Research Grants 2001

Dr. Armen Aprikian, Surgery Department, Urology Division, McGill University

It is impossible to predict in which prostate cancer patients, when and how fast prostate cancer will spread. We have shown that an important protein called Focal Adesion kinase (FAK) was significantly increased in cases of advanced prostate cancer and associated with prostate cancer cell movement. We seek to better understand how FAK is related to prostate cancer progression and determine if alterations in FAK activation lead to changes in aggressiveness of the disease. We hope that these studies will lead to potential diagnostic markers of prostate cancer progression risks and new therapeutic strategies directed at this important protein.

Dr. J. Thomas Buckley, Department of Biochemistry, University of Victoria

One unique characteristic of prostate cells is that they are the only cells that produce prostate specific antingen (PSA). PSA is a protease, an enzyme that cuts other proteins into smaller pieces in a very specific way. We are working on an engineered protein toxin that is activated by the protease and kills PSA producing tumour cells, but is much less toxic against normal cells. We plan to investigate if it is possible that the toxin can completely destroy prostate tumours when it is injected into the tumour. The results of this research may lead to a new therapy for prostate cancer.

Dr. Cheryl Helgason, Department of Cancer Endocrinology, BC Cancer Agency

Prostate cancer is the second leading cause of cancer deaths among North American men. As such, there is an urgent need for the development of innovative and effective new therapeutic strategies. Immunotherapy approaches that attempt to induce or enhance the immune response against prostate cancer offer an exciting alternative to conventional treatment. However, the success of such strategies has been limited by the lack of identified tumour-specific proteins and the immunosuppression often observed in cancer patients. A population of T cells responsible for preventing the development of immune responses against normal cells and tissues is present in both mice and man. Since tumour cells resemble normal cells in many respects, it is possible that this T cell population, called regulatory T (Tr) cells, protects the tumour cells from the immune system. The objectives of my research are to determine if these Tf cells play a role in allowing tumour growth and to examine the possibility that elimination of this cell population will allow the immune system to kill the tumour. These studies will assist in the development of improved strategies to treat prostate cancer. 

Dr. Claude Labrie, Department of Anatomy and Physiology, Laval University

Androgens play a key role in the development and functions of the normal human prostate as well as in the control of prostate cancer cell proliferation. In the course of our study of prostate cancer cells in mice, we have identified a new mediator of androgen action in the prostate, a gene called AlbZIP, localized on a region of Chromosome 1 that is amplified in prostate cancer. We aim to explore the effects of this gene expression and cell proliferation in prostate cancer cells and examine what the consequences are of deleting the AlbZIP gene in mice. Our answers will speed doing parallel work in human prostate cancer cells.

Dr. Louis Lacombe, Department of Surgery, Laval University

Prostate cancer follows widely varying clinical courses. The gene expressions of p21 and p27 in prostate specimens are tumour markers which can assist physicians with appropriate timing of radical treatments such as prostatectomy or radiation therapy and the usefulness and timing of hormonal manipulation. Some tumours behave in an indolent fashion while others are headed for metastasis right from the start. The most promising tumour markers for understanding the course of prostate cancer are p53, p21, p27, pRb, MDM2, bci-2, and p19. We plan to test these markers on a very large number of prostate specimens with large tissue microarrays to survey the clinical potential of how the presence and level of each tumour marker can affect the outcome of the patient, which markers predict PSA failure, which markers predict metastasis and which markers predict progression of hormonal-resistant prostate cancer. The ability to determine the biological potential of individual tumours would help identify patients who may require more intensive treatment strategies.

Dr. Fred Saad, Centre de Recherche, CHUM-Hopital Notre-Dame 

Science does not yet understand what triggers the uncontrolled growth of prostate cancer cells. It is difficult to determine whether or not the tumour will develop into an aggressive malignancy. Recent research has suggested that deregulation of cell death is implicated in the development and progression of prostate cancer. NF-kB is a molecule that is involved in the normal cell death process and has been shown to be deregulated in many cancers. We are testing whether NF-kB could be used as a marker to predict patient outcomes and analyze the mechanisms by which this molecule affects prostate cancer progression and/or resistance to therapy. These experiments may eventually lead to the development of new therapeutic strategies targeting the NF-kB molecule.

Dr. Damu Tang, Department of Medicine, McMaster University, 

Cancers may arise because the functions of certain genes, called tumour suppressors, are lost. One newly discovered tumour suppressor is called pTEN. We know how pTEN acts to prevent cancerous change in the cells, but how pTEN itself is controlled is unknown. Usually tumour suppressor functions are lost because of mutations in their genes (DNA), but pTEN function may also be lost by failure of the protein to function. Two out of three prostate cancer cell lines have mutated pTEN genes, but one, called DU-145 does not. When we add extra pTEN into DU-145, it doesn't stop growing, suggesting that pTEN's function is lost or suppressed. We are performing laboratory experiments to determine how DU-145 prevents pTEN from doing its anti-cancer job. The answers to this would have important implications in providing potential therapeutic targets in advanced prostate cancer that retains the tumour suppressor gene pTEN.

Dr. Mark Trifiro, Sir Mortimer B. Davis Jewish General Hospital

In identifying preclinical prostate cancer in patients, we currently have a few biomarkers, such as PIN, PSA, and AAH (atypical hyperplasia). Tissues from prostate cancer patients also display a short repeat size on the genetic chromosome level (CAG). The shorter repeat size is the largest risk factor for prostate cancer at a young age. Prostate cancer is a disease that evolves as a continual process and early disease is androgen (hormone) dependent but invariably progresses to androgen independence at later stages. We will fully analyze over 100 different prostate cancer lab specimens and correlate the occurrence of androgen receptor (AR) mutations, CAG instability and androgen receptor mutations with different tumour tissues and known various biomarkers in order to better understand hormone resistance in prostate cancer.

Dr. John Tsihlias, University Health Network, Princess Margaret Hospital

In healthy multicellular organisms, a process of programmed cell death occurs normally and routinely. This process of cell death allows renewal; fresh cells replace old ones. A defect in this process appears to be an important mechanism contributing to prostate cancer progression. A novel protein called PIDD (p53 induced protein) is involved somehow as a trigger for the process of cell death. We will introduce PIDD into prostate cancer cells and identify whether PIDD can induce cell death and enhance the cell sensitivity to radiation, chemotherapy and hormones. This research may identify PIDD as a target for development of new treatments for prostate cancer.

Dr. Yuzhuo Wang, Department of Cancer Endocrinology, BC Cancer Agency

We have developed a successful method of grafting low-grade human prostate cancer cells into mice. We now will collect tissue samples of low-grade human prostate cancer and graft the samples into mice. For specimens that progress, we will determine the genetic alterations associated with disease progression. Similar analysis will be used to assess the known tumour markers in prostate cancer and the tumour suppressor genes involved in prostate cancer. This will offer unique opportunities to study progression of human prostate cancer in vivo under experimental conditions and it will also allow prostate cancer cell samples from specific patients to be tested with different experimental therapies.

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