Cancer → Compound Matrix

Cancer type	Compound	Pathway	Evidence	Adjunctive context	Mechanistic rationale
Breast cancer	Tamoxifen	estrogen-receptor, apoptosis	Established Oncology Use; Clinical / Human Evidence	Labelled endocrine therapy context	Established SERM therapy for hormone-receptor-positive breast cancer according to labelled oncology practice. Tissue-specific agonist/antagonist balance still applies.
Breast cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Breast cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Breast cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Breast cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Breast cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Breast cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Breast cancer	Propranolol	angiogenesis, invasion	Early Clinical; In Vivo; In Vitro	Adrenergic / vascular adjunctive research	β-adrenergic signalling can support angiogenesis and invasion in selected tumours. Oncology uses remain investigational except where a specific vascular indication is separately established.
Breast cancer	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
Breast cancer	Melatonin	oxidative-stress, apoptosis	In Vitro; In Vivo; Mechanistically Plausible	Circadian / redox adjunctive research	Circadian receptor and antioxidant chemistry with adjunctive hypotheses. Not an antineoplastic standard.
Breast cancer	Omega-3 fatty acids	cox-inflammation, immune-suppression	Clinical / Human Evidence; Mechanistically Plausible	Inflammation / cachexia supportive research	Eicosanoid rebalancing and cachexia/inflammation research. Not cytotoxic oncology.
Breast cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
ER+ breast cancer	Tamoxifen	estrogen-receptor, apoptosis	Established Oncology Use; Clinical / Human Evidence	Labelled endocrine therapy context	Established SERM therapy for hormone-receptor-positive breast cancer according to labelled oncology practice. Tissue-specific agonist/antagonist balance still applies.
ER+ breast cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
ER+ breast cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
ER+ breast cancer	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
ER+ breast cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
PR+ breast cancer	Tamoxifen	estrogen-receptor, apoptosis	Established Oncology Use; Clinical / Human Evidence	Labelled endocrine therapy context	Established SERM therapy for hormone-receptor-positive breast cancer according to labelled oncology practice. Tissue-specific agonist/antagonist balance still applies.
PR+ breast cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
HER2+ breast cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
HER2+ breast cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
HER2+ breast cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
HER2+ breast cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
Triple-negative breast cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Triple-negative breast cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Triple-negative breast cancer	Fenbendazole	apoptosis, glycolysis	In Vitro; Hypothesis-Generating	Preclinical microtubule hypothesis	Veterinary benzimidazole with preclinical microtubule and glucose-handling reports. Human oncology evidence is insufficient.
Triple-negative breast cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Triple-negative breast cancer	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Triple-negative breast cancer	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Triple-negative breast cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Triple-negative breast cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Triple-negative breast cancer	AICAR	ampk, mtor	In Vitro; In Vivo; Hypothesis-Generating	Experimental AMPK agonism	Pharmacologic AMPK activation is a research tool.
Triple-negative breast cancer	N-acetylcysteine	oxidative-stress, nrf2, ferroptosis	In Vitro; Mechanistically Plausible; Hypothesis-Generating	Redox-buffering cautionary context	GSH repletion is dual-edged in oncology models and must not be framed as anticancer.
Lung cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Lung cancer	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Lung cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Lung cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Lung cancer	Sulforaphane	nrf2, oxidative-stress	In Vitro; In Vivo; Mechanistically Plausible	NRF2 / chemoprevention research	KEAP1/NRF2 activation and epigenetic reports in models. Chemoprevention hypotheses are not treatment proof.
Lung cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Lung cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
Non-small-cell lung cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Non-small-cell lung cancer	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Non-small-cell lung cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Non-small-cell lung cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Non-small-cell lung cancer	Sulforaphane	nrf2, oxidative-stress	In Vitro; In Vivo; Mechanistically Plausible	NRF2 / chemoprevention research	KEAP1/NRF2 activation and epigenetic reports in models. Chemoprevention hypotheses are not treatment proof.
Non-small-cell lung cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Non-small-cell lung cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Non-small-cell lung cancer	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Small-cell lung cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Small-cell lung cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Small-cell lung cancer	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Small-cell lung cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Small-cell lung cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
EGFR-mutant NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
EGFR-mutant NSCLC	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
EGFR-mutant NSCLC	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
EGFR-mutant NSCLC	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
ALK-rearranged NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
ALK-rearranged NSCLC	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
KRAS-driven NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
KRAS-driven NSCLC	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
KRAS-driven NSCLC	Sulforaphane	nrf2, oxidative-stress	In Vitro; In Vivo; Mechanistically Plausible	NRF2 / chemoprevention research	KEAP1/NRF2 activation and epigenetic reports in models. Chemoprevention hypotheses are not treatment proof.
