Running interference
Dana-Farber clinical researcher Robert Ross, MD, and biostatistician Meredith Regan, ScD, here observing a prostate cancer model, work together to design and analyze many clinical trials around this disease.
The challenge of devising better therapies for prostate cancer — indeed, for any malignancy — is to eliminate tumor cells without harming normal ones. One strategy is to block genes that tumor cells (but not normal ones) need to survive. The issue is whether prostate cancer cells contain such genes; if so, how can they be found?
A reasonable approach might be to shut down the genes associated with prostate cancer, one at a time, and watch the effect in prostate cancer cells and normal cells. Until recently, however, the technical challenges were too daunting.
That changed with the introduction of a laboratory technique known as RNA interference (RNAi, for short), which uses bits of RNA (the cell's template for protein assembly) as molecular circuit breakers to shut down the activity of selected genes (see related story, Silence is golden). "We've built a library of thousands of RNAi reagents that we use to assess the function of genes," says Dana-Farber's William Hahn, MD, PhD, who is leading the effort. "It's like a fuse box at home: You disconnect a single fuse and see which lights go off — except we have a box containing hundreds of fuses."
Powerful as RNAi is, it would be inefficient to use on each of the 22,000 to 25,000 genes in the human genome. That's why Hahn and his colleagues are focusing on certain "candidate" genes which researchers have already identified as likely contributors to prostate cancer.
Hahn's team has also genetically re-wired normal prostate cells so they behave like cancerous cells. "We've found that putting a small number of candidate genes into prostate cells causes them to look and act like prostate cancer cells in animal models," Hahn relates. "It enables us to study cells in which we know precisely what the genetic abnormalities are. In real prostate cancer cells, there can be thousands of genetic mistakes and misspellings, not all of which are essential to the cancer process."
Over the next couple of years, the team will be combining data from both research projects to see if they point to the same set of prostate cancer-critical genes. "If the two approaches produce overlapping results," says Hahn, "it will be a very powerful indication that the spotlighted genes play a central role in prostate cancer and should be considered as prime targets for future therapies."
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