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Drug Shown to Break Down Cancer’s Defenses

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A drug that strips cancer cells of their defenses against chemotherapy could improve treatment for cancer patients with drug resistant tumors, scientists in Britain said on Thursday.

The drug attacks a molecule called P-glycoprotein which is produced by cancerous cells and acts like a bouncer to resist the damaging impact of chemotherapy. “We knew that P-glycoprotein was found in large numbers of tumors, but we didn’t know how important the molecule was for their resistance to drugs,” Dr Richard Callaghan, of the John Radcliffe Hospital in Oxford, England, said in a statement. In a study reported in the European Journal of Cancer, Callaghan and his team showed that the molecule was not only a vital element in drug resistance but that something could be done to counteract it. Tumors may initially respond to chemotherapy treatment, which kills the cancerous cells, but can later develop a resistance to the toxic drugs. An estimated 30-80 percent of cancer patients may develop multi-drug resistant tumors. To study how and why it happens scientists grew balls of cancerous cells in the laboratory to mimic the reaction of tumors to a drug called XR9576. One group of cells had high levels of P-glycoproteins while the other group had low levels of the molecule. After treating both types of cells with either vinblastine or doxorubicin, two chemotherapy drugs, the scientists found that cells with low amounts of P-glycoprotein were more sensitive to the drugs. Cells with high levels of the molecule were 20 times more resistant to doxorubicin and up to 300 times more resistant to vinblastine than the balls of cells with lower levels. But when the scientists repeated the experiment and pre-treated the cells with the XR9576 drug the cells were much more sensitive to the treatments. “It raises the possibility of new types of treatment to overcome a tumor’s resistance to chemotherapy,” Callaghan explained. (Source: Reuters Health: February 2004)


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Dates

Posted On: 19 February, 2004
Modified On: 3 December, 2013

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