RAS/RAF

Scientific explanation

RAS GTPases and RAF kinases are frequent oncogenic nodes. KRAS, NRAS and BRAF mutations lock mitogenic signalling on in a ligand-independent way in many tumours.

Cancers where relevant

Lung cancer Non-small-cell lung cancer KRAS-driven NSCLC BRAF-mutant NSCLC Colorectal cancer MSS colorectal cancer KRAS-mutant colorectal cancer BRAF-mutant colorectal cancer Pancreatic cancer Cholangiocarcinoma Melanoma BRAF-driven melanoma NRAS-driven melanoma Skin cancers Thyroid cancer

Compounds that intersect this pathway

Statins (HMG-CoA reductase inhibitors)

Inhibit HMG-CoA reductase, depleting mevalonate-pathway isoprenoids needed for RAS/RHO prenylation and some sterol-dependent growth programmes. Observational oncology signals are mixed and not a licence to treat cancer with statins.

Evidence in mapped cancers: Clinical / Human Evidence · In Vitro · Mechanistically Plausible

Convergence partners

Other pathways that co-occur with RAS/RAF on mapped adjunct records: Fatty-acid metabolism.

This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.