Oncology pathway explorer
JAK/STAT
Scientific explanation
receptors signal through JAKs to STATs. in particular supports survival, invasion and inflammatory gene programmes in many solid and hematologic tumours.
Cancers where relevant
Compounds that intersect this pathway
uncoupler in cestodes; mammalian models report , Wnt/β-catenin and modulation. Those host-signalling findings are investigational/preclinical.
Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible
Glutamate-gated chloride channel in invertebrates. Reported mammalian effects on nuclear transport and signalling pathways come from experimental systems and do not constitute proven anticancer therapy.
Antiparasitic interfering with PFOR in anaerobes. Broader in-vitro reports include metabolic and -related readouts; these are not clinical oncology indications.
Curcumin
Polyphenol with promiscuous in-vitro NF-κB, and ROS effects. Bioavailability is poor; dish activity does not establish clinical anticancer efficacy.
Evidence in mapped cancers: In Vitro · Mechanistically Plausible
Convergence partners
Other pathways that co-occur with JAK/STAT on mapped adjunct records: NF-κB, Wnt/β-catenin, mTOR.
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.