Written and medically validated by Hanne Kjær Uhlig, registered nurse (see author info at the bottom of the page).

Always consult your healthcare provider! ❤

Treatments

Block cancer’s growth pathways

Metaboliske strategier ved neurologiske kræftformer, herunder glioblastom, symboliseret ved skitse af hjerne med rygsøjle og neuroner stikkende ud fra 4 sider med følenerver. Sarte farver i rosa, lyseblå og hvid.

Brain cancer – other types – chart overview
Metabolic strategy against cancer – Pathways blocking

NOTE: To view all content in the chart, you must swipe/scroll to the right. (There are also many rows.)Metabolic Strategy Against Cancer – Pathways Blocking.

Content:

Short summary about metabolic approach

This is a page that provides an overview of which strategies may be appropriate if you want to challenge cancer’s metabolism.

Tools

  • Here you will find detailed overviews of a number of supplements and repurposed drugs (drugs for other purposes) that are being researched for these effects.
Metaboliske strategier symboliseret ved nogle kræfteller på kongeblå baggrund. Man kan se hvordan deres forsyning blokeres ved gule og lyseblå blokeringer der er sat ind som skiver. Røde linjer der illustrerer blodforsyning er også afbrudt.

Strategy – Block cancer’s signaling pathways (pathways)

Combination is crucial:

  • Cancer cells have great adaptability and can often find a “detour” if only one pathway is blocked.
  • Therefore, a central part of the metabolic approach is a “multi-target” strategy where multiple drugs are combined to target cancer’s vulnerabilities from multiple angles simultaneously.

How it is structured

  • The information is divided into an overview of individual drugs/supplements and their effects, as well as a number of overviews for specific cancer types that show which drugs may be relevant for these.

Purpose

  • To provide a knowledge base for a conversation with a qualified practitioner about additional treatment options/preventive measures.

Important

  • For a deeper and necessary understanding of the principles behind metabolic strategies against cancer, it is highly recommended that you read about this here: Metabolic Strategy.

This is not a self-treatment guide

  • Factors such as correct dosing, interactions with ongoing treatment, and unexpected side effects are real risks that require monitoring by a healthcare professional with insight into the area. Preferably one with experience in Integrative Oncology.

Also see Supplements and Chemotherapy – How does it work

To be continued…

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❤

What you read on Jeg har Kræft is not a recommendation. Seek competent guidance

Brain cancer – other types – Overview

Content:

Metabolic strategies for brain cancer – other types

Metaboliske strategier ved neurologiske kræftformer, herunder glioblastom, symboliseret ved skitse af hjerne med rygsøjle og neuroner stikkende ud fra 4 sider med følenerver. Sarte farver i rosa, lyseblå og hvid.

Find your cancer type in the chart below.

⚠️ The chart is not a clinical recommendation

This overview is based on a collection of knowledge about the mechanisms of action of selected repurposed drugs and supplements in relation to cancer cell vulnerabilities. The chart is not a list of preparations that should be taken simultaneously.

Be aware that cancer cells have the unfortunate ability to quickly find new supply routes (energy and signaling pathways/metabolic detours) if only one of these is blocked. Therefore, you should always choose at least 5 to 7 agents from categories (1) and (2) (Main strategy and high relevance) in consultation with your practitioner.

How to read the tables

Strength of Effect

(1) Main strategy: The most central and well-documented agents for this specific vulnerability.

(2) High relevance: Agents with strong data from laboratory experiments that are very precise.

(3) Supporting relevance: Agents that target an important “plan B” or supporting mechanism.

(4) General support: Agents that are beneficial for the body’s overall balance (e.g., immune support or anti-inflammation).

(5) Theoretical / Lacking data: Agents where the connection is more speculative, or where specific research is lacking.How to Read the Tables

Independent attack routes:

To ensure that the attack is multi-pronged, you should choose at least one preparation from each of the following five independent strategic groups/codes:

  • (A) Main motor: Blocks the growth accelerator (PI3K/Akt/mTOR).
  • (B) Waste system: Stops the recycling station (Autophagy).
  • (C) Fat factory: Blocks building blocks for cell membranes (Mevalonate pathway).
  • (D) Inflammation signal: Turns off chronic inflammation (NF-κB/STAT3).
  • (E) Cell death via stress: Kills via oxidative stress/iron stress (Ferroptosis).

Guide to selecting a column

When selecting a strategy to block cancer, you should find the column in the chart that is most relevant to your situation. Here, the cancer cell’s biological type (e.g., a specific mutation or a subtype such as triple-negative breast cancer) is the most crucial factor for selecting the protocol/column.

  • Specific type is listed: If your specific mutation or subtype is included, you should focus on that column.
  • Type is not listed: If your type is rare, unknown, or not specifically listed, you should focus on the last column labeled ‘General strategy / unspecified type’. Select 5-7 agents that cover the 5 attack groups (A-E) from this column. This general strategy targets the vulnerabilities common to almost all aggressive cancers.

Warning

This chart is solely for information and inspiration for a dialogue with a qualified doctor. It is not a treatment guide.

