Friday, February 06, 2015
In what could be termed path-breaking, scientists from Fox Chase Cancer Center have found that pancreatic cancer cells successfully sidestep chemotherapy by employing vitamin D receptors, making this a deadly and difficult to treat cancer. They believe that inactivating these receptors could render chemotherapy effective in killing the cancerous cells.
These results were published in the journal Cell Cycle. Most patients with pancreatic cancer are treated with gemcitabine; however, even with treatment, the prognosis is poor as many of them succumb to death within a few months of treatment.
To understand the mechanism by which pancreatic cells evade chemotherapy, the research team removed all of the approximately 24,000 genes, one by one, in the pancreatic cancer cells and exposed them to gemcitabine. They then observed which gene "knockout" caused the cells to be more sensitive to the drug. They found that one of the ‘knocked-out’ genes, which codes a protein that normally binds to vitamin D was particularly significant.
The researchers hit gold when they discovered that inactivating this vitamin D receptor in cancer cells and adding gemcitabine killed almost all of the cancer cells. Therefore, to ensure chemotherapeutic effectiveness, they suggest finding a drug that can inactivate the vitamin D receptor allowing gemcitabine to selectively kill the pancreatic cancerous cells. They found that only pancreatic cancer cells need vitamin D receptors to survive. This could mean that inactivation of vitamin D receptors during the treatment of pancreatic cancer may not result in a lot of collateral damage/side effects, provided that the patients drink lots of milk or take calcium supplements.
Commenting on the findings, lead researcher Dr. Yen said, “We suspect that cancer cells hijacked the vitamin D receptor and reassigned it to perform other cellular functions, such as repairing the DNA damage caused by gemcitabine, so that the cancer can continue to divide and spread. By knocking out the vitamin D receptor, we could inactivate that DNA repair process that is allowing drug-treated tumor cells to live. As a result, we could eliminate more cancer cells at the outset.”
The positive findings of this study have thus set the ball rolling for future research on ways to combat pancreatic cancer.
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