New molecule Concurrently Targets Key Cancer Genes, Offering Hope for Wider Treatment Options
Chapel Hill, NC – Researchers at the University of North Carolina (UNC) School of Medicine have developed a novel molecule capable of simultaneously reducing the expression of both KRAS and MYC genes, two critical drivers of cancer development. This breakthrough, detailed in a recent study, holds critically important promise for expanding treatment options for a wide range of cancers.
“This research represents a significant step forward in understanding the complex interplay driving cancer evolution, and thus has the potential for broader applications in oncological treatments,” explained Dr. Chad V. Pecot, lead author of the study and a professor at UNC School of Medicine.
KRAS and MYC oncogenes frequently collaborate to fuel aggressive tumor growth. They achieve this by triggering inflammation,bolstering cancer cell survival mechanisms,and inhibiting programmed cell death – a natural process that eliminates damaged cells. Mutations in the KRAS gene are found in approximately 25% of all human cancers, particularly in common and aggressive tumor types. MYC is implicated in an even larger proportion of cancers, with disruptions occurring in 50-70% of cases.Importantly, studies have demonstrated that blocking MYC activity can slow or even halt tumor development, making it a highly attractive target for new therapies. Though, despite its importance, effective drugs targeting MYC have remained elusive. “MYC appears to be a target almost as crucial as the oncogene KRAS, but currently, there are no effective drugs capable of directly targeting this gene,” Dr. Pecot stated. “Our study is among the first to thoroughly investigate the therapeutic effects of simultaneously targeting both of these genes. We’ve also created the first molecule demonstrably capable of reducing the expression of both KRAS and MYC proteins.”
The meaning of this dual-targeting approach lies in the fact that most cancers arise from a combination of genetic mutations. by simultaneously attacking two key genetic factors, this technology offers a more comprehensive strategy for combating the disease. This is particularly valuable when both genes are essential for cancer cell survival, yet have historically proven arduous to treat with conventional drugs.
The innovative molecule’s design also allows for the potential to simultaneously deactivate up to three genetic targets, further expanding its therapeutic possibilities.
This success builds upon previous research from the UNC laboratory, published in Cancer Cell in June, which outlined a targeted drug delivery mechanism for a specific KRAS variant, KRAS G12V. The current study expands on this work by developing an RNA molecule capable of reducing the expression of all KRAS mutations found in cancer.
While this broader approach is less specific than the previous method focused solely on KRAS G12V, it offers a significant advantage: applicability to a much larger patient population, including those with the most prevalent KRAS mutations associated with lung, colorectal, and pancreatic cancers.The American Cancer Society estimates that these cancers alone could account for nearly half a million cases in the United States this year.
These advancements pave the way for new treatment avenues for cancers driven by KRAS mutations, offering renewed hope for patients and furthering the fight against this devastating disease.
(Image caption): A schematic depiction of a ligand targeting EGFR (left) alongside a hybrid chemical molecule designed to simultaneously target KRAS and MYC genes. Credit: Chad Pecot’s laboratory, UNC Lineberger Comprehensive cancer Center, and martin Egli, vanderbilt Faculty.
Sources:
https://www.eurekalert.org/news-releases/1093561
https://www.cell.com/cancer-cell/fulltext/S1535-6108(25)00225-900225-9)