Brain cancer – other types – Block pathways

Substance1.1 Astro: Grade 2 (low)1.2 Astro: Grade 3 (anapl.)Substance1.3 Astro: Grade 4 (IDH-mut)1.4 Astro: CDKN2A-lossSubstance1.5 Astro: PIK3CA-mut2.1 Oligo: Grade 2Substance2.2 Oligo: Grade 32.3 Oligo: CIC-mutSubstance2.4 Oligo: FUBP1-mut2.5 Oligo: Notch-drivenSubstance3.1 Ependym: ST-ZFTA (RELA)3.2 Ependym: ST-YAP1Substance3.3 Ependym: PFA (Grp A)3.4 Ependym: PFB (Grp B)Substance3.5 Ependym: SP-MYCN3.6 Ependym: SP-MPESubstance4.1 Chordoma: common/ conventional4.2 Chordoma: chondroidSubstance4.3 Chordoma: dediff.4.4 Chordoma: poorly diff.SubstanceGeneral strategy / unspecified type
— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —— Repurposed Drugs —
Benzimidazoles (Mebendazole)(2) (A (C)) Inhibits microtubules / Secondary Inhibits glucose uptake.(2) (A (C)) Inhibits cell division / Secondary Inhibits angiogenesis.Benzimidazoles (Mebendazole)(1) (A (C)) Main strategy. Inhibits rapid division / Secondary Inhibits VEGF.(2) (A (E)) Inhibits mitosis / Secondary Promotes mitotic stress.Benzimidazoles (Mebendazole)(2) (A (C)) Inhibits growth / Secondary Inhibits glucose.(2) (A (E)) Inhibits microtubules / Secondary Inhibits Wnt signal.Benzimidazoles (Mebendazole)(2) (A (C)) Inhibits cell division / Secondary Inhibits VEGF.(3) (A (D)) Inhibits division / Secondary Stresses MAPK pathway.Benzimidazoles (Mebendazole)(3) (A (E)) Inhibits growth / Secondary Stresses MYC.(3) (A (C)) General inhibition / Secondary Interferes with Notch.Benzimidazoles (Mebendazole)(2) (A (D)) Inhibits growth / Secondary Attenuates signaling.(2) (A (E)) Inhibits YAP transport / Secondary Growth arrest.Benzimidazoles (Mebendazole)(1) (A (C)) Main strategy. Inhibits aggressive growth / Secondary Inhibits invasion.(3) (A (E)) Inhibits division / Secondary Stabilizes cells.Benzimidazoles (Mebendazole)(2) (A (E)) Inhibits growth / Secondary Inhibits MYC targets.(3) (A (D)) Inhibits division / Secondary Attenuates inflammation.Benzimidazoles (Mebendazole)(2) (A (C)) Inhibits microtubules / Secondary Inhibits invasion.(1) (A (C)) Main strategy. Inhibits microtubules / Secondary Inhibits matrix formation.Benzimidazoles (Mebendazole)(1) (A (C)) Main strategy. Aggressive growth inhibition / Secondary Inhibits spread.(1) (A (E)) Main strategy. Inhibits mitosis / Secondary Inhibits spread.Benzimidazoles (Mebendazole)(1) (A (C)) Main strategy. Inhibits microtubules broadly / Secondary Inhibits sugar metabolism.
Celecoxib(3) (D (A)) Attenuates inflammation / Secondary Prevents progression.(3) (D (C)) Attenuates microenvironment / Secondary Inhibits vessel growth.Celecoxib(2) (D (C)) High Relevance. Attenuates edema / Secondary Inhibits VEGF.(3) (D (E)) Supportive treatment / Secondary Attenuates cell stress.Celecoxib(3) (D (A)) Attenuates inflammation / Secondary Inhibits Akt signal.(3) (D (A)) Attenuates inflammation / Secondary Modulates Wnt.Celecoxib(3) (D (C)) Attenuates angiogenesis / Secondary Stabilizes microenvironment.(3) (D (A)) Attenuates inflammation / Secondary Supports MAPK blockade.Celecoxib(3) (D (E)) Attenuates inflammation / Secondary Supports stress response.(3) (D (A)) Attenuates signaling / Secondary Supports Notch blockade.Celecoxib(1) (D (A)) Main strategy. Inhibits NF-kB (RELA) / Secondary Blocks COX-2.(3) (D (A)) Attenuates inflammation / Secondary Supports Hippo blockade.Celecoxib(2) (D (C)) Attenuates inflammation / Secondary Stabilizes microenvironment.(3) (D (A)) General support / Secondary Increases stability.Celecoxib(3) (D (A)) Attenuates inflammation / Secondary General support.(1) (D (A)) Main strategy. Inhibits COX-2 / Secondary Attenuates pain and growth.Celecoxib(3) (D (C)) Attenuates inflammation / Secondary Controls matrix.(3) (D (C)) Attenuates inflammation / Secondary Controls matrix.Celecoxib(3) (D (E)) Attenuates inflammation / Secondary Attenuates pain.(3) (D (A)) Attenuates inflammation / Secondary Supports immune system.Celecoxib(3) (D (A)) Attenuates inflammation / Secondary Inhibits growth signals.
Desloratadine(4) (B (D)) Stabilizes lysosomes / Secondary Attenuates histamine.(4) (B (A)) Lysosome stress / Secondary Attenuates growth.Desloratadine(3) (B (E)) Increases chemo effect / Secondary Destabilizes lysosomes.(4) (B (E)) Lysosome stress / Secondary Supportive treatment.Desloratadine(4) (B (A)) Lysosome stress / Secondary General support.(4) (B (D)) Stabilizes lysosomes / Secondary General support.Desloratadine(4) (B (E)) Lysosome stress / Secondary General support.(4) (B (D)) Lysosome stress / Secondary General support.Desloratadine(4) (B (D)) Lysosome stress / Secondary General support.(4) (B (D)) Lysosome stress / Secondary General support.Desloratadine(3) (B (D)) Attenuates inflammation / Secondary Lysosome stress.(4) (B (E)) Lysosome stress / Secondary General support.Desloratadine(3) (B (E)) Lysosome stress / Secondary Increases cell death.(4) (B (D)) Lysosome stress / Secondary General support.Desloratadine(4) (B (E)) Lysosome stress / Secondary General support.(3) (B (D)) Attenuates inflammation / Secondary Lysosome stress.Desloratadine(4) (B (E)) Lysosome stress / Secondary General support.(4) (B (D)) Lysosome stress / Secondary General support.Desloratadine(4) (B (E)) Lysosome stress / Secondary General support.(4) (B (D)) Lysosome stress / Secondary General support.Desloratadine(4) (B (D)) Stabilizes lysosomes / Secondary Attenuates growth.
Dipyridamole(3) (D (C)) Inhibits adenosine uptake / Secondary Attenuates hypoxia signal.(3) (D (C)) Increases chemo effect / Secondary Attenuates platelet shield.Dipyridamole(2) (D (C)) High Relevance. Inhibits thrombosis risk / Secondary Inhibits angiogenesis.(3) (D (A)) Attenuates signaling / Secondary Supports chemo.Dipyridamole(3) (D (A)) Attenuates growth / Secondary Inhibits adenosine.(3) (D (C)) Inhibits platelets / Secondary Attenuates spread.Dipyridamole(3) (D (C)) Increases chemo effect / Secondary Attenuates spread.(3) (D (A)) Inhibits signaling / Secondary Support.Dipyridamole(3) (D (A)) Attenuates growth / Secondary Support.(3) (D (C)) Inhibits spread / Secondary Attenuates signal.Dipyridamole(3) (D (A)) Attenuates inflammation / Secondary Inhibits growth.(3) (D (C)) Attenuates blood supply / Secondary Support.Dipyridamole(2) (D (C)) High Relevance. Inhibits metastasis / Secondary Platelet inhibition.(3) (D (C)) Inhibits spread / Secondary Support.Dipyridamole(3) (D (C)) Inhibits spread / Secondary Inhibits adenosine.(3) (D (A)) Attenuates inflammation / Secondary Support.Dipyridamole(3) (D (C)) Inhibits metastasis / Secondary Attenuates signaling.(3) (D (C)) Inhibits spread / Secondary Attenuates signaling.Dipyridamole(2) (D (C)) Inhibits aggressive spread / Secondary Increases chemo effect.(3) (D (C)) Inhibits spread / Secondary Support.Dipyridamole(3) (D (C)) Inhibits platelets / Secondary Attenuates spread.
Disulfiram (Antabuse)(2) (E (D)) Inhibits stem cells / Secondary Creates copper toxicity.(2) (E (A)) High Relevance. Inhibits ALDH / Secondary Creates stress.Disulfiram (Antabuse)(2) (E (D)) Inhibits resistance / Secondary Inhibits NF-kB.(2) (E (A)) Targets dividing cells / Secondary Creates stress.Disulfiram (Antabuse)(2) (E (A)) Inhibits survival / Secondary Creates stress.(2) (E (D)) High Relevance. Targets stem cells / Secondary Creates stress.Disulfiram (Antabuse)(2) (E (C)) Inhibits ALDH / Secondary Inhibits angiogenesis.(2) (E (A)) Targets stem cells / Secondary Creates stress.Disulfiram (Antabuse)(2) (E (A)) Targets stem cells / Secondary Creates stress.(2) (E (D)) Targets stem cells / Secondary Creates stress.Disulfiram (Antabuse)(1) (D (E)) Main strategy. Inhibits NF-kB directly / Secondary Targets stem cells.(3) (E (D)) Inhibits stem cells / Secondary Creates stress.Disulfiram (Antabuse)(2) (E (B)) Inhibits stem cells / Secondary Creates epigenetic stress.(3) (E (D)) Inhibits stem cells / Secondary Creates stress.Disulfiram (Antabuse)(2) (E (A)) Inhibits stem cells / Stresses MYC cells.(2) (D (E)) Inhibits NF-kB / Secondary Targets stem cells.Disulfiram (Antabuse)(2) (E (A)) High Relevance. Inhibits Brachyury pathways / Secondary Targets stem cells.(2) (E (C)) Inhibits stem cells / Secondary Affects matrix.Disulfiram (Antabuse)(1) (E (D)) Main strategy. Inhibits resistance / Secondary Inhibits NF-kB.(2) (E (D)) Inhibits stem cells / Secondary Modulates immune response.Disulfiram (Antabuse)(2) (E (A)) High Relevance. Targets stem cells / Secondary Inhibits growth.
Doxycycline(2) (E (C)) Inhibits mitochondria / Secondary Inhibits stem cells.(2) (E (C)) Metabolic stress / Secondary Inhibits invasion (MMP).Doxycycline(2) (E (C)) High Relevance. Inhibits invasion / Secondary Creates energy failure.(2) (E (C)) Metabolic stress / Secondary Inhibits MMP enzymes.Doxycycline(2) (E (A)) Inhibits energy / Secondary Stresses Akt pathway.(2) (E (C)) Inhibits mitochondria / Secondary Inhibits MMP enzymes.Doxycycline(2) (E (C)) Metabolic stress / Secondary Inhibits MMP enzymes.(3) (E (C)) Inhibits energy / Secondary Inhibits MMP.Doxycycline(3) (E (C)) Inhibits energy / Secondary Inhibits MMP.(3) (E (C)) Inhibits energy / Secondary Inhibits MMP.Doxycycline(3) (E (D)) Inhibits MMP-9 / Secondary Targets mitochondria.(3) (E (C)) Inhibits energy / Secondary Inhibits MMP.Doxycycline(2) (E (C)) High Relevance. Inhibits metastasis / Secondary Removes energy.(3) (E (C)) Inhibits energy / Secondary Inhibits MMP.Doxycycline(2) (E (C)) Inhibits energy / Secondary Inhibits MMP.(2) (E (D)) Inhibits inflammation (MMP) / Secondary Removes energy.Doxycycline(2) (E (C)) High Relevance. Inhibits MMP (Matrix) / Secondary Targets mitochondria.(1) (E (C)) Main strategy. Inhibits MMP (Cartilage) / Secondary Removes energy.Doxycycline(2) (E (C)) Inhibits invasion / Secondary Removes energy.(2) (E (C)) Inhibits invasion / Secondary Removes energy.Doxycycline(2) (E (C)) High Relevance. Targets the energy factories / Secondary Inhibits spread.
