Cancer / Oncology/BRAF-mutant NSCLC
Thoracic · subtype
BRAF-mutant NSCLC
Subtype of Non-small-cell lung cancer
Clinical / Scientific
BRAF V600 and non-V600 alterations activate . V600-targeted combinations are established in selected NSCLC; non-V600 biology is less uniform.
Core Biological Drivers
BRAF mutation
lock.
Key Pathways
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.
Scientific explanation
The RAS–RAF–MEK–ERK cascade transmits mitogenic RTK signals to programmes for proliferation and differentiation.
Pathway Convergence
Target → pathway → downstream effect → biological consequence. Shared intersections are mechanistic maps, not protocols.
Growth-factor signalling
Ligand or mutation-driven RTK input feeds PI3K/AKT and mTORC1, supporting anabolic growth. This is a map of signalling, not a treatment protocol.
Metabolic Vulnerabilities
Aerobic supports ATP, biomass and acidification even when oxygen is available. Extent varies by tumour and remains a vulnerability hypothesis rather than a uniform target.
Tumor Microenvironment
Disordered vasculature creates , HIF-1α stabilization, induction and immune-suppressive adenosine/lactate milieus.
Metastasis Module
, protease-mediated invasion, , circulating tumour-cell survival and organ-specific colonization form the metastatic cascade. Pre-metastatic niches and vascular permeability influence tropism.
Resistance Biology
reactivation and RTK adaptive signalling.
Cancer Stemness
Wnt, Notch, Hedgehog, ALDH and CD44-associated programmes can mark stem-like fractions with quiescence and therapy tolerance. These markers are not interchangeable across tumour types.
Mechanism-Based Adjunctive Strategies
Compounds appear only where a mechanistic overlap exists for this cancer. Evidence tiers are not equivalent. Nothing here is a treatment recommendation.
Statins (HMG-CoA reductase inhibitors)
Target / Mechanism
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.
Cancer relevance
Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Mevalonate / prenylation mechanistic overlap. Convergence: RAS/RAF, Fatty-acid metabolism.
Target / Mechanism
Modest complex I inhibition raises AMP:ATP, activating and restraining hepatic and -linked anabolism. Direct antineoplastic efficacy is not established from that pharmacology alone.
Cancer relevance
activation and restraint provide a metabolic rationale in - and -linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Metabolic adjunctive research context. Convergence: AMPK, mTOR, Glycolysis.
Research Context
- BRAF. Davies H, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949-954. https://doi.org/10.1038/nature00766
- Resistance. Holohan C, Van Schaeybroeck S, Longley DB, Johnston PG. Cancer drug resistance: an evolving paradigm. Nat Rev Cancer. 2013;13(10):714-726. https://doi.org/10.1038/nrc3599
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.