In his mouse, he used a synthetic drug that turned the re-engineered fibroblast growth factor receptor on. As the gene product was activated, the prostate gland began dramatic, synchronized changes characteristic of cancer. However, when he withdrew the drug that turned the receptor on, the changes reversed over several weeks until the prostate gland appeared normal.

However, at a certain point, changes in the tissue reach a point of no-return and transform in to a kind of cancer called adenocarcinoma that does not appear to be reversible, although withdrawing the drug can slow the cancer, too.

During this study, Spencer, his graduate student, Victor Acevedo and their colleagues also studied the changes prostate cells undergo while they spread outside the gland and into surrounding tissue. Understanding the events that take place in cells during the transition from normal to cancer can provide important clues about cancer and potential treatments.

From this study, he has identified some of the genes involved in the transition from normal prostate cells within a secretory gland to more migratory, malignant cells outside the gland. Using special gene chips called tumor microarrays, they have also discovered the up regulation or increase in cellular levels of Fzd4, a gene that might prove to be a new marker for human prostate cancer.

“Victor started out looking for a role of fibroblast growth factor receptor 1 in prostate cancer progression and ended up with a new cancer marker and a model for epithelial cell plasticity, rounding out his productive thesis,” Spencer added.

Others who took part in this work include Rama D. Gangula, Kevin W. Freeman, Rile Li, Gustavo E, Ayala, Leif E. Peterson and Michael Ittmann, all of BCM, and Youngyou Zhang and Fen Wang of Texas A&M University Health Science Center in Houston.

Funding for this research came from the National Institutes of Health.

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