Aspirin(3) (D (C)) Attenuates inflammation / Secondary Inhibits platelet aggregation.(3) (D (C)) Inhibits vessel growth / Secondary Attenuates microenvironment.Aspirin(2) (D (C)) High Relevance. Inhibits VEGF and edema / Secondary Attenuates inflammation.(3) (D (A)) Attenuates signaling / Secondary Inhibits platelets.Aspirin(3) (D (A)) Attenuates growth / Secondary Inhibits platelets.(3) (D (C)) Inhibits platelets / Secondary Attenuates spread.Aspirin(3) (D (C)) Attenuates angiogenesis / Secondary Inhibits thrombocytes.(3) (D (A)) Attenuates inflammation / Secondary Support.Aspirin(3) (D (A)) Attenuates inflammation / Secondary Support.(3) (D (C)) Attenuates signaling / Secondary Inhibits platelets.Aspirin(2) (D (A)) High Relevance. Inhibits NF-kB / Secondary Inhibits COX-1.(3) (D (C)) Attenuates inflammation / Secondary Inhibits platelets.Aspirin(2) (D (C)) Attenuates inflammation / Secondary Inhibits spread.(3) (D (C)) General support / Secondary Inhibits platelets.Aspirin(3) (D (C)) Attenuates inflammation / Secondary Inhibits spread.(2) (D (A)) Inhibits inflammation / Secondary Pain and growth.Aspirin(3) (D (C)) Attenuates inflammation / Secondary Inhibits spread.(3) (D (C)) Attenuates inflammation / Secondary Inhibits spread.Aspirin(3) (D (C)) Attenuates inflammation / Secondary Inhibits spread.(3) (D (A)) Attenuates inflammation / Secondary Supports immune system.Aspirin(3) (D (C)) Attenuates inflammation / Secondary Inhibits spread.
Hydroxychloroquine(1) (B (E)) Main strategy. Blocks autophagy (IDH requirement) / Secondary Sensitizes the cell.(1) (B (E)) Main strategy. Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(1) (B (D)) Main strategy. Critical stress / Secondary Modulates immune response.(2) (B (A)) Blocks autophagy / Secondary Stresses cell cycle.Hydroxychloroquine(1) (B (A)) Main strategy. Inhibits PI3K escape / Secondary Creates stress.(1) (B (E)) Main strategy. Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(1) (B (E)) Main strategy. Blocks autophagy / Secondary Creates stress.(2) (B (E)) Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(2) (B (E)) Blocks autophagy / Secondary Creates stress.(2) (B (E)) Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(2) (B (D)) Blocks autophagy / Secondary Stresses NF-kB.(3) (B (E)) Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(1) (B (E)) Main strategy. Hypoxia stress / Secondary Sensitizes the cell.(3) (B (E)) Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(2) (B (A)) Blocks autophagy / Stresses MYC cells.(3) (B (D)) Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(2) (B (A)) Blocks autophagy / Secondary Stresses Brachyury cells.(2) (B (C)) Blocks autophagy / Secondary Creates stress.Hydroxychloroquine(1) (B (E)) Main strategy. Stresses aggressive cells / Secondary Inhibits resistance.(2) (B (D)) Blocks autophagy / Secondary Immune effect.Hydroxychloroquine(1) (B (E)) Main strategy. Blocks autophagy / Secondary Creates stress.
Ivermectin(2) (A (E)) Inhibits Wnt/PAK1 / Secondary Inhibits growth.(2) (A (E)) Inhibits signaling / Secondary Induces apoptosis.Ivermectin(3) (A (E)) Inhibits stem cells / Secondary Blockade of Wnt.(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.Ivermectin(3) (A (C)) Inhibits growth / Secondary Inhibits Akt pathway.(1) (A (E)) Main strategy. Wnt blockade (Important) / Secondary Induces apoptosis.Ivermectin(2) (A (E)) High Relevance. Wnt/PAK1 / Secondary Induces apoptosis.(3) (A (E)) Inhibits signaling / Secondary Induces apoptosis.Ivermectin(3) (A (E)) Inhibits signaling / Secondary Induces apoptosis.(2) (A (D)) Inhibits Notch crosstalk / Secondary Induces apoptosis.Ivermectin(3) (A (D)) Inhibits PAK1 / Secondary Attenuates inflammation.(3) (A (E)) Inhibits PAK1 / Secondary Supports YAP blockade.Ivermectin(3) (A (E)) Inhibits signaling / Secondary Induces apoptosis.(3) (A (E)) Inhibits signaling / Secondary Induces apoptosis.Ivermectin(3) (A (E)) Inhibits signaling / Secondary Induces apoptosis.(3) (A (D)) Inhibits signaling / Secondary Induces apoptosis.Ivermectin(3) (A (E)) Inhibits Wnt / Secondary Induces apoptosis.(3) (A (E)) Inhibits Wnt / Secondary Induces apoptosis.Ivermectin(3) (A (E)) Inhibits Wnt / Secondary Induces apoptosis.(3) (A (E)) Inhibits Wnt / Secondary Induces apoptosis.Ivermectin(3) (A (E)) Inhibits Wnt signal / Secondary Promotes cell death.
Low-dose Naltrexone (LDN)(4) (D (A)) Immune modulation / Secondary Attenuates OGF factor.(4) (D (A)) Immune support / Secondary Inhibits growth.Low-dose Naltrexone (LDN)(4) (D (C)) Immune support / Secondary Modulates microenvironment.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (A)) Immune support / Secondary Creates balance.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (A)) Immune support / Secondary Creates balance.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (A)) Immune support / Secondary Creates balance.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(3) (D (A)) Attenuates inflammation / Secondary Immune support.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (E)) Immune support / Secondary Creates balance.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (A)) Immune support / Secondary Creates balance.(2) (D (A)) High Relevance. Attenuates glial inflammation / Secondary Attenuates pain.Low-dose Naltrexone (LDN)(4) (D (A)) Immune support / Secondary Creates balance.(4) (D (A)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (E)) Immune support / Secondary Creates balance.(4) (D (E)) Immune support / Secondary Creates balance.Low-dose Naltrexone (LDN)(4) (D (A)) Strengthens immune system / Secondary Attenuates growth signals.
Metformin(1) (A (E)) Main strategy. Lowers insulin/IGF-1 / Secondary Activates AMPK.(1) (A (C)) Main strategy. Inhibits mTOR / Secondary Glucose starvation.Metformin(1) (A (C)) Main strategy. Metabolic blocking / Secondary Inhibits stroma.(2) (A (E)) Inhibits growth / Secondary Supports cell cycle arrest.Metformin(1) (A (C)) Main strategy. Direct mTOR antidote / Secondary Lowers insulin.(1) (A (E)) Main strategy. Metabolic control / Secondary Activates AMPK.Metformin(1) (A (C)) Main strategy. Metabolic control / Secondary Activates AMPK.(2) (A (C)) Inhibits mTOR / Secondary Crosses with MAPK.Metformin(2) (A (C)) Inhibits mTOR / Secondary Starves MYC cells.(2) (A (D)) Inhibits mTOR / Secondary Crosses with Notch.Metformin(2) (A (D)) Inhibits mTOR / Secondary Supports NF-kB blockade.(2) (A (C)) Inhibits mTOR / Secondary Crosses with Hippo.Metformin(2) (A (E)) High Relevance. Metabolic pressure / Secondary Inhibits hypoxia.(3) (A (E)) General metabolic control / Secondary Creates stress.Metformin(1) (A (C)) Main strategy. Starves MYC cells / Secondary Activates AMPK.(3) (A (D)) Metabolic control / Secondary Attenuates inflammation.Metformin(2) (A (E)) High Relevance. Inhibits mTOR / Secondary Crosses with Brachyury.(2) (A (C)) Metabolic control / Secondary Affects matrix.Metformin(1) (A (C)) Main strategy. Metabolic blockade / Secondary Inhibits mTOR.(2) (A (D)) Metabolic control / Secondary Supports immune response.Metformin(1) (A (E)) Main strategy. Lowers blood sugar / Secondary Activates emergency brake.
Propranolol(3) (C (A)) Attenuates stress signals / Secondary Inhibits invasion.(2) (C (A)) High Relevance. Inhibits angiogenesis / Secondary Attenuates stress.Propranolol(1) (C (A)) Main strategy. Inhibits vessel growth (VEGF) / Secondary Attenuates stress.(3) (C (E)) Attenuates stress / Secondary Inhibits growth.Propranolol(3) (C (A)) Attenuates stress / Secondary Inhibits growth.(3) (C (A)) Attenuates stress / Secondary Inhibits growth.Propranolol(2) (C (A)) High Relevance. Inhibits angiogenesis / Secondary Attenuates stress.(3) (C (A)) Attenuates stress / Secondary Inhibits growth.Propranolol(3) (C (A)) Attenuates stress / Secondary Inhibits growth.(3) (C (D)) Attenuates stress / Secondary Inhibits growth.Propranolol(2) (C (D)) Attenuates angiogenesis / Secondary Attenuates stress.(3) (C (A)) Attenuates stress / Secondary Inhibits growth.Propranolol(2) (C (E)) High Relevance. Inhibits blood supply / Secondary Attenuates stress.(3) (C (A)) Attenuates stress / Secondary Inhibits growth.Propranolol(2) (C (A)) Inhibits angiogenesis / Secondary Attenuates stress.(3) (C (D)) Attenuates stress / Secondary Inhibits growth.Propranolol(3) (C (A)) Attenuates stress / Secondary Inhibits growth.(3) (C (A)) Attenuates stress / Secondary Inhibits growth.Propranolol(2) (C (A)) Inhibits vessel growth / Secondary Attenuates stress.(2) (C (D)) Inhibits vessel growth / Secondary Attenuates stress.Propranolol(3) (C (D)) Blocks blood vessel formation / Secondary Blocks stress signals.
