Our immune system could detect cancer cells easily, which could boost the development of new treatments for the disease. What if drugs could cause cancer cells in the body to become visible to the immune system? This could allow them to be targeted and killed.
This is the basic approach to cancer treatment that a rapidly growing form — still being tested in humans.
The treatment involves drawing the protein from the KRAS cancer-causing gene to the surface of the cancer cell. The treatment then transforms the protein’s surface into an enormous “eat me!” signal for the body’s immune systems, according to the press release.
Kevin Shokat, a UCSF chemist and study co-author, stated in the release that “the immune system already has potential to recognize mutated KRAS but it often can’t find it very easily.” The immune system will find it much easier to recognize mutated KRAS proteins when we place this marker on them.”
Although it sounds simple and logical, doctors still struggle to implement this concept.
It’s difficult for drugs to attach to cancer-causing KRAS proteins. This is assuming that you can reach them. Most of them are hidden within cells, so it doesn’t get detected by the immune system.
Scientists have been able, partly thanks to Shokat’s years of research on KRAS, to create drugs such as sotorasib (aka lumakras) that block KRAS from growing tumors. The researchers then turned to ARS1620 to kill and weed out KRAS cells.
The Cancer Cellstudy found that ARS1620 was not only binding to KRAS proteins, blocking their tumorous effects but also drew them closer to the cell’s surface. Even better, when they were bound together, the drug/KRAS complex that they formed alerted immune system to get rid of the particular cell they were on.
Charles Craik, one the study’s authors, is a professor of pharmaceutical chemistry at UCSF. He said in the same release that “this mutated protein is often flying under the radar because its so similar to the healthy proteins.” It is easy to spot if you attach the drug to it.
The researchers claim that they were able develop an immunotherapy that stimulates the immune system and targets cancerous KRAS bound to ARS1620. Even though KRAS cells were resistant to the drug, the treatment worked.
Although it’s a positive development, there is still much to do before the treatment can be applied to humans. Still, Craik remains optimistic.
Craik stated that this is a platform technology. “We would like to pursue other targets that could also move molecules to cells surface and make them more susceptible to immunotherapy.”