Marwa Zaied, Head of the Department of Medical Oncology at the Birket Elsaba General Hospital, shared a post on LinkedIn:
“KRAS was never the whole problem — and maybe never the solution.
For decades, we have known that >90% of pancreatic ductal adenocarcinomas (PDAC) are driven by oncogenic KRAS mutations.
And for just as long, KRAS was considered ‘undruggable.’
Recent preclinical work from Prof Mariano Barbacid’s group does not announce a new KRAS inhibitor.
Instead, it reframes the question:
What pathways do KRAS-mutant cancer cells depend on to survive?
By targeting KRAS dependency networks and exploiting synthetic lethality, the study demonstrated:
- Selective vulnerability of KRAS-driven PDAC cells
- Relative sparing of normal tissue
- Strong tumor regression in preclinical models
This reinforces a fundamental lesson in oncology:
The real target is often not the oncogene itself, but the biology it creates.
While these findings are preclinical, they provide a strong rationale for future combination strategies and translational trials in one of the most therapy-resistant malignancies.
Sometimes progress in oncology doesn’t come from a new drug — but from asking a better question.
Reference:
Guerra C, Liaki V, Barrambana S, et al. A targeted combination therapy achieves effective pancreatic cancer regression and prevents tumor resistance. Proc Natl Acad Sci U S A. 2025.
Dr. Marwa Zaied
Oncologist | Nutritionist.”
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