Tumor resistance: weakening the pulse.

Tumor resistance: Weakening the pulse

Cancer patients receiving chemotherapy often suffer from a phenomenon known as multidrug resistance, in which their tumors develop resistance to drugs previously effective and even to drugs the patient has never taken (SN: 8/6/88, p.87). Researchers know that in some (but not all) cases of multidrug resistance, tumor cells make a so-called p-glycoprotein that seems to pump anticancer drugs out of these cells before the drugs accomplish their cell-icidal task. New research by Thomas P. Miller and his colleagues at the University of Arizona in Tucson strengthens evidence that p-glycoprotein is a major culprit in multidrug resistance, and sugggests that a drug commonly prescribed for heart rhythm abnormalities can reverse multidrug resistance in lymphoma patients.

In the first prospective trial of its kind, the researchers examined tumors in 49 newly diagnosed cancer patients and found only one patient with p-glycoproetin-containing cells. Subsequent biopsies on the 10 patients who went on to relapse with multidrug resistance showed that seven now had the glycoprotein.

Previous research by the same group had shown that verapamil, a drug that corrects electrical-conduction abnormalities in the heart, seemed to reverse multidrug resistance in patients with multiple myeloma, another form of cancer. The researchers now report that verapamil reversed drug resistance in 12 of 17 lymphoma patients, allowing the patients to respond again to their original drug. Encouraged by the expanded findings, Miller suggests verapamil may prevent multidrug resistance if given "up front" with chemotherapy, and may prove especially valuable in bladder or other cancers that tend to produce lots of p-glycoprotein.