Statins(2) (C (A)) High Relevance. Inhibits mevalonate / Secondary Stabilizes cell membranes.(2) (C (A)) Inhibits proliferation / Secondary Inhibits Rho pathway.Statins(2) (C (A)) High Relevance. Synergy with metformin / Secondary Inhibits growth.(2) (C (E)) Inhibits cell cycle (p21) / Secondary Inhibits mevalonate.Statins(2) (C (A)) Inhibits PI3K via Ras / Secondary Inhibits mevalonate.(2) (C (A)) Inhibits mevalonate / Secondary Inhibits growth.Statins(2) (C (A)) Inhibits proliferation / Secondary Inhibits Rho pathway.(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.Statins(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.Statins(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.Statins(3) (C (E)) Inhibits growth / Secondary Inhibits mevalonate.(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.Statins(2) (C (A)) High Relevance. MYC-dependent fatty acid / Secondary Inhibits growth.(3) (C (D)) Inhibits growth / Secondary Inhibits mevalonate.Statins(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.(3) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.Statins(2) (C (A)) Inhibits growth / Secondary Inhibits mevalonate.(3) (C (D)) Inhibits growth / Secondary Inhibits mevalonate.Statins(2) (C (A)) High Relevance. Shuts down building blocks (Mevalonate) / Secondary Inhibits growth.
— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —— Supplements —
AHCC(4) (D (A)) Strengthens NK cells / Secondary Supports immune defense.(4) (D (A)) General immune support / Secondary Attenuates growth.AHCC(4) (D (C)) General immune support / Secondary Supports chemo.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (C)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Attenuates inflammation.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General immune support / Secondary Support.(4) (D (A)) General immune support / Secondary Support.AHCC(4) (D (A)) General strengthening of the immune system / Secondary Supports the body’s fight.
Alpha-lipoic acid (ALA)(3) (A (E)) Supports mitochondria / Secondary Antioxidant.(3) (A (C)) Inhibits glycolysis / Secondary Supports metabolism.Alpha-lipoic acid (ALA)(2) (A (C)) High Relevance. IDH metabolic regulator / Secondary Antioxidant.(3) (A (E)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (C)) Supports metabolism / Secondary Antioxidant.(2) (A (C)) High Relevance. Metabolic support / Secondary Antioxidant.Alpha-lipoic acid (ALA)(2) (A (C)) Inhibits glycolysis / Secondary Antioxidant.(3) (A (C)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (C)) Supports metabolism / Secondary Antioxidant.(3) (A (C)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (D)) Attenuates inflammation / Secondary Metabolic support.(3) (A (C)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (C)) Supports metabolism / Secondary Antioxidant.(3) (A (C)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (C)) Supports metabolism / Secondary Antioxidant.(3) (A (D)) Attenuates neuropathy / Secondary Metabolic support.Alpha-lipoic acid (ALA)(3) (A (C)) Supports metabolism / Secondary Antioxidant.(3) (A (C)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (C)) Supports metabolism / Secondary Antioxidant.(3) (A (C)) Supports metabolism / Secondary Antioxidant.Alpha-lipoic acid (ALA)(3) (A (C)) Helps regulate blood sugar / Secondary Supports metabolism.
Apigenin(3) (D (A)) Attenuates inflammation / Secondary Inhibits CD38.(3) (A (D)) Inhibits growth / Secondary Attenuates edema.Apigenin(3) (D (A)) Anti-inflammatory / Secondary Inhibits invasion.(3) (A (D)) Inhibits growth / Secondary Support.Apigenin(3) (A (D)) Inhibits growth / Secondary Support.(3) (D (A)) Attenuates inflammation / Secondary Inhibits Wnt.Apigenin(3) (A (D)) Inhibits angiogenesis / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.Apigenin(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits Notch / Secondary Support.Apigenin(1) (D (A)) Main strategy. Inhibits NF-kB (RELA) / Secondary Inhibits growth.(3) (A (D)) Inhibits growth / Secondary Support.Apigenin(3) (D (A)) Attenuates inflammation / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.Apigenin(3) (A (D)) Inhibits growth / Secondary Support.(2) (D (A)) High Relevance. Attenuates glial inflammation / Secondary Support.Apigenin(2) (D (A)) High Relevance. Inhibits CK2/Brachyury / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.Apigenin(3) (D (A)) Attenuates inflammation / Secondary Support.(3) (D (A)) Immune modulation / Secondary Support.Apigenin(3) (D (A)) Attenuates inflammation / Secondary Inhibits growth signals.
Artemisinin(3) (E (C)) Iron-dependent stress / Secondary Inhibits growth.(2) (E (C)) High Relevance. Induces ferroptosis / Secondary Inhibits vessels.Artemisinin(2) (E (C)) Induces ferroptosis / Secondary Inhibits angiogenesis.(2) (E (A)) Induces apoptosis / Secondary Support.Artemisinin(3) (E (A)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces ferroptosis / Secondary Inhibits growth.Artemisinin(2) (E (C)) Induces ferroptosis / Secondary Inhibits vessels.(3) (E (A)) Induces apoptosis / Secondary Support.Artemisinin(3) (E (A)) Induces apoptosis / Secondary Support.(3) (E (A)) Induces apoptosis / Secondary Support.Artemisinin(3) (E (D)) Attenuates inflammation / Secondary Cell death.(3) (E (A)) Induces apoptosis / Secondary Support.Artemisinin(2) (E (C)) High Relevance. Inhibits metastasis / Secondary Ferroptosis.(3) (E (A)) Induces apoptosis / Secondary Support.Artemisinin(2) (E (A)) Induces apoptosis / Secondary Support.(3) (E (D)) Attenuates inflammation / Secondary Cell death.Artemisinin(3) (E (C)) Induces ferroptosis / Secondary Support.(3) (E (C)) Induces ferroptosis / Secondary Support.Artemisinin(2) (E (C)) High Relevance. Induces ferroptosis / Secondary Aggressive growth.(3) (E (A)) Induces apoptosis / Secondary Support.Artemisinin(2) (E (C)) High Relevance. Utilizes iron to kill cancer / Secondary Inhibits blood vessels.
Astragalus(4) (D (A)) Immune support / Secondary Attenuates growth.(4) (D (A)) Immune support / Secondary Attenuates growth.Astragalus(3) (D (C)) Attenuates edema / Secondary Immune support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Astragalus(3) (D (A)) Anti-inflammatory / Secondary Immune support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) Immune support / Secondary Support.(3) (D (A)) Attenuates inflammation / Secondary Immune support.Astragalus(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Astragalus(4) (D (A)) General strengthening of the body / Secondary Immune system.
Berberine(1) (A (C)) Main strategy. Inhibits metabolism / Secondary IDH synergy.(1) (A (C)) Main strategy. Inhibits mTOR / Secondary Inhibits glucose.Berberine(1) (A (C)) Main strategy. Inhibits invasion / Secondary Inhibits EGFR.(2) (A (E)) Cell cycle arrest / Secondary Inhibits mTOR.Berberine(1) (A (C)) Main strategy. Inhibits mTOR / Secondary Inhibits Akt.(1) (A (D)) Main strategy. Metabolic inhibition / Secondary Inhibits Wnt.Berberine(1) (A (D)) Main strategy. Inhibits mTOR / Secondary Inhibits Wnt.(2) (A (C)) Inhibits MAPK / Secondary Metabolic inhibition.Berberine(2) (A (C)) Inhibits growth / Secondary Links to MYC.(2) (A (D)) Inhibits growth / Secondary Inhibits Notch.Berberine(2) (A (D)) Inhibits NF-kB / Secondary Inhibits metabolism.(2) (A (E)) Inhibits growth / Secondary Inhibits Hippo.Berberine(2) (A (C)) High Relevance. Inhibits growth / Secondary Inhibits metabolism.(3) (A (C)) General inhibition / Secondary Inhibits metabolism.Berberine(2) (A (C)) High Relevance. MYC inhibition / Secondary Inhibits metabolism.(3) (A (D)) Attenuates inflammation / Secondary Inhibits metabolism.Berberine(1) (A (C)) Main strategy. Inhibits EGFR / Secondary Inhibits metabolism.(2) (A (C)) Inhibits growth / Secondary Inhibits metabolism.Berberine(1) (A (C)) Main strategy. Inhibits aggressive growth / Secondary Inhibits metabolism.(2) (A (E)) Inhibits growth / Secondary Inhibits metabolism.Berberine(1) (A (D)) Main strategy. Activates the emergency brake (AMPK) / Secondary Attenuates inflammation.
Boswellia(3) (D (A)) Attenuates edema / Secondary 5-LOX inhibition.(3) (D (A)) Attenuates inflammation / Secondary 5-LOX inhibition.Boswellia(2) (D (A)) High Relevance. Alternative to steroid / Secondary 5-LOX inhibition.(3) (D (E)) Attenuates edema / Secondary Inhibits inflammation.Boswellia(3) (D (A)) Attenuates inflammation / Secondary General support.(3) (D (A)) Attenuates edema / Secondary 5-LOX inhibition.Boswellia(3) (D (A)) Attenuates inflammation / Secondary 5-LOX inhibition.(3) (D (A)) Attenuates inflammation / Secondary General support.Boswellia(3) (D (E)) Attenuates inflammation / Secondary General support.(3) (D (A)) Attenuates inflammation / Secondary General support.Boswellia(2) (D (A)) High Relevance. Attenuates NF-kB / Secondary 5-LOX inhibition.(3) (D (A)) Attenuates inflammation / Secondary General support.Boswellia(3) (D (E)) Attenuates inflammation / Secondary General support.(3) (D (A)) Attenuates inflammation / Secondary General support.Boswellia(3) (D (A)) Attenuates inflammation / Secondary General support.(1) (D (A)) Main strategy. Inhibits inflammation / Secondary Attenuates pain.Boswellia(3) (D (C)) Attenuates inflammation / Secondary General support.(3) (D (C)) Attenuates inflammation / Secondary General support.Boswellia(3) (D (E)) Attenuates inflammation / Secondary General support.(3) (D (A)) Attenuates inflammation / Secondary General support.Boswellia(3) (D (A)) Potent attenuation of inflammation / Secondary Inhibits growth.
