A method to eliminate a dangerous genetic cancer trigger has been foundScientists have made a breakthrough in the fight against cancer, discovering a method to neutralize a dangerous genetic factor that provokes the development of malignant tumors. Resear

Breakthrough in oncology: scientists reveal molecular secrets of dangerous cancer mutation KRAS-G12V

A research team from Northwestern University has made a significant scientific breakthrough, revealing previously unknown molecular mechanisms of one of the most common oncogenic mutations - KRAS-G12V. The results of this important study have already been published in the prestigious scientific journal Nature Chemical Biology (NCB).

As reported by TUT.AZ, mutations in the KRAS gene are frequent "culprits" in the development of pancreatic cancer, colon cancer, and non-small cell lung cancer. These genetic changes trigger a sinister process of malignancy, in which normal cells transform into cancerous ones. Until today, the structural features of the mutated protein made it virtually invulnerable to direct drug intervention.

In the past, the scientific community concentrated its efforts on studying another variant of the mutation - KRAS-G12C, for which effective drugs that inhibit the growth of cancerous tumors have already been developed. Inspired by this success, scientists decided to challenge the KRAS-G12V mutation, which had long been considered practically inaccessible for therapeutic intervention.

Using advanced CRISPR-Cas9 whole-genome screening technology, researchers made an amazing discovery: the ELOVL6 gene can reduce KRAS-G12V levels. This gene is responsible for synthesizing an enzyme - fatty acid elongase, which plays an important role in cell membrane formation. The lipids produced by this enzyme effectively serve as an "anchor", holding the mutated KRAS protein on the cell membrane. Scientists found that when these lipids are eliminated, the mutated protein detaches from the membrane, after which it breaks down and is removed from the cell.

In experiments on laboratory mice with tumors caused by KRAS-G12V, suppression of ELOVL6 activity led to slower growth of cancer formations and a significant increase in the lifespan of the test animals.

"When we blocked the action of this lipid elongase, the mutated KRAS detached from the membrane and was destroyed," noted Kelley. "This was an unexpected and significant discovery."

According to the researcher, identifying the key role of ELOVL6 as a regulator of mutated KRAS could lay the foundation for revolutionary new approaches in the treatment of oncological diseases. Currently, the scientific team is actively working on creating a startup to transform this promising discovery into effective anti-cancer therapy.