KRAS-driven NSCLC	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
ROS1-rearranged NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
MET-altered NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
MET-altered NSCLC	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
RET-rearranged NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
BRAF-mutant NSCLC	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
BRAF-mutant NSCLC	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Mesothelioma	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Mesothelioma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Mesothelioma	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Mesothelioma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Mesothelioma	Losartan	tgfb, angiogenesis	Early Clinical; In Vivo; Mechanistically Plausible	Stroma / perfusion adjunctive research	AT1 blockade can reduce TGF-β-linked desmoplasia and improve perfusion in models, notably pancreatic. Stromal decompression is not cytotoxicity.
Colorectal cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Colorectal cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Colorectal cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Colorectal cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Colorectal cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Colorectal cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Colorectal cancer	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
Colorectal cancer	Omega-3 fatty acids	cox-inflammation, immune-suppression	Clinical / Human Evidence; Mechanistically Plausible	Inflammation / cachexia supportive research	Eicosanoid rebalancing and cachexia/inflammation research. Not cytotoxic oncology.
Colorectal cancer	Sulforaphane	nrf2, oxidative-stress	In Vitro; In Vivo; Mechanistically Plausible	NRF2 / chemoprevention research	KEAP1/NRF2 activation and epigenetic reports in models. Chemoprevention hypotheses are not treatment proof.
Colorectal cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
MSI-high colorectal cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
MSI-high colorectal cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
MSI-high colorectal cancer	Beta-glucans / medicinal-mushroom polysaccharides	immune-suppression	Early Clinical; In Vivo; Mechanistically Plausible	Innate-immune adjunctive research	Innate-immune engagement via Dectin-1-related biology. Adjunctive immunomodulation is not tumour-selective cytotoxicity.
MSI-high colorectal cancer	Omega-3 fatty acids	cox-inflammation, immune-suppression	Clinical / Human Evidence; Mechanistically Plausible	Inflammation / cachexia supportive research	Eicosanoid rebalancing and cachexia/inflammation research. Not cytotoxic oncology.
MSS colorectal cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
MSS colorectal cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
MSS colorectal cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
MSS colorectal cancer	Losartan	tgfb, angiogenesis	Early Clinical; In Vivo; Mechanistically Plausible	Stroma / perfusion adjunctive research	AT1 blockade can reduce TGF-β-linked desmoplasia and improve perfusion in models, notably pancreatic. Stromal decompression is not cytotoxicity.
MSS colorectal cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
KRAS-mutant colorectal cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
KRAS-mutant colorectal cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
KRAS-mutant colorectal cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
BRAF-mutant colorectal cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
BRAF-mutant colorectal cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
BRAF-mutant colorectal cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
APC-driven colorectal cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
APC-driven colorectal cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
APC-driven colorectal cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
HER2-amplified colorectal cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
HER2-amplified colorectal cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Pancreatic cancer	Losartan	tgfb, angiogenesis	Early Clinical; In Vivo; Mechanistically Plausible	Stroma / perfusion adjunctive research	AT1 blockade can reduce TGF-β-linked desmoplasia and improve perfusion in models, notably pancreatic. Stromal decompression is not cytotoxicity.
Pancreatic cancer	Candesartan	tgfb, angiogenesis	In Vivo; Mechanistically Plausible	Stroma / TGF-β class-level research	ARBs share AT1-blockade stromal hypotheses with losartan. Class-level biology is not tumour-type-proven treatment.
Pancreatic cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Pancreatic cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Pancreatic cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Pancreatic cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Pancreatic cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Pancreatic cancer	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Pancreatic cancer	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Pancreatic cancer	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
Gastric cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Gastric cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Gastric cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Gastric cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Gastric cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Gastric cancer	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Esophageal cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Esophageal cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Esophageal cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Esophageal cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
Hepatocellular carcinoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Hepatocellular carcinoma	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Hepatocellular carcinoma	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Hepatocellular carcinoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Hepatocellular carcinoma	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Hepatocellular carcinoma	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Hepatocellular carcinoma	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
Liver cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Liver cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Cholangiocarcinoma	Losartan	tgfb, angiogenesis	Early Clinical; In Vivo; Mechanistically Plausible	Stroma / perfusion adjunctive research	AT1 blockade can reduce TGF-β-linked desmoplasia and improve perfusion in models, notably pancreatic. Stromal decompression is not cytotoxicity.
Cholangiocarcinoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Cholangiocarcinoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Cholangiocarcinoma	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Ovarian cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Ovarian cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Ovarian cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Ovarian cancer	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Ovarian cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Ovarian cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Ovarian cancer	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Cervical cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Cervical cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Cervical cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Cervical cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
Endometrial cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Endometrial cancer	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
Endometrial cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Endometrial cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Endometrial cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Uterine cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Prostate cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Prostate cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Prostate cancer	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Prostate cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Prostate cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Prostate cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Prostate cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Androgen-sensitive prostate cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Androgen-sensitive prostate cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Castration-resistant prostate cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Castration-resistant prostate cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Castration-resistant prostate cancer	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Castration-resistant prostate cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Castration-resistant prostate cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Neuroendocrine prostate cancer	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Neuroendocrine prostate cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Neuroendocrine prostate cancer	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Neuroendocrine prostate cancer	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Kidney / renal cell carcinoma	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Kidney / renal cell carcinoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Kidney / renal cell carcinoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Kidney / renal cell carcinoma	Propranolol	angiogenesis, invasion	Early Clinical; In Vivo; In Vitro	Adrenergic / vascular adjunctive research	β-adrenergic signalling can support angiogenesis and invasion in selected tumours. Oncology uses remain investigational except where a specific vascular indication is separately established.
Kidney / renal cell carcinoma	Sulforaphane	nrf2, oxidative-stress	In Vitro; In Vivo; Mechanistically Plausible	NRF2 / chemoprevention research	KEAP1/NRF2 activation and epigenetic reports in models. Chemoprevention hypotheses are not treatment proof.
Bladder cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Bladder cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Bladder cancer	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Bladder cancer	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
Bladder cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Testicular cancer	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Testicular cancer	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Leukemias	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Leukemias	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Leukemias	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Acute myeloid leukemia	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Acute myeloid leukemia	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Acute myeloid leukemia	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Acute myeloid leukemia	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Acute myeloid leukemia	Berberine	ampk, mtor, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Metabolic energy-stress hypothesis	Complex I / AMPK pharmacology overlaps metformin-like energy stress in models. Bioavailability and lack of oncology indication keep this mechanistic.
Acute myeloid leukemia	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Acute lymphoblastic leukemia	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Acute lymphoblastic leukemia	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Acute lymphoblastic leukemia	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Hodgkin lymphoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Hodgkin lymphoma	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Hodgkin lymphoma	Omega-3 fatty acids	cox-inflammation, immune-suppression	Clinical / Human Evidence; Mechanistically Plausible	Inflammation / cachexia supportive research	Eicosanoid rebalancing and cachexia/inflammation research. Not cytotoxic oncology.
Hodgkin lymphoma	Beta-glucans / medicinal-mushroom polysaccharides	immune-suppression	Early Clinical; In Vivo; Mechanistically Plausible	Innate-immune adjunctive research	Innate-immune engagement via Dectin-1-related biology. Adjunctive immunomodulation is not tumour-selective cytotoxicity.
Non-Hodgkin lymphoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Non-Hodgkin lymphoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Non-Hodgkin lymphoma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Non-Hodgkin lymphoma	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Non-Hodgkin lymphoma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Multiple myeloma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Multiple myeloma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Multiple myeloma	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Multiple myeloma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Multiple myeloma	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Brain tumors	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Brain tumors	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Glioblastoma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Glioblastoma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Glioblastoma	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
Glioblastoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Glioblastoma	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Glioblastoma	Niclosamide	wnt, jak-stat, mtor	In Vitro; In Vivo; Mechanistically Plausible	Wnt / STAT3 signalling models	Models report Wnt/β-catenin, STAT3 and mTOR effects. Host signalling findings remain investigational.
Glioblastoma	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Glioblastoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Glioblastoma	Fenbendazole	apoptosis, glycolysis	In Vitro; Hypothesis-Generating	Preclinical microtubule hypothesis	Veterinary benzimidazole with preclinical microtubule and glucose-handling reports. Human oncology evidence is insufficient.
IDH-mutant glioma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
IDH-mutant glioma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
IDH-wildtype glioma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
IDH-wildtype glioma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
IDH-wildtype glioma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
MGMT-methylated glioma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
MGMT-methylated glioma	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.