Cat’s Claw(4) (D (E)) Anti-inflammatory / Secondary Induces apoptosis.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(3) (D (E)) Inhibits NF-kB / Secondary Apoptosis.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Pain.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) Attenuates inflammation / Secondary Support.(4) (D (E)) Attenuates inflammation / Secondary Support.Cat’s Claw(4) (D (E)) General attenuation of inflammation / Secondary Attenuates stress.
Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) Supports mitochondria / Secondary Cell protection.(4) (A (E)) Supports mitochondria / Secondary Cell protection.Coenzyme Q10(4) (A (E)) General cellular energy support / Secondary Antioxidant.
Curcumin(2) (D (A)) Attenuates inflammation / Secondary Inhibits IDH growth.(2) (A (D)) Inhibits mTOR / Secondary Inhibits NF-kB.Curcumin(2) (D (A)) High Relevance. Synergy with chemo / Secondary Attenuates edema.(1) (A (D)) Main strategy. Inhibits Cyclin D1 / Secondary Inhibits growth.Curcumin(2) (A (D)) Inhibits mTOR/Akt / Secondary Inhibits NF-kB.(2) (D (A)) Attenuates inflammation / Secondary Inhibits Notch.Curcumin(2) (A (D)) Inhibits growth / Secondary Inhibits Notch.(2) (A (D)) Inhibits MAPK / Secondary Inhibits NF-kB.Curcumin(2) (A (C)) Inhibits growth / Secondary Inhibits MYC.(1) (A (D)) Main strategy. Inhibits Notch signal / Secondary Inhibits Wnt.Curcumin(1) (D (A)) Main strategy. Inhibits NF-kB (RELA) / Secondary Inhibits growth.(2) (A (D)) Inhibits YAP/TAZ / Secondary Inhibits growth.Curcumin(2) (D (E)) Attenuates inflammation / Secondary Epigenetic support.(3) (D (A)) Attenuates inflammation / Secondary Inhibits growth.Curcumin(2) (D (A)) Attenuates inflammation / Secondary Inhibits MYC.(1) (D (E)) Main strategy. Anti-inflammatory / Secondary Attenuates pain.Curcumin(2) (D (A)) High Relevance. Inhibits EGFR / Secondary Inhibits Brachyury.(2) (D (C)) Attenuates inflammation / Secondary Controls matrix.Curcumin(2) (D (A)) Attenuates inflammation / Secondary Inhibits growth.(1) (D (A)) Main strategy. Immune modulation (INI1) / Secondary Inhibits growth.Curcumin(1) (D (A)) Main strategy. Targets inflammation / Secondary Targets growth and blood supply.
DIM / I3C(3) (A (D)) Inhibits growth signals / Secondary Attenuates inflammation.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Attenuates edema.(3) (A (D)) Inhibits cycle / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits Wnt / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(2) (A (D)) Attenuates NF-kB / Secondary Inhibits growth.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (D (A)) Attenuates inflammation / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(3) (A (D)) Inhibits growth / Secondary Support.(3) (A (D)) Inhibits growth / Secondary Support.DIM / I3C(3) (A (D)) May inhibit growth signals / Secondary Attenuates inflammation.
EGCG (Green Tea)(2) (A (C)) Inhibits glutaminase / Secondary Inhibits IDH growth.(2) (A (C)) Inhibits vessel growth / Secondary Inhibits glutamine.EGCG (Green Tea)(1) (A (C)) Main strategy. Metabolic blocking / Secondary Inhibits angiogenesis.(2) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(2) (A (C)) Inhibits PI3K / Secondary Inhibits glutamine.(2) (A (D)) Inhibits glutaminase / Secondary Inhibits Wnt.EGCG (Green Tea)(2) (A (C)) Inhibits growth / Secondary Inhibits angiogenesis.(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.(3) (A (C)) Inhibits growth / Secondary Inhibits Notch.EGCG (Green Tea)(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(2) (A (C)) Inhibits glutamine (MYC requirement) / Secondary Inhibits growth.(3) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(2) (A (C)) Inhibits EGFR / Secondary Inhibits glutamine.(2) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(2) (A (C)) Inhibits growth / Secondary Inhibits glutamine.(2) (A (C)) Inhibits growth / Secondary Inhibits glutamine.EGCG (Green Tea)(2) (A (C)) High Relevance. Inhibits growth and sugar uptake / Secondary Inhibits blood vessels.
High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Inhibits glycolysis.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(2) (E (C)) High Relevance. Pro-oxidant in IDH mutant / Secondary Stress.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Support.(2) (E (C)) High Relevance. Pro-oxidant effect / Secondary Stress.High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(2) (E (C)) High Relevance. Inhibits metabolic stress / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(3) (E (C)) Pro-oxidant effect / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(2) (E (C)) High Relevance. Pro-oxidant in rapid growth / Secondary Support.(3) (E (C)) Pro-oxidant effect / Secondary Support.High-dose Vit C (IV)(1) (E (C)) Main strategy. Creates targeted stress / Secondary Targets energy.
Ginger(3) (D (E)) Anti-inflammatory / Secondary Antiemetic.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(2) (D (E)) High Relevance. Attenuates edema / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(2) (D (E)) Attenuates NF-kB / Secondary Antiemetic.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(2) (D (E)) High Relevance. Attenuates inflammation / Secondary Pain.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Support.(3) (D (E)) Attenuates inflammation / Secondary Support.Ginger(3) (D (E)) Attenuates inflammation / Secondary Attenuates growth.
IP6 & Inositol(3) (A (C)) Inhibits glycolysis / Secondary Normalizes cells.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(2) (A (C)) High Relevance. Inhibits angiogenesis / Secondary Inhibits growth.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits PI3K / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits growth / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits growth / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (D)) Attenuates inflammation / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits growth / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits growth / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits growth / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) Inhibits growth / Secondary Support.(3) (A (C)) Inhibits growth / Secondary Support.IP6 & Inositol(3) (A (C)) May inhibit growth / Secondary Affects sugar metabolism.
Dandelion root(3) (E (B)) Induces apoptosis / Secondary Induces autophagy.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Inhibits resistance.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) Induces apoptosis / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(2) (E (B)) High Relevance. Targets resistant cells / Secondary Support.(3) (E (B)) Induces apoptosis / Secondary Support.Dandelion root(3) (E (B)) May promote cell death / Secondary Stresses the cell.
Maitake(4) (D (A)) Immune modulation / Secondary Attenuates growth.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) Immune support / Secondary Support.(4) (D (A)) Immune support / Secondary Support.Maitake(4) (D (A)) General immune support / Secondary May promote cell death.
Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Attenuates STAT3.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Attenuates edema.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Attenuates inflammation.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Support.(3) (D (A)) Liver protection / Secondary Support.Milk Thistle (Silymarin)(3) (D (A)) Liver protection / Secondary Attenuation of inflammation.
Melatonin(2) (A (D)) High Relevance. Inhibits growth / Secondary Sleep and immune support.(3) (A (C)) Inhibits angiogenesis / Secondary Improves sleep.Melatonin(3) (A (D)) Inhibits growth factors / Secondary Improves sleep.(3) (A (E)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (C)) Inhibits growth / Secondary Improves sleep.(3) (A (D)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (C)) Inhibits angiogenesis / Secondary Improves sleep.(3) (A (D)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (D)) Inhibits growth / Secondary Improves sleep.(3) (A (D)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (D)) Attenuates NF-kB / Secondary Improves sleep.(3) (A (D)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (E)) Inhibits growth / Secondary Improves sleep.(3) (A (E)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (C)) Inhibits growth / Secondary Improves sleep.(2) (D (A)) High Relevance. Attenuates inflammation / Secondary Improves sleep.Melatonin(3) (A (C)) Inhibits growth / Secondary Improves sleep.(3) (A (C)) Inhibits growth / Secondary Improves sleep.Melatonin(3) (A (E)) Inhibits growth / Secondary Improves sleep.(3) (A (D)) Inhibits growth / Secondary Improves sleep.Melatonin(2) (A (D)) High Relevance. Growth inhibition / Secondary Immune support.
Modified Citrus Pectin (MCP)(2) (A (D)) Inhibits Galectin-3 / Secondary Inhibits spread.(2) (A (D)) Inhibits invasion / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Attenuates fibrosis.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Attenuates inflammation.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(3) (A (D)) Inhibits spread / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(2) (A (D)) High Relevance. Inhibits metastasis / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(2) (A (D)) High Relevance. Inhibits metastasis / Secondary Support.(3) (A (D)) Inhibits spread / Secondary Support.Modified Citrus Pectin (MCP)(2) (A (D)) High Relevance. Blocks proliferation / Secondary Attenuates inflammation.
