Washington, January 29 (ANI): University of Missouri scientists in the United States say that a small molecule drug has the potential as a novel chemotherapeutic treatment for breast cancer accelerated by the hormone progestin.
The researchers have revealed that the drug called PRIMA-1 targets the most common mutated gene, p53, in human cancer cells.
"We demonstrated that PRIMA-1 was an effective drug to treat and prevent emergence of progestin-accelerated mammary tumors in rats," said Salman Hyder, professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center.
"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," he added.
The researchers pointed out that mutated p53 plays a key role in promoting tumour cell survival and tumour cell resistance to chemotherapeutic drugs.
According to him, over 50 percent of breast cancer cases are found to be associated with mutated p53.
Studies conducted in the past have shown that when p53 is functionally abnormal, tumour cells are prolific and develop quickly.
PRIMA-1 targets and returns normal function to the mutated p53, says the researcher.Hyder revealed that his study examined the ability of PRIMA-1 to suppress growth of progestin-accelerated, mammary tumours in an animal model.
When tumors reached a certain size, he and his colleagues administrated PRIMA-1 twice a day for three days.
The researchers found that PRIMA-1 caused regression of approximately 40 percent of progestin-accelerated mammary tumours.
However, the drug did not induce regression of native, non-progestin accelerated tumours.
Hyder also revealed that PRIMA-1 suppressed the emergence of any new progestin-accelerated tumours in the animal model.
"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 Hyder, who is also the Zalk Endowed Professor of Tumor Angiogenesis.
"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," the researcher added. (ANI)