Papilloma Virus-Dependent Tumours
New papilloma virus-dependent tumours
It is well established that infection with certain strains of the papilloma virus is responsible for the majority of cases of cervical cancer. Drs. S. Wen & L. Ghali have demonstrated that they can identify an involvement of the virus in a given tumour by immunohistochemical staining (revealing a molecule in a tissue section through binding of an antibody linked to a colour-producing moiety) of paraffin embedded tumour tissue and by DNA analysis. The team has preliminary evidence that the virus can be detected in a minority of breast cancer patients from Austria and Nigeria and they wish to follow this up with a larger well-defined population, looking also to probe the possibility of there being a genetic predisposition to this subsection of breast and other cancers (e.g. major histocompatibility complex genes).
Goal
Identify tumour types not previously linked to papilloma virus.
Project team
Dr. S. Wen
Leader
Dr. L. Ghali Scientific support
Dr. Dong Li Immunohistochemistry
Dr. P. Cohen (Histopath., Imperial)
Supply clinical materials
Project B: Prostate cancer
Infections with high-risk human papilloma viruses (HPVs), causatively linked to cervical cancer, might also play a role in the development of prostate cancer due to the proximity in the type of the cervical transitional zone epithelium and prostate epithelium per se in terms of the histological characteristics and the embryologic origin.
Infection with a number of human polyomaviruses has been described (BKV, JCV, KIPyV, MUPyV & MCPyV) and some have been associated with tumour development, for example, it has been suggested that BK is associated with brain tumours, adenocarcinomas, and prostate carcinomas. As is the case for all polyomaviruses, BKV encodes two proteins that deregulate the ability of the cell to control its growth, namely 'large' and 'small' T antigens. BKV, like JCV and the similar simian virus, SV40, is recognised as a tumour virus because of its ability to cause changes in cell growth and tumour formation in cultured cells and animal models, respectively. BKV and JCV oncogenically transform non-permissive rodent cells in culture and immortalize permissive human cells alone or in the presence of other oncogenes.
We will examine prostate cancer operation specimens for evidence of viral infection and relate this to the clinical status of the patient.
Goals
1) To establish the prevalence of infection with human papillomaviruses and polyomaviruses in prostate cancer.
2) To find out if there is any correlation between viral load or genome expression and the clinical grading on the hyperplasia or tumour.
Project team and indicative budget
Dr. Christopher Ring
Leader
Dr. Mahmoud Naase
Scientific support
Ph.D. student
Analyse clinical samples for viral infection
Dr. R. Persad (Bristol)
Provide clinical samples