The scientist finds black plain tumour cancer cell drug resistance mechanism

The scientist finds black plain tumour cancer cell drug resistance mechanism
All of us know cancer is very difficult to cure for at present, and very great relation exists with drug resistance of the cancer cell in this, it has already become a big bottleneck of treatment of cancer. According to U.S.A.>Websites report recently, American researchers have already found the drug resistance mechanism of the black plain tumour cancer cell, it can point out the direction in order to solve this difficult problem.
The researchers of the Los Angeles comprehensive cancer research center of branch school Johnson of University of California find in a clinical trial, a test medicine named PLX4032 is very effective to suffering from the cancer patient of the black plain tumour because mutation takes place in BRAF gene. But this kind of curative effect duration is very short, had 7 to 9 months only on average, because though PLX4032 oriented BRAF of 50% to 60% of the black plain tumour patients and made a variation, but the cancer cell will get around the blockade that it is set up.
Reputable author, dermatology assistant professor Dr. Roger of this research explain, in some cases, he finds after PLX4032 has prevented the surviving route of BRAF, the cancer cell begins to express a kind of cell surface albumen in over quantity, create another existence route; Among other cases, another kind of the intersection of oncogene and NRAS morph, make originally BRAF genetic mutation that PLX4032 inhibit from and the short circuit has taken place, activate the surviving thorough fare of BRAF again in this way. Because PLX4032 has no function on NRAS, the cancer cell begins to regrow.
This research has already been issued in Britain >On the magazine . Dr. Roger says, this research will be guided to the new research and development to the treatment of cancer target, situation in order to deal with patients and present the drug resistance of cancer and even recur.
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