Cancer / Oncology/Skin cancers
Skin · umbrella
Skin cancers
Clinical / Scientific
Skin cancers include keratinocyte carcinomas (BCC, cSCC) and melanoma. BCC is Hedgehog-driven; cSCC is TP53/UV with immune context; melanoma is /TMB. Do not collapse them.
Core Biological Drivers
Hedgehog in BCC
PTCH/SMO.
UV/TP53 in cSCC
Keratinocyte carcinoma.
MAPK in melanoma
Separate lineage.
Key Pathways
Scientific explanation
Hedgehog–GLI signalling patterns development and can support basal-cell and some stromal/stem-like tumour programmes. Ligand-dependent stromal Hedgehog is distinct from mutation-driven ligand-independent activation.
Scientific explanation
TP53 encodes a stress-responsive factor controlling cell-cycle arrest, and metabolic adaptation. Loss or mutation is among the most common cancer events.
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
PD-1 on T cells engaging PD-L1/PD-L2 restrains cytotoxic function. Tumour or myeloid PD-L1 is a canonical adaptive immune-evasion axis.
Scientific explanation
family ligands drive endothelial sprouting and vascular permeability, a canonical tumour axis.
Pathway Convergence
Target → pathway → downstream effect → biological consequence. Shared intersections are mechanistic maps, not protocols.
Inflammatory survival
Chronic cytokine tone activates NF-κB and STAT3 transcriptional programmes that favour survival, invasion and sometimes immune evasion.
Hypoxia to vessels
Low oxygen stabilizes HIF-1α, inducing VEGF and endothelial sprouting. Anti-angiogenic pharmacology intersects this axis but does not erase the tumour ecosystem.
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
Resistance can arise from drug efflux, secondary mutations, bypass RTK signalling, apoptotic threshold elevation, -mediated survival, metabolic adaptation and lineage plasticity.
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.
Target / Mechanism
Azole antifungal; off-target reports include Hedgehog-pathway antagonism and anti-angiogenic endothelial effects in experimental and early clinical settings. Not a licensed antineoplastic.
Cancer relevance
Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Hedgehog / angiogenesis research. Convergence: Hedgehog, Angiogenesis.
Celecoxib
Target / Mechanism
Selective -2 reducing PGE2. Relevant to -associated epithelial neoplasia; cardiovascular risk and lack of broad anticancer approval constrain interpretation.
Cancer relevance
-2/PGE2 biology is relevant in some epithelial neoplasias. Cardiovascular risk and lack of broad anticancer approval apply. Do not equate polyp or biomarker studies with tumour cure.
Inflammation-associated epithelial neoplasia research. Convergence: COX / inflammatory signalling, Angiogenesis.
Curcumin
Target / Mechanism
Polyphenol with promiscuous in-vitro NF-κB, and ROS effects. Bioavailability is poor; dish activity does not establish clinical anticancer efficacy.
Cancer relevance
In-vitro NF-κB/ effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Inflammatory-signalling dish models. Convergence: NF-κB, JAK/STAT.
Research Context
- Hallmarks. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-674. https://doi.org/10.1016/j.cell.2011.02.013
- Checkpoints. Pardoll DM. The blockade of immune checkpoints in cancer immunotherapy. Nat Rev Cancer. 2012;12(4):252-264. https://doi.org/10.1038/nrc3239
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.