Experimental drug causes cell death in prostate cancer
An experimental drug that blocks the breakdown of a compound derived from vitamin A could one day provide a new treatment for prostate cancer, researchers have said.
Vitamin A is converted by the body into retinoic acid, which is known to help maintain normal cell growth. Previous studies have shown that prostate cancer cells contain less retinoic acid than normal prostate cells.
Researchers at the University of Maryland, Baltimore, have now found that regularly injecting mice with VN/14-1, a synthetic compound that blocks the breakdown of retinoic acid, causes a 50 per cent decrease in the size of transplanted prostate tumours.
The compound works by preventing the breakdown of all-trans retinoic acid (ATRA) within cancer cells, which seems to return the cells to normal growth patterns.
It also appears to allow them to be able to 'commit suicide' via a mechanism called 'apoptosis', or programmed cell death - a key mechanism by which damaged cells avoid turning into cancer cells.
The study, which was presented at a conference of the American Association for Cancer Research, is still in its early stages but suggests that if proved safe and effective, the compound could potentially be injected or even administered orally for the treatment of prostate cancer.
Senior investigator Dr Vincent Njar, associate professor in the university's Department of Pharmacology and Experimental Therapeutics, explained: "This potent agent causes cancer cells to differentiate, forcing them to turn back to a non-cancerous state - which is what we expected it would do - but it also stops cancer growth by arresting the cell cycle and pushes cells to die by inducing programmed cell death."
Dr Njar described the findings as "unexpected and wonderfully surprising", adding that the "promiscuous" agent targets more pathways than any existing prostate cancer drug.
The researchers have also tested the compound in breast cancer cells and plan to move on to preclinical studies and eventually trials in humans.