The receptor known as HER3 is present in two of the most fatal forms of cancer – pancreatic and breast – and as such it’s been gaining interest among cancer researchers. Its close relatives, HER2 and EGFR, are already the targets of a number of effective cancer drugs. Now, new research shows how "turning off" HER3 might stop cancer call growth in its tracks, and lead to promising new treatments.
The team tested the method in six different types of cancer cells and found it to be effective in all of them.
The discovery began with a chance finding by a researcher who was studying bone regeneration. He found that pairing two receptors sometimes had an unexpected effect: it occasionally shut down growth, rather than promoting it.
Author of the current study, Linda Griffith, said that "[i]t was not something we were expecting to see – you don’t expect to shut off a receptor with something that normally activates it – but in retrospect it seemed obvious to try this approach for HER3. We pursued it only because we had people in the lab working with cancer cells, and we thought, ‘Since it had these effects in stem cells, let’s just try this in tumor cells, and see if something interesting happens.’"
The team tested the method in six different types of cancer cells and found it to be effective in all of them. It even halted the growth of one cell type that is resistant to anticancer medications that target the EGFR receptor.
Griffith herself was diagnosed with a form of breast cancer that can over-express EGFR. The team is currently working on developing a form of the molecule that can be tested in living animals, rather than in the Petri dish. Though the study is preliminary, it points to exciting new possibilities for anticancer drugs.
Dr. Griffith is a researcher at MIT; the study was published in the May 26, 2011 issue of the Journal of Biological Chemistry.