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David Neal
Molecular mechanisms and the development of novel treatment strategies in genitourinary cancers
ProtecT: Prostate cancer screening
In this clinical trial, 250,000 men will be contacted to be screened for prostate cancer. Men with prostate cancer are invited to enter a randomised study of treatment and will be followed for 10 to 15 years. Tissue, blood and DNA are being stored for studies of cancer genomics.
PROMPT: laboratory and translational studies in prostate cancer
We are coordinating this collaborative research programme which involves tissue banking and genomic studies of prostate cancer.
Ian Mills is investigating the molecular basis of the transition to androgen-independent prostate cancer. We will determine how these changes relate to the sorting, down-regulation and signalling of growth factor receptors in the prostate. We will determine the contribution of endocytic proteins to growth factor cross-talk with the androgen receptor and the development of hormone refractory prostate cancer.
Evaluation of MCM5 as a biomarker in bladder and prostate cancer
This project led by John Kelly is a translational study of the protein MCM5, which is found in increased quantities in the urine of patients with bladder and prostate cancer. We will determine MCM5 levels in urine samples from 3,000 patients. This study is a collaboration between Cambridge University, University College London and Newcastle University.
Genomic studies in genitourinary malignancies
We are evaluating prognostic expression patterns using array based technology in bladder, renal and prostate cancer. We are interested in the response of these cancers to small molecule therapies and have initiated a number of trials involving novel molecules. We have developed clinical trial protocols in which pharmacodynamic endpoints are assessed in normal and neoplastic tissues before and after therapy.
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This figure shows androgen receptor (AR) labeled with the green fluorescent protein GFP. The AR is initially in the cytoplasm, but moves to the nucleus after the application of androgen.
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RACK1 binds both Protein Kinase C (PKC) and the androgen receptor (AR). The AR normally resides in the cytoplasm under basal conditions (top row), but moves to the nucleus in response to the application of androgen (middle row) or to PKC activation in the absence of androgen (bottom row). In both cases, nuclear translocation results in gene activation. AR is shown in green and RACK1 in red.
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- Donovan, J., Mills, N., Smith, M., Brindle, L., Jacoby, A., Peters, T., Frankel, S., Neal, D. and Hamdy, F. (2002)
Improving design and conduct of randomized trials by embedding them in qualitative research: ProtecT (prostate testing for cancer and treatment) study.
Brit Med J 325, 766-770.
- Gaughan, L., Logan, I.R., Cook, S., Neal, D.E. and Robson, C.N. (2002)
Tip60 and HDAC1 regulate androgen receptor activity through changes to the acetylation status of the receptor.
J Biol Chem 277, 25904-25913.
- Gnanapragasam, V.J., Robson, C.N., Neal, D.E. and Leung, H.Y. (2002)
Regulation of FGF8 expression by the androgen receptor human prostate cancer.
Oncogene 21, 5069-5080.
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