Journal
JOURNAL OF MEDICAL GENETICS
Volume 49, Issue 5, Pages 341-344Publisher
B M J PUBLISHING GROUP
DOI: 10.1136/jmedgenet-2012-100807
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Funding
- Genetic Counseling Programme in Hereditary Cancer (Junta de Castilla y Leon) [FIS PI10/00219]
- Spanish Association Against Cancer (AECC) [FIS PI08-1120]
- Red Tematica de investigacion Cooperativa en Cancer [RETICC RD06/0020/1060, RETICC 06/0020/0021]
- Xunta de Galicia [10PXIB 9101297PR]
- Fundacion Mutua Madrilena
- Cancer Research UK
- The Francis Crick Institute [10124] Funding Source: researchfish
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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=1.0x10(-18)). Conclusion These findings indicate that TL could be a risk factor for early onset ovarian cancer.
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