Scientists at Manchester University may have identified a new way of treating deadly melanoma cancer. They discovered that MITF (a protein which helps cells to produce pigment, but also allows melanoma cells to grow and survive) is able to provide cancer cells with resistance to a new class of drugs, called MEK inhibitors, which were being tested in clinical trials.
This is exciting news as one of the big problems with developing anti-cancer drugs is that cancer cells often develop resistance to even the most advanced treatments. Having identified how that mechanism works against MEK inhibitors will help scientists ultimately make the drug more effective.
Dr Claudia Wellbrock working at the Wellcome Trust Centre for Cell-Matrix Research found, by comparing human melanoma cells that respond to the drug to those that don’t, that the protein SMURF2 was present in higher levels in cells which didn’t respond to the drug. Further experiments seemed to suggest that this was because high levels of SMURF2 were linked to high levels of MITF, the protein responsible for resistance to MEK inhibitors.
Following these discoveries, Dr Wellbrock’s team carried out an experiment on mice with tumours to show that there was a substantial decrease in tumour growth when the removal of SMUF2 was used alongside MEK inhibitors.
This discovery could have very real implications for cancer patients: the current MEK inhibitor drug suffers from the huge disadvantage that it targets all cells, as although MEK is present in elevated levels in cancer cells, it can be found in all healthy cells as well. Consequently the drug must be given in small doses over a long period of time to avoid harming healthy cells. Reducing SMURF2 to increase the effectiveness of the drug specifically in the tumour would mean that smaller doses could be given over a shorter time period, therefore reducing damage to the healthy parts of the patient’s body.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=127134&CultureCode=en
http://jnci.oxfordjournals.org/content/early/2012/12/17/jnci.djs471.full.pdf+html