N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E) Increases glutathione / Secondary Cell protection.(4) (E) Increases glutathione / Secondary Cell protection.N-acetyl-cysteine (NAC)(4) (E (D)) General antioxidant support / Secondary Supports immune system.
Omega-3 (Fish oil)(3) (D (C)) Attenuates inflammation / Secondary Supports cell membranes.(3) (D (C)) Inhibits angiogenesis / Secondary Attenuates inflammation.Omega-3 (Fish oil)(2) (D (C)) High Relevance. Attenuates edema / Secondary Counteracts cachexia.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(3) (D (C)) Attenuates inflammation / Secondary General support.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(3) (D (C)) Inhibits angiogenesis / Secondary Attenuates inflammation.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(3) (D (C)) Attenuates inflammation / Secondary General support.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(2) (D (A)) High Relevance. Attenuates NF-kB / Secondary Attenuates inflammation.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(3) (D (E)) Attenuates inflammation / Secondary General support.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(3) (D (C)) Attenuates inflammation / Secondary General support.(1) (D (A)) Main strategy. Anti-inflammatory / Secondary Attenuates pain.Omega-3 (Fish oil)(3) (D (C)) Attenuates inflammation / Secondary General support.(3) (D (C)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(3) (D (E)) Attenuates inflammation / Secondary General support.(3) (D (A)) Attenuates inflammation / Secondary General support.Omega-3 (Fish oil)(1) (D (C)) Main strategy. Attenuates inflammation / Secondary Counteracts weight loss.
Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Inhibits angiogenesis.(3) (E (C)) Inhibits growth / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Inhibits vessels.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) Induces apoptosis / Secondary Support.(3) (E (C)) Induces apoptosis / Secondary Support.Pau D’Arco(3) (E (C)) May promote cell death / Secondary Inhibits blood vessels.
Probiotics(4) (D (E)) Immune modulation / Secondary Gut-brain axis.(4) (D (E)) Immune support / Secondary Support.Probiotics(2) (D (E)) High Relevance. Gut microbiota support / Secondary Attenuates inflammation.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(4) (D (E)) Immune support / Secondary Support.(4) (D (E)) Immune support / Secondary Support.Probiotics(2) (D (E)) High Relevance. Optimizes immune system / Secondary Attenuates inflammation.
Quercetin(2) (A (C)) High Relevance. Inhibits IDH metabolism / Secondary Inhibits glutamine.(2) (A (E)) Inhibits Hsp27 (stress) / Secondary Inhibits angiogenesis.Quercetin(2) (A (C)) Inhibits invasion / Secondary Attenuates edema.(1) (A (E)) Main strategy. Inhibits CDK/Cyclin / Secondary Inhibits growth.Quercetin(2) (A (C)) Inhibits PI3K / Secondary Inhibits growth.(1) (A (D)) Main strategy. Inhibits Wnt/β-catenin / Secondary Inhibits growth.Quercetin(2) (A (C)) Inhibits angiogenesis / Secondary Inhibits Wnt.(3) (A (E)) Inhibits growth / Secondary Creates stress.Quercetin(3) (A (E)) Inhibits growth / Secondary Creates stress.(3) (A (E)) Inhibits growth / Secondary Creates stress.Quercetin(2) (D (A)) Attenuates inflammation / Secondary Inhibits growth.(3) (A (E)) Inhibits growth / Secondary Creates stress.Quercetin(3) (A (E)) Inhibits growth / Secondary Creates stress.(3) (A (E)) Inhibits growth / Secondary Creates stress.Quercetin(3) (A (C)) Inhibits growth / Secondary Creates stress.(3) (D (A)) Attenuates inflammation / Secondary Inhibits growth.Quercetin(2) (A (E)) Inhibits Brachyury (weakly) / Secondary Inhibits growth.(2) (A (C)) Inhibits matrix / Secondary Inhibits growth.Quercetin(2) (A (E)) Inhibits growth / Secondary Creates stress.(2) (A (D)) Inhibits growth / Secondary Creates stress.Quercetin(2) (A (C)) High Relevance. Inhibits growth and sugar uptake / Secondary Inhibits blood vessels.
Resveratrol(3) (E (C)) Induces apoptosis / Secondary Inhibits metabolism.(2) (A (E)) Inhibits invasion / Secondary Induces apoptosis.Resveratrol(3) (E (A)) Induces apoptosis / Secondary Inhibits growth.(2) (E (A)) Induces apoptosis / Secondary Affects cell cycle.Resveratrol(2) (A (E)) Inhibits Akt / Secondary Induces apoptosis.(2) (A (E)) High Relevance. Inhibits Wnt / Secondary Induces apoptosis.Resveratrol(2) (A (C)) Inhibits Wnt / Secondary Inhibits angiogenesis.(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.Resveratrol(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.(1) (A (D)) Main strategy. Inhibits Notch / Secondary Inhibits growth.Resveratrol(2) (D (E)) Attenuates NF-kB / Secondary Induces apoptosis.(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.Resveratrol(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.Resveratrol(3) (A (E)) Inhibits growth / Secondary Induces apoptosis.(3) (D (E)) Attenuates inflammation / Secondary Induces apoptosis.Resveratrol(1) (A (E)) Main strategy. Inhibits Brachyury / Secondary Inhibits growth.(2) (A (C)) Inhibits growth / Secondary Inhibits Brachyury.Resveratrol(1) (A (E)) Main strategy. Inhibits Brachyury / Secondary Induces apoptosis.(2) (E (A)) Inhibits growth / Secondary Inhibits Brachyury.Resveratrol(2) (A (C)) High Relevance. Inhibits growth / Secondary Attenuates inflammation.
Selenium(4) (E (D)) Important antioxidant / Secondary Attenuates inflammation.(4) (E) Important antioxidant / Secondary Support.Selenium(3) (E (D)) Attenuates inflammation / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E) Important antioxidant / Secondary Support.(4) (E) Important antioxidant / Secondary Support.Selenium(4) (E (D)) General antioxidant support / Secondary Supports immune system.
Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Inhibits growth.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) Cell-killing effect / Secondary Support.(3) (E (A)) Cell-killing effect / Secondary Support.Black Walnut (Juglone)(3) (E (A)) May promote cell death / Secondary Inhibits growth.
Sulforaphane(2) (E (D)) Targets stem cells / Secondary HDAC inhibition.(2) (E (A)) Inhibits growth / Secondary Targets stem cells.Sulforaphane(2) (E (D)) Inhibits resistance / Secondary Targets stem cells.(2) (E (A)) Inhibits growth / Secondary Affects cell cycle.Sulforaphane(2) (E (A)) Inhibits growth / Secondary Targets stem cells.(2) (A (E)) Inhibits Wnt / Secondary Targets stem cells.Sulforaphane(2) (A (C)) Inhibits growth / Secondary Inhibits Wnt.(3) (E (A)) Targets stem cells / Secondary Inhibits growth.Sulforaphane(3) (E (A)) Targets stem cells / Secondary Inhibits growth.(3) (E (D)) Targets stem cells / Secondary Inhibits growth.Sulforaphane(2) (D (E)) Attenuates NF-kB / Secondary Targets stem cells.(3) (E (A)) Targets stem cells / Secondary Inhibits growth.Sulforaphane(1) (E (D)) Main strategy. HDAC inhibition (Epigenetics) / Secondary Targets stem cells.(3) (E (D)) Targets stem cells / Secondary Inhibits growth.Sulforaphane(2) (E (A)) Targets stem cells / Secondary Inhibits growth.(3) (D (E)) Attenuates inflammation / Secondary Targets stem cells.Sulforaphane(3) (E (A)) Inhibits growth / Secondary Targets stem cells.(3) (E (C)) Inhibits growth / Secondary Targets stem cells.Sulforaphane(2) (E (D)) High Relevance. HDAC inhibition / Secondary Targets stem cells.(1) (E (D)) Main strategy. HDAC inhibition / Secondary Immune support.Sulforaphane(2) (A (D)) High Relevance. Targets stem cells / Secondary Attenuates inflammation.
Turkey Tail(2) (D (A)) High Relevance. Strengthens immune response / Secondary Inhibits growth.(3) (D) General immune support / Secondary Support.Turkey Tail(2) (D (A)) High Relevance. Strengthens immune response / Secondary Inhibits growth.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(3) (D) General immune support / Secondary Support.(3) (D) General immune support / Secondary Support.Turkey Tail(2) (D (A)) High Relevance. Potent immune support / Secondary Can inhibit growth.
Vitamin C (Oral)(4) (E (D)) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E) General antioxidant / Secondary Immune support.(4) (E) General antioxidant / Secondary Immune support.Vitamin C (Oral)(4) (E (D)) General antioxidant support / Secondary Supports immune system.
Vitamin D(3) (D (A)) Immune support / Secondary Promotes differentiation.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (C)) Immune support / Secondary Inhibits growth.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (A)) Immune support / Secondary Inhibits growth.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (A)) Immune support / Secondary Inhibits growth.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (A)) Immune support / Secondary Inhibits growth.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (A)) Immune support / Secondary Inhibits growth.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (E)) Immune support / Secondary Inhibits growth.(3) (D (A)) Immune support / Secondary Inhibits growth.Vitamin D(3) (D (A)) Immune support / Secondary Inhibits growth.(2) (D (A)) High Relevance. Strengthens bones and spine / Secondary Immune support.Vitamin D(3) (D (C)) Immune support / Secondary Bone health.(3) (D (C)) Immune support / Secondary Bone health.Vitamin D(3) (D (E)) Immune support / Secondary Bone health.(3) (D (A)) Immune support / Secondary Immune support.Vitamin D(2) (D (A)) High Relevance. Promotes cell maturation / Secondary Important for the immune system.