MGMT-methylated glioma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Melanoma	Propranolol	angiogenesis, invasion	Early Clinical; In Vivo; In Vitro	Adrenergic / vascular adjunctive research	β-adrenergic signalling can support angiogenesis and invasion in selected tumours. Oncology uses remain investigational except where a specific vascular indication is separately established.
Melanoma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Melanoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Melanoma	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Melanoma	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Melanoma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
BRAF-driven melanoma	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
BRAF-driven melanoma	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
BRAF-driven melanoma	Propranolol	angiogenesis, invasion	Early Clinical; In Vivo; In Vitro	Adrenergic / vascular adjunctive research	β-adrenergic signalling can support angiogenesis and invasion in selected tumours. Oncology uses remain investigational except where a specific vascular indication is separately established.
NRAS-driven melanoma	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
NRAS-driven melanoma	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
NRAS-driven melanoma	Propranolol	angiogenesis, invasion	Early Clinical; In Vivo; In Vitro	Adrenergic / vascular adjunctive research	β-adrenergic signalling can support angiogenesis and invasion in selected tumours. Oncology uses remain investigational except where a specific vascular indication is separately established.
KIT-associated melanoma	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
KIT-associated melanoma	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Skin cancers	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Skin cancers	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Skin cancers	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Head and neck cancers	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Head and neck cancers	Curcumin	nfkb, jak-stat	In Vitro; Mechanistically Plausible	Inflammatory-signalling dish models	In-vitro NF-κB/STAT3 effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Head and neck cancers	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Head and neck cancers	EGCG	egfr, pi3k-akt	In Vitro; Mechanistically Plausible	RTK / redox dish models	Catechin effects on RTKs and redox in vitro. Clinical anticancer efficacy is not established.
Head and neck cancers	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Head and neck cancers	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Thyroid cancer	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Thyroid cancer	Statins (HMG-CoA reductase inhibitors)	ras-raf, fatty-acid-metabolism	Clinical / Human Evidence; In Vitro; Mechanistically Plausible	Mevalonate / prenylation mechanistic overlap	Mevalonate-pathway blockade can affect prenylation of RAS-family GTPases. Observational human signals are mixed and confounding is substantial.
Thyroid cancer	Celecoxib	cox-inflammation, angiogenesis	Clinical / Human Evidence; In Vivo; In Vitro	Inflammation-associated epithelial neoplasia research	COX-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.
Neuroendocrine tumors	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Neuroendocrine tumors	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Neuroendocrine tumors	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Neuroendocrine tumors	Hydroxychloroquine	autophagy	Early Clinical; In Vivo; In Vitro	Autophagy-modulation research combinations	Lysosomal pH elevation impairs autophagy flux. Early combination trials exist; benefit is not established and toxicity/retinal risk remain labelled concerns.
Sarcomas	Itraconazole	hedgehog, angiogenesis	Early Clinical; In Vivo; In Vitro	Hedgehog / angiogenesis research	Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Sarcomas	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Sarcomas	Propranolol	angiogenesis, invasion	Early Clinical; In Vivo; In Vitro	Adrenergic / vascular adjunctive research	β-adrenergic signalling can support angiogenesis and invasion in selected tumours. Oncology uses remain investigational except where a specific vascular indication is separately established.
Sarcomas	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Sarcomas	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Bone cancers	Mebendazole	apoptosis, tp53	In Vitro; In Vivo; Mechanistically Plausible	Experimental antimitotic / microtubule stress	Microtubule disruption can trigger mitotic stress and apoptosis in cell and animal models. This is not an established oncology use.
Bone cancers	Doxycycline	invasion, stemness, oxphos	In Vitro; In Vivo; Mechanistically Plausible	Anti-invasive / mitochondrial experimental context	MMP inhibition and experimental mitochondrial effects map to invasion and stem-like states in models.
Bone cancers	Metformin	ampk, mtor, glycolysis	Clinical / Human Evidence; In Vivo; In Vitro; Mechanistically Plausible	Metabolic adjunctive research context	AMPK activation and mTOR restraint provide a metabolic rationale in insulin- and glycolysis-linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Bone cancers	Disulfiram	stemness, nfkb, oxidative-stress	In Vitro; In Vivo; Early Clinical	ALDH / redox experimental context	ALDH and copper-dependent proteasome/NF-κB stress in models; clinical oncology remains limited.

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.