instability contribute to malignant transformation, and it is therefore likely that people with shorter telomeres are at higher risk for different types of cancer. Recently, the authors demonstrated that the genes BRCA1 and BRCA2 are modifiers of telomere length (TL) in familial breast cancer. The present study analysed TL in peripheral blood leucocytes of hereditary and sporadic ovarian cancer cases, as well as in female controls, to evaluate whether TL contributes to ovarian cancer risk.
  
  
  METHODS
  TL was measured by quantitative PCR in 178 sporadic and 168 hereditary ovarian cases (46 BRCA1, 12 BRCA2, and 110 BRCAX) and compared to TL in 267 controls.
  
  
  RESULTS
  Both sporadic and hereditary cases showed significantly shorter age adjusted TLs than controls. Unconditional logistic regression analysis revealed an association between TL and ovarian cancer risk with a significant interaction with age (p<0.001). Risk was higher in younger women and progressively decreased with age, with the highest OR observed in women under 30 years of age (OR 1.56, 95% CI 1.34 to 1.81; p=1.0×10(-18)).
  
  
  CONCLUSIONS
  These findings indicate that TL could be a risk factor for early onset ovarian cancer.
authors.affiliation: Human Genetics Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. bmartinez@cnio.es
authors.forename: Beatriz
authors.initials: B
authors.lastname: Martinez-Delgado
authors.forename: Kira
authors.initials: K
authors.lastname: Yanowsky
authors.forename: Lucia
authors.initials: L
authors.lastname: Inglada-Perez
authors.forename: Miguel
authors.initials: M
authors.lastname: de la Hoya
authors.forename: Trinidad
authors.initials: T
authors.lastname: Caldes
authors.forename: Ana
authors.initials: A
authors.lastname: Vega
authors.forename: Ana
authors.initials: A
authors.lastname: Blanco
authors.forename: Teresa
authors.initials: T
authors.lastname: Martin
authors.forename: Rogelio
authors.initials: R
authors.lastname: Gonzalez-Sarmiento
authors.forename: Maria
authors.initials: M
authors.lastname: Blasco
authors.forename: Mercedes
authors.initials: M
authors.lastname: Robledo
authors.forename: Miguel
authors.initials: M
authors.lastname: Urioste
authors.forename: Honglin
authors.initials: H
authors.lastname: Song
authors.forename: Paul
authors.initials: P
authors.lastname: Pharoah
authors.forename: Javier
authors.initials: J
authors.lastname: Benitez
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D004247:DNA / Q000032:analysis / Q000097:blood; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology / Q000235:genetics*; D006801:Humans; D007963:Leukocytes, Mononuclear; D016015:Logistic Models; D008875:Middle Aged; D010051:Ovarian Neoplasms / Q000453:epidemiology / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D012307:Risk Factors; D013030:Spain / Q000453:epidemiology; D016615:Telomere / Q000235:genetics*; D059506:Telomere Shortening / Q000235:genetics
chemical_list: D004247:DNA