Early Telomere Shortening and Genomic Instability in Tubo-Ovarian Preneoplastic Lesions—Letter

In a recent article, Chene and colleagues reported that telomere length shortened gradually when comparing tubo-ovarian dysplasia with serous tubal intraepithelial carcinoma, and shorter telomere length was associated with BRCA1/2 mutations (1). However, we have several concerns in regards to these findings.

First, it is well known that telomere length is inversely correlated with increasing age in both healthy and cancer populations (2, 3). In addition, estrogen deficiency has been found to decrease telomerase activity and shorten telomere length in the ovary of mice (4). Unfortunately, no information about age or menopausal status was supplied in the present study.

Second, telomere length has been previously investigated in a panel of 178 sporadic and 168 hereditary ovarian cancer cases (5). Both sporadic and hereditary ovarian cancers exhibited showed shorter telomeres than the age-matched normal controls and even much shorter telomeres were found in the BRCA1/2 mutation carriers. Interestingly, Chene and colleagues mention that the telomeres of patients with cancer were longer than those in the dysplasia cases. Given that BRCA1/2 status was not provided for the cancer group, we wonder whether this is just a bias caused by a different incidence of BRCA1/2 mutations?

In summary, we suggest that age and menopausal status should be taken into considerations for this study and that BRCA1/2 mutation status in both the control and cancer groups needs to be clarified.

See the Response, p. 5255