A new study has shown positive results that PRIMA-1 could potentially become a new chemotherapy treatment for progestin-accelerated human breast cancer.
A new study conducted by the University of Missouri has shown positive results that PRIMA-1, a small-molecule drug that targets p53 and is the most commonly mutated gene in human cancer cells, could potentially become a new chemotherapy treatment for progestin-accelerated human breast cancer.
“Postmenopausal women worldwide are exposed to exogenous progestin in the form of hormone replacement therapy, and clinical studies have associated combined exposure to progestin and estrogen with an increased incidence of human breast cancer in this population,” said Salman Hyder, professor of biomedical sciences at the College of Veterinary Medicine and the Dalton Cardiovascular Research Center.
Additional research has shown that the risk for breast cancer increases from outside exposure to the progestin, like when taken as part of hormone replacement therapy. PRIIMA-1 could now become a successful treatment option for patients with this specific type of breast cancer.
Researchers looked at how PRIMA-1 could limit the growth of progestin-accelerated mammary tumors in the animal model. Once the tumors had reached a certain size, PRIMA-1 was given two times a day for three days. The results showed that approximately 40% of the progestin-accelerated tumors regressed with the treatment.
“We demonstrated that PRIMA-1 was an effective drug to treat and prevent emergence of progestin-accelerated mammary tumors in rats,” said Hyder. “The results of this study may have significant implications for the treatment and prevention of human breast cancer because such a large fraction of human breast cancers are dependent on estrogens and progestins for growth.”
More than half of breast cancer cases involve the mutated p53 gene; prior research has shown that abnormal function of p53 causes tumor cells to grow and develop much more quickly. PRIMA-1 targets the gene and causes the normal function of p53 to resume.
The drug suppressed new progestin-accelerated tumors in the animal model, but it did not regress any native, non-progestin accelerated ones.
“Because PRIMA-1 blocked the formation of new tumors following progestin stimulation in this experimental model, it is tempting to speculate that this agent could be used to prevent progestin-accelerated tumors in women on hormone replacement therapy. However, this needs to be tested thoroughly in a clinical setting,” said Hyder.
For more information, click here.