Oncology pathway explorer
Immune suppression
Scientific explanation
Tumours recruit Tregs, MDSCs and M2-like macrophages, and secrete TGF-β, IL-10, adenosine and IDO-related metabolites to blunt effector immunity.
Cancers where relevant
Compounds that intersect this pathway
Lysosomotropic agent that raises endosomal/autophagosomal pH, impairing flux. Combination trials in oncology have been mixed; blockade is not equivalent to proven benefit.
Macrolide with immunomodulatory properties and experimental / observations. Not an anticancer indication.
Celecoxib
Selective -2 reducing PGE2. Relevant to -associated epithelial neoplasia; cardiovascular risk and lack of broad anticancer approval constrain interpretation.
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).
Omega-3 fatty acids
EPA/DHA alter eicosanoid balance and membrane signalling. Cachexia and hypotheses exist; they are not cytotoxic oncology drugs.
Evidence in mapped cancers: Clinical / Human Evidence · Mechanistically Plausible
Beta-glucans / medicinal-mushroom polysaccharides
β-glucans can engage Dectin-1 and complement pathways, modulating innate immunity in models and some adjunctive clinical settings. They are not tumour-selective cytotoxics.
Evidence in mapped cancers: Early Clinical · In Vivo · Mechanistically Plausible
Convergence partners
Other pathways that co-occur with Immune suppression on mapped adjunct records: COX / inflammatory signalling.
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.