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    Research Grants Awarded

    Human papilloma viruses and human breast cancer

    Study Section:
    Risk, Prevention and Epidemiology

    Scientific Abstract:
    HPV is considered to be a candidate virus associated with breast cancer because: breast epithelial cells can be immortalised/transformed by HPV in culture ; areas remote to the cervix, such as head/neck cancer, are also associated with HPV ; and the histology of breast cancer cells is very similar to those of cervical cancer . Involvement of HPV in breast cancer is supported by studies which reported HPV is present in 29%-84% of breast cancer specimens. This is consistent with our preliminary data which indicated 48% of breast tumours are HPV 18 positive . Hypotheses: We hypothesise as follows: 1. that HPVs types 16 and 18 may be associated with the etiology of 45% of invasive ductal carcinomas. 2. that HPV types 6 and 11 may be associated with the etiology of nipple duct wart like breast carcinomas. These hypotheses are based on the identification of HPV types 16 and 18 in invasive ductal carcinomas (Lawson et al 2006, Kan et al 2005) and that HPV types 6 and 11 are associated with cervical condylomatas (Topley and Wilson's Microbiology and Microbial Infections Vol 1, VirologyStudy aims The specific aims are to: (i) determine the basic epidemiology of HPV positive human breast cancer, (ii) to determine the types of HPV that may be involved in breast carcinogenesis, (iii) identify the cellular location of HPVs in breast cancer specimens (iii) conduct histopathological assessments of HPV positive breast tumors to determine if they are typical of HPV positive cervical cancer morphology, (iv) confirm that the mechanisms used by HPV to induce breast cancer are the same as for cervical(v) investigate the integration site of HPV, Study aims The specific aims are to: (i) determine the basic epidemiology of HPV positive human breast cancer, (ii) to determine the types of HPV that may be involved in breast carcinogenesis, (iii) identify the cellular location of HPVs in breast cancer specimens (iv) conduct histopathological assessments of HPV positive breast tumors to determine if they are typical of HPV positive cervical cancer morphology, (v) confirm or deny that the mechanisms used by HPV to induce breast cancer are the same as for cervical cancer (v) investigate the integration site of HPV in breast cancer. Methods Step 1.Specimen collection (12 months). Step 2. Development of fluorescent PCR technology (12 to 24 months). Step 3. Confirmation of the presence of HPV genetic material in fresh breast tumors as compared with normal controls using standard PCT analyses. Identification of HPV types (12 to 24 months). Step 4. Assessment of histological characteristics of HPV positive breast tumors (first 12 months). Step 5. Identification of the cellular location of HPVs in breast cancer specimens (12 to 24 months). Step 6. Confirm that the mechanisms used by HPVs to induce breast cancer are the same as for cervical cancer (24 to 36 months). Step 7. Investigation of the integration sites of HPV in the breast cancer genome using

    Lay Abstract:
    Human papilloma viruses (HPVs) have emerged as major candidate viruses as potential causes of possibly 45% of human breast cancers. The development of preventive vaccines for high risk HPVs is a major reason for seeking conclusive evidence of a role for HPVs in breast cancer. HPV genetic material has been identified in breast tumors from women in Europe, the US, China, Japan and Australia. Because such identification is rare in normal breast tissues there is a possibility that HPVs may be associated with breast tumors. However, the presence of such genetic material is not evidence of a causal role as these viruses may be parasites. It is very difficult to establish conclusive evidence of a causal role for viruses in human breast cancer. The aim of the present proposal is to overcome those difficulties. The specific aims are to: (i) determine the basic epidemiology of HPV positive human breast cancer, (ii) identify the cellular location of HPVs in breast cancer specimens (iii) conduct histopathological assessments of HPV positive breast tumors to determine if they are typical of HPV positive cervical cancer morphology, (iv) investigate the mechanisms used by HPV to induce breast cancer (v) investigate the integration site of HPV, (vi) to determine the types of HPV that may be involved in breast carcinogenesis. Because of our experience in this field of research we can accomplish these aims over a 3 years period. Successful outcomes will provide a basis for basing conclusions about the role of HPVs in human breast cancer. Finally, if conclusive evidence for a causal role for HPVs can be established, primary prevention by proven vaccines will become a reality for the first time.