About types of Brain cancer – other types

The strategy’s effectiveness depends on whether one attacks the genetic engine (e.g., IDH or RELA), the epigenetic profile (how the genes are turned on and off (methylation)) or the specific tissue type (chordoma).

Astrocytoma (genetic driver: IDH mutation)

1.1. Astro – Grade 2 (low):

  • Choose this, if your medical report says diffuse astrocytoma, IDH-mutant, WHO Grade 2. It is a low-grade astrocytoma that grows slowly. The strategy focuses on keeping the tumor at rest via metabolic blockade (IDH).

1.2. Astro – Grade 3 (anapl.):

  • Choose this, if your medical report says anaplastic astrocytoma, IDH-mutant, WHO Grade 3. It is a more aggressive form with faster cell division. The strategy increases focus on slowing down cell division and beginning vessel formation.

1.3. Astro – Grade 4 (IDH-mut):

  • Choose this, if your medical report says astrocytoma, IDH-mutant, WHO Grade 4 (formerly called secondary glioblastoma). Even though it is grade 4, it is driven by the IDH mutation, which requires a different approach than standard glioblastoma.

1.4. Astro – CDKN2A loss:

  • Choose this, if your medical report specifically mentions CDKN2A homozygous deletion or loss of p16/p14. This is an aggressive marker that trumps the grade itself. The strategy requires specific and intense blockade of the cell cycle (CDK4/6) to slow down division.

1.5. Astro – PIK3CA-mut:

  • Choose this, if the tumor has returned, or if a genetic test shows a mutation in the PIK3CA gene. The strategy is directed at blocking the growth engine (mTOR/Akt), which is overactive here.

Oligodendroglioma (genetic driver: 1p/19q codeletion)

2.1. Oligo – Grade 2:

  • Choose this for standard oligodendroglioma, IDH-mutant and 1p/19q codeleted, WHO Grade 2. The strategy focuses on blocking Wnt signaling and the cell’s energy supply.

2.2. Oligo – Grade 3:

  • Choose this for anaplastic oligodendroglioma, WHO Grade 3. A more aggressive form that requires focus on both metabolism and inhibition of blood vessels (angiogenesis).

2.3. Oligo – CIC mutated:

  • Choose this, if your tissue sample (histological examination / microscopy) shows a mutation in the CIC gene (capicua), which is very frequent (approx. 60-70%). The strategy is to block the MAPK signaling pathway, which becomes overactive when CIC is defective.

2.4. Oligo – FUBP1 mutated:

  • Choose this, if your tissue sample (histological examination / microscopy) shows a mutation in FUBP1. This genetic error prevents the cell from dying naturally and regulates the oncogene MYC.

2.5. Oligo – Notch driven:

  • Choose this in case of resistance or specific notch activation. The strategy focuses on blocking the Notch signaling pathway (e.g., with curcumin or gamma-secretase inhibitors).

Ependymoma (location-based and fusion-driven types)

3.1. Ependym – ST-ZFTA (RELA):

  • Choose this, if the tumor is located in the cerebrum (supratentorial) and is ZFTA fusion positive. This type is extremely dependent on inflammation. The strategy is an effort to block the NF-kB signaling pathway.

3.2. Ependym – ST-YAP1:

  • Choose this, if the tumor is located in the cerebrum and is YAP1 fusion positive. A rarer type, most often in young children, driven by the hippo signaling pathway.

3.3. Ependym – PFA (Grp A):

  • Choose this, if the tumor is located in the cerebellum/back of the head (posterior fossa) and is classified as Group A (most often young children). The strategy is directed at epigenetic errors (EZH2) and hypoxia (oxygen deprivation).

3.4. Ependym – PFB (Grp B):

  • Choose this, if the tumor is located in the cerebellum/back of the head (posterior fossa) and is classified as Group B (most often older children/adults). The strategy focuses on genomic stability.

3.5. Ependym – SP-MYCN (spinal):

  • Choose this, if the tumor is located in the spinal cord and is MYCN amplified. The strategy focuses on metabolic starvation of the aggressive MYC oncogene (cancer gene).

3.6. Ependym – SP-MPE (myxopapillary):

  • Choose this for myxopapillary ependymoma, which is typically located in the lower back. The strategy focuses on dampening inflammation (COX-2) and pain.

Chordoma (tissue-specific bone tumor)

4.1. Chordoma – classic (common / “conventional”):

  • Choose this for the most widespread type (in pathology reports often called conventional or classic). The strategy is unique to this form of cancer and focuses on blocking the transcription factor (the gene switch) brachyury (TBXT) as well as the growth factor EGFR.

4.2. Chordoma – chondroid:

  • Choose this, if the tumor contains cartilage-like tissue (chondroid chordoma). The strategy focuses on controlling matrix formation (MMP).

4.3. Chordoma – dediff.:

  • Choose this for dedifferentiated chordoma, which is more aggressive and has lost its original features (often INI1 loss). The strategy requires a more aggressive, broad-spectrum blockade of both growth and epigenetics.

