Abstract
9635 Background: Viruses are known to be associated with human malignancies, e.g.,; Epstein-Barr virus, human papilloma virus (HPV) and human T-cell leukemia virus type I. HPV DNA has been found in uterine cervix, anogenital, oral cavity and esophagus tumors. HPV also has been shown to immortalize the breast epithelial cells and increase their proliferation in vitro. We conducted a prospective study to define the role of HPV in breast cancer. Materials and Methods: The malignant and normal breast tissue samples of 30 consecutive breast cancer patients were obtained postoperatively within the 1st hour of operation. All tissue samples were proven to be invasive ductal/lobular carcinoma histopathologically. DNA extracted from all tissues was amplified with the polymerase chain reaction using HPV consensus primer (MY11; 5'GCMCAGGGWCATAAYAATGG-3'; MY9; 5'CGTCCMARRGGAWACTGATC-3') and HPV type specific primers. HPV 11, 16, 18, 33 subtypes were searched in HPV-DNA positive samples. Results: The median age was 53 (range 30–75). Twenty-five samples (83.3%) of tumoral breast tissue expressed HPV-DNA, 13 normal breast tissue samples (43.3%) were positive as well. But there was a significant difference in HPV-DNA positivity between normal and tumoral breast tissue samples (p= 0.003; Fisher's exact test). HPV 18 was detected in 20 of the HPV-DNA positive tumoral tissue (80%) and in 9 of the HPV-DNA positive normal tissue (69.2%) (p=0.689). HPV-33 also was detected in 24 (96 %) of the HPV-DNA positive tumoral tissue and in 12 (92.3 %) of the HPV-DNA positive normal tissue samples (p= 1.000). The distribution of HPV types 18 and 33 between the normal tissue and tumoral tissue was not significantly different. HPV-11 and 16 were not found in any of the HPV-DNA positive samples. Conclusion: HPV DNA was significantly associated with breast tumor tissue compared to normal breast tissue. Our study could not define the specific HPV subtype involved in breast cancer etiology due to the small number of samples and the possible presence of other HPV subtypes which are not analyzed in the present study. Additional studies looking at other HPV subtypes are needed to clarify the etiological role of the HPV in breast cancer. No significant financial relationships to disclose.
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