Oncology pathway explorer
Angiogenesis
Scientific explanation
New vessel formation supplies oxygen and routes for dissemination. It is driven by , angiopoietins, FGF and inflammatory cytokines under .
Cancers where relevant
Compounds that intersect this pathway
Azole antifungal; off-target reports include Hedgehog-pathway antagonism and anti-angiogenic endothelial effects in experimental and early clinical settings. Not a licensed antineoplastic.
Evidence in mapped cancers: Early Clinical · In Vivo · In Vitro
Celecoxib
Selective -2 reducing PGE2. Relevant to -associated epithelial neoplasia; cardiovascular risk and lack of broad anticancer approval constrain interpretation.
Evidence in mapped cancers: Clinical / Human Evidence · In Vivo · In Vitro
Propranolol
Non-selective β-adrenergic . Adrenergic signalling can support and invasion in some tumours; selected clinical experiences (e.g. infantile haemangioma is established vascular biology, oncology uses are a different question).
Evidence in mapped cancers: Early Clinical · In Vivo · In Vitro
Losartan
AT1- . In desmoplastic models, angiotensin blockade can reduce TGF-β-linked stromal compression and improve perfusion; this is adjunctive stromal biology, not cytotoxic oncology.
Evidence in mapped cancers: Early Clinical · In Vivo · Mechanistically Plausible
Candesartan
ARBs share AT1-blockade biology with losartan. Tumour- hypotheses are class-level and not tumour-type-proven treatments.
Evidence in mapped cancers: In Vivo · Mechanistically Plausible
Convergence partners
Other pathways that co-occur with Angiogenesis on mapped adjunct records: COX / inflammatory signalling, Invasion, Hedgehog, TGF-β.
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.