Researchers at Mayo Clinic in Florida's study, found that in the lab and in animals, the drug Decitabine turns on a gene coding for protein kinase D1 (PRKD1) that halts the ability of cancer cells to separate from a tumor and spread to distant organs.
Study's senior investigator, Peter Storz, Ph.D., a biochemist and molecular biologist at Mayo Clinic in Florida, said that treatment with low doses of decitabine in an animal model of breast cancer restored PRKD1 expression, reduced tumor size, and blocked metastasis to the lung.
He said that the outcome of patients with invasive breast cancer is less than optimal despite many attempts to improve treatment, including advanced chemotherapy and hormonal therapy.
Storz asserted that they are hoping that this study may offer a new avenue to prevent breast cancer from becoming aggressive and untreatable.
First author Sahra Borges, Ph.D., a postdoctoral researcher in Dr. Storz's lab, found that the gene coding for PRKD1 was silenced in all but one subtype of invasive breast cancer, including aggressive triple negative breast cancer. That subtype is invasive lobular carcinoma.
She also developed an assay that can be used to measure the amount of PRKD1 that is silenced in patients' breast tumors.
Borges said that because they found that PRKD1 is increasingly silenced as breast cancer becomes aggressive and spreads, the hope is that this test can be further developed and used to predict which patients are at risk for cancer metastasis, and thus may benefit from decitabine.
Storz said that treating genes that are silenced is much easier than trying to restore function of a mutated gene.
The study has been published online in Breast Cancer Research.
--ANI (Posted on 27-08-2013)