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SAN ANTONIO, Texas—A recent study by the Cancer Therapy & Research Center (CTRC) showed a correlation between levels of certain proteins in human tumor cells and the effectiveness of two of the most common chemotherapy drugs for lung, prostate and breast cancer. The findings, published in the July-August issue of Cancer Genomics & Proteomics could suggest future methods for both determining an individual patient's susceptibility to cancer and to help design the most effective treatment regimen for individual patients.
 
"There is still a lot or work to be done, but this could indicate and lead to individualized medicine for the treatment of cancer which is something everyone has dreamed about," says Dr. Elzbieta Izbicka, who headed the study for the CTRC's Institute of Drug Development.
 
The study tested two of the most common cancer drugs, docetaxel (Taxotere) and paclitaxel (Taxol), both of which inhibit cell growth by stopping cell division.
 
Notable findings in the study included the discovery that docetaxel was determined to be superior to paclitaxel in inhibiting growth of human lung and prostate cancer cells that had low levels of Bcl-2, an "anti-death" protein that protects cancer cells and allows them to multiply. Yet the effectiveness of docetaxel and paclitaxel against breast cancers showed no marked difference in tumors with high Bcl-2 levels.
 
"The findings on tumors with little Bcl-2 was interesting and we need to do more work in this area to perhaps identify biomarkers for drug sensitivity based on protein profiling," Izbicka notes. "These finding provide a proof of concept that through proteomic profiling we may be able to identify biomarkers that exist in certain types of cancers and not others."
 
The work also shines a light on why some patients show better therapeutic results from their cancer regimen than others and the potential to identify those whose treatment regimens are less effective. "People are finding different activity that you would not immediately expect from drugs of the same class," says Izbicka. "They are similar and they are targeting similar biological targets, but they are working differently. This was part of the problem."
 
CTCR's research may be the first step to understanding why this happens and eventually how to address it.

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