New protein gives hope in cancer fight
26 February 2015 08:54
Prostate cancer: Scientists claim they have found another clue in the hunt to discover how to prevent it
The hope of finding drugs which prevent prostate cancers that are immune to treatment has moved a step closer.
The clue could lie in GPR158, a previously undiscovered protein in the human body.
Scientists found that prostate cancer sufferers with increased levels of this molecule were most at risk from the disease returning.
The illness initially responds well to drugs which stop male hormones triggering tumour expansion. But then it gets immune to this kind of medication and rapid death can regularly follow.
Prostate Cancer UK's Matthew Hobbs said that finding out why this happens could be key to generating fresh life-saving treatments.
Dr Hobbs, a research deputy director, said the new report's results provide the world with one more clue, but he admitted there is still plenty to be done.
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Like many of the world's greatest discoveries, this new finding was stumbled upon by accident.
Southern California scientists were looking for drugs to help with glaucoma, the eye disease.
Nitin Patel, the study's lead scientist, is hopeful that the GPR158 molecule could hold the clue for generating fresh prostate cancer medications.
This is because it is associated with a procedure which relates to how the cancer ceases to respond to normal hormone therapies.
Dr Patel said that in the embryonic stages, these cancer tumours rely on androgen hormones to expand.
These then grow into a more deadly form, becoming immune to medications that usually prevent androgen receptors.
The expert said GPR158 is unique among its genus in that it is triggered by androgens. This leads to the growth of tumours.
Dr Hobbs admitted that humankind still has much to learn about prostate cancer in its advanced form.
The Public Library of Science ONE has published the study.
Prostate cancer is found in about 40,000 males in the UK every year.
As many as 10,000 men die because of the condition.