New York, Aug 9 (IANS) Researchers including one of Indian-origin have shown that a first-in-class drug could prevent breast cancer growth when traditional therapies stop working.
First-in-class drugs are drugs that work by a unique mechanism, in this case a molecule that targets a protein on the estrogen receptor of tumour cells.
The potential drug offers hope for patients whose breast cancer has become resistant to traditional therapies.
“This is a fundamentally different, new class of agents for estrogen-receptor-positive breast cancer,” said Ganesh Raj, Professor of Urology and Pharmacology at the University of Texas Southwestern Medical Center in the US.
“Its unique mechanism of action overcomes the limitations of current therapies,” Raj said.
All breast cancers are tested to determine if they require estrogen to grow and about 80 per cent are found to be estrogen-sensitive.
These cancers can often be effectively treated with hormone therapy, such as tamoxifen, but as many as a third of these cancers eventually become resistant.
The new compound, detailed online in the journal eLife, is a potential highly effective, next-line treatment for these patients, said Raj.
The new molecule, dubbed ERX-11, mimics a peptide, or protein building block, and works by blocking other molecules. So far, it has been tested in mice and in cancer cells removed from patients and works well in both models, and there have been no signs of toxicity in the tests.
If successfully translated to a human therapy, another advantage of ERX-11 is that it could be taken orally by patients, rather than as an infusion.
The team is hoping to get a clinical trial under way in about a year, Raj said.
The notion of blocking protein co-factors has implications for treatment of other cancers as well.
“This could be a first-line breast cancer therapy down the line. It could even lead to new treatments for other hormone-sensitive cancers. For now, it offers hope for women with estrogen-sensitive breast cancer for whom conventional therapies fail,” Raj said.