In trying to better predict a patient's response to chemotherapy for cancer treatment, a team of investigators at The Cancer Institute of New Jersey (CINJ) and Rutgers, The State University of New Jersey, has identified a way to better manipulate a gene product to cause cancer cells to die. And in order to further examine this mechanism, researchers also created a new vehicle for pre-clinical testing of cancer treatments that acts as a bridge between experimental models and human subjects. CINJ is a Center of Excellence of UMDNJ-Robert Wood Johnson Medical School.
A gene common in many cancers known as Bcl-2 produces a protein that plays a role in blocking programmed cell death (apoptosis). Bcl-2 is often over produced in tumors, thus helping to maintain a cancer cell's existence and resulting in resistance to cancer-fighting drugs. By looking at ways to block Bcl-2's actions thereby promoting apoptosis of cancer cells, scientists believe promising new cancer therapies can be developed.
Researchers in this study -- led by Eileen White, PhD, associate director for basic science at CINJ and Robert S. DiPaola, MD, CINJ director, and recently published in Molecular Cancer Research (2009; 7 (9))
(http://mcr.aacrjournals.org/content/7/9/1487.abstract) -- looked at the role of Bcl-2 in prostate cancer that does not respond to therapy. Study has shown it is difficult to kill prostate cancer in particular due to blockage of apoptosis by Bcl-2 and thus few therapeutic options are available. There is now great excitement in the field of cancer research with the development of a Bcl-2 inhibitor, ABT-737, by Abbott laboratories with the potential to overcome this block to apoptosis. And while positive response in stimulating apoptosis has been seen in laboratory tests in human small cell lung cancer and lymphoma cell lines, whether or not a Bcl-2 inhibitor would be effective in prostate cancer was not known.