Breast cancer and human papillomavirus infection: no evidence of HPV etiology of breast cancer in Indian women.

BACKGROUND: Two clinically relevant high-risk HPV (HR-HPV) types 16 and 18 are etiologically associated with the development of cervical carcinoma and are also reported to be present in many other carcinomas in extra-genital organ sites. Presence of HPV has been reported in breast carcinoma which is the second most common cancer in India and is showing a fast rising trend in urban population. The two early genes E6 and E7 of HPV type 16 have been shown to immortalize breast epithelial cells in vitro, but the role of HPV infection in breast carcinogenesis is highly controversial. Present study has therefore been undertaken to analyze the prevalence of HPV infection in both breast cancer tissues and blood samples from a large number of Indian women with breast cancer from different geographic regions. METHODS: The presence of all mucosal HPVs and the most common high-risk HPV types 16 and 18 DNA was detected by two different PCR methods - (i) conventional PCR assays using consensus primers (MY09/11, or GP5+/GP6+) or HPV16 E6/E7 primers and (ii) highly sensitive Real-Time PCR. A total of 228 biopsies and corresponding 142 blood samples collected prospectively from 252 patients from four different regions of India with significant socio-cultural, ethnic and demographic variations were tested. RESULTS: All biopsies and blood samples of breast cancer patients tested by PCR methods did not show positivity for HPV DNA sequences in conventional PCRs either by MY09/11 or by GP5+/GP6+/HPV16 E6/E7 primers. Further testing of these samples by real time PCR also failed to detect HPV DNA sequences. CONCLUSIONS: Lack of detection of HPV DNA either in the tumor or in the blood DNA of breast cancer patients by both conventional and real time PCR does not support a role of genital HPV in the pathogenesis of breast cancer in Indian women.

Persistence of genetic damage in mice exposed to low dose of X rays.

PURPOSE: The aim of this work was to evaluate the persistence of genetic damage in CBA/J mice treated with a single irradiation of 0.1 or 1 Gy of X rays. MATERIALS AND METHODS: Peripheral blood was collected from irradiated and control mice after 30 min, 24 h, 7 days, 1, 3 and 6 months from exposure and analysed by comet assay. To investigate if the whole-body irradiation affect DNA repair, half of the sampled blood cells were in vitro-irradiated with additional 4 Gy and immediately analysed. Six months from exposure haematopoietic organs were sampled for measuring apoptotic index. RESULTS: In mice exposed to 1 Gy genetic damage was initially high and decreased during the experimental-time, while in the 0.1 Gy group damage, at first low, persisted and slightly increased. The 0.1 Gy-irradiated mice showed also a time-dependent increasing sensitivity to the in vitro-irradiation. Six months after whole-body irradiation, the percentage of apoptotic cells observed in haematopoietic compartments from 0.1 Gy-irradiated mice was significantly higher compared to controls and to 1 Gy mice. CONCLUSIONS: Results demonstrated that a single exposure to low-dose might induce long-term damage. Persistence of genetic damage might have relevant implications for estimating risk for low doses.