4.4. Chordoma – poorly diff.:

  • Choose this for poorly differentiated chordoma (often children/adolescents, loss of SMARCB1/INI1). The strategy focuses on the immune system and epigenetic (gene regulation) blockade.

Universal fallback

5.1. General strategy / unspecified:

  • If your type is rare, unknown, or not specifically listed, you should focus on the last column to the right, which is named ‘General strategy / unspecified type’. Choose the main strategy (1), as well as 5-7 remedies that cover the 5 attack groups (A-E), based on this column. This general strategy attacks the vulnerabilities that are common to almost all aggressive cancer.

Se also Brain metastases and the blood-brain barrier

Who can help

Here you can get help with repurposed drugs (the prescription part – self-payment) Holistic doctors DK.

Note

You can use the above chart to get an impression of which repurposed drugs and supplements could theoretically have a metabolically beneficial effect on your cancer type.

According to the Warburg effect, such an approach could help starve the cancer.

If this approach feels right for you, discuss it with your practitioner.

See also Cancer as a Metabolic Disease

See also About the Mitochondria – what are they

See also It must feel right

See also Evidence vs Experience

See also Holistic Doctors DK

See also Blood cancer

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Page created: June 12, 2025

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What you read on “Jeg har Kræft” (I have Cancer) is not a recommendation. Seek competent guidance.

Metabolic strategy
Overview 1 – Drugs

Content:

Overview of metabolic strategy – Drugs

Metaboliske strategier - Lægemidler, symboliseret ved 6-7 forskellige piller - gule og hvide mod lys blå baggrund.

Overview 1: Repurposed Drugs

SubstanceTypePrimary Mechanism(s)Potential SynergiesEvidence Level (indicative)Important Remarks
Benzimidazoles (scroll to)AntiparasiticsInhibits microtubules (cell division). Disrupts glucose uptake.Certain chemotherapies (e.g., taxanes), DCA.Primarily preclinical. Many case reports.May require high doses. Potential liver toxicity.
Celecoxib (scroll to)NSAID (Selective COX-2 inhibitor)Inhibits COX-2 and PGE2. Blocks AKT/ERK signaling pathways.Chemotherapy (e.g., cisplatin), immunotherapy.Preclinical, observational studies.Note cardiovascular risk. Gentle on the stomach.
Desloratadine (scroll to)AntihistamineH1 receptor antagonist. Anti-inflammatory. Induces lysosomal cell death.Certain chemotherapies (e.g., cisplatin), immunotherapy.Preclinical, observational studies.High safety profile. Non-drowsy. Part of the CAD group.
Disulfiram (Antabuse) (scroll to)AntabuseInhibits the ALDH enzyme, important for cancer stem cells. Requires copper.Copper, certain chemotherapies.Preclinical. Few early clinical studies.Must never be combined with alcohol.
Dipyridamole (scroll to)Blood thinnerInhibits adenosine uptake, which otherwise protects cancer cells from the immune system.Certain chemotherapies (e.g., Methotrexate).Few older studies.Must be monitored if taking other blood-thinning medication.
Doxycycline (scroll to)AntibioticInhibits mitochondrial protein synthesis (targets cancer stem cells).High-dose Vit. C, Metformin.Primarily preclinical. Conceptually strong.Can cause photosensitivity and affect intestinal flora.
Aspirin (Hjertemagnyl) (scroll to)NSAIDAnti-inflammatory (COX inhibition). Affects platelets.Immunotherapy, certain targeted treatments.Strong evidence (especially for colorectal cancer).Risk of stomach ulcers and bleeding.
Hydroxychloroquine (scroll to)AntimalarialInhibits autophagy – the ability to use a survival mechanism by recycling cell parts.Many chemo & targeted therapies (by blocking resistance).Many clinical trials, often with mixed results.Can have eye and heart side effects with long-term use.
Ivermectin (scroll to)AntiparasiticSeveral proposed mechanisms, including inhibition of WNT signaling.Certain chemotherapies (e.g., taxanes).Primarily preclinical.Controversial. Requires caution with dosage.
Low-dose Naltrexone (LDN) (scroll to)Opiate antagonistUp-regulates the body’s own endorphins and enkephalins (immuno-modulating).Immunotherapy, certain chemotherapies (low-dose).Primarily case reports and smaller studies.Very few side effects. Must not be taken with opioids.
Metformin (scroll to)Diabetes medicationInhibits complex I in mitochondria, activates AMPK, lowers blood sugar/insulin.Glycolysis inhibitors, mTOR inhibitors, Statins, diet (keto).Very strong evidence (preclinical and epidemiological).Very safe. Mild stomach discomfort at the start.
Propranolol (scroll to)Beta-blockerBlocks beta-adrenergic receptors (stress signals), inhibits angiogenesis.Certain chemotherapies (e.g., taxanes), anti-angiogenic agents.Several case reports and smaller clinical trials.Can cause low blood pressure and pulse.
Statins (scroll to)Cholesterol-loweringInhibits the Mevalonate pathway, important for many growth processes.Metformin, PI3K/Akt inhibitors.Strong preclinical and epidemiological evidence.Can cause muscle pain.

Overview 1: Here you will find a table for Repurposed Drugs. This can be used to look up a specific substance and quickly get an overall impression of its mechanism of action, evidence level, and any remarks.

To be continued..

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Page created: June 10, 2025

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What you read on I have Cancer (Jeg har Kræft) is not a recommendation. Seek competent guidance.

Metabolic strategy
Supplements Overview 2

Indhold:

Overview of metabolic strategy – Supplements

Metabolisk strategi, Kosttilskud, symboliseret ved nærbillede af ingefærrod der ligger på bord. over en overskåret ingefær. Foran en porcelænsske med gurkemejefarvet pulver.

Overview 2: Supplements

SubstanceTypePrimary Mechanism(s)Potential SynergiesEvidence Level (indicative)Important Remarks
AHCC (rul til)Mushroom extractImmuno-modulating (increases NK cell activity).Chemotherapy (immune support), other immuno-modulators.Several human studies.Very safe.
Alfa-lipon acid (ALA) (rul til)AntioxidantPotent antioxidant. Improves insulin sensitivity. Affects glycolysis.Metformin, other antioxidants.Clinical studies for neuropathy. Increasing preclinical cancer research.Can affect blood sugar levels.
Apigenin (rul til)FlavonoidAnti-inflammatory, inhibits the PI3K/Akt signaling pathway, induces apoptosis.Certain chemotherapies (e.g., Paclitaxel).Strong preclinical evidence.Found in parsley and chamomile, among others.
Artemisia (rul til)Herbal extractReacts with iron in cancer cells and creates oxidative stress (ferroptosis).Iron, IV Vitamin C.Strong preclinical evidence. Smaller human studies.Must be taken away from antioxidants. Breaks in intake are necessary.
Astragalus (rul til)Herbal extractImmuno-modulating. Used in TCM alongside chemo.Platinum-based chemotherapy (improves effect, reduces side effects).Several human studies (especially from China).Very safe.
Berberine (rul til)Herbal extractActivates AMPK (like Metformin), anti-inflammatory.Metformin.Strong preclinical evidence.Can affect intestinal flora and cause stomach discomfort.
Boswellia (rul til)Herbal extractAnti-inflammatory (inhibits 5-LOX).Curcumin (synergistic anti-inflammatory effect).Several human studies (especially for brain edema).Very safe.
Cat’s Claw (rul til)Herbal extractStrongly anti-inflammatory (inhibits NF-kB), immuno-modulating.Other anti-inflammatory substances.Primarily preclinical.Can affect blood pressure and blood thinning.
Coenzym Q10 (rul til)Vitamin-likeCritical for mitochondrial energy production. Potent antioxidant.Statins (counteracts side effects).Good evidence for cardiovascular health and statin side effects.Choose the ubiquinol form for better absorption.
Curcumine (rul til)Herbal extractStrongly anti-inflammatory (inhibits NF-kB), affects many signaling pathways.Piperine (for absorption), Boswellia.Very strong preclinical evidence. Many human studies.Poor bioavailability alone.
DIM / I3C (rul til)Plant substanceModulates estrogen metabolism into beneficial metabolites.Hormone therapy (e.g., Tamoxifen), Sulforaphane.Strong preclinical evidence for hormone-sensitive cancers.Found in cruciferous vegetables.
EGCG (Green tea) (rul til)PolyphenolAntioxidant in low doses, pro-oxidant in high. Inhibits many signaling pathways.Curcumin, Quercetin.Strong preclinical evidence.High doses as extract can affect the liver.
High-dose Vit. C (IV) (rul til)VitaminPro-oxidant in high doses (creates hydrogen peroxide).Doxycycline, certain chemotherapies