Pairing KRAS-targeted drugs with medicines that stop cancer cells from dividing may keep those therapies working longer in pancreatic and lung cancers, according to a preclinical study published Oct. 28 in Cancer Research.
Researchers from Buffalo, N.Y.-based Roswell Park Comprehensive Cancer Center analyzed laboratory and animal models of pancreatic and lung cancers to assess why tumors stop responding to KRAS and RAS inhibitors, a class of drugs that include the recently FDA-approved daraxonrasib.
Here are three notes from the study:
- Cancer cells became resistant to both KRAS inhibitors and the broader RAS inhibitor daraxonrasib by finding other ways to keep dividing, even as the drugs blocked their targets.
- Adding CDK4/6 or CDK2 inhibitors, drugs that halt cell division, made resistant cancer cells respond to KRAS and RAS inhibitors again. CDK2 inhibitors had a longer-lasting effect and delayed regrowth after treatment ended.
- In animal models developed from resistant tumors, combining a KRAS inhibitor with either type of cell-cycle drug controlled tumor growth longer than KRAS inhibition alone.
Read the full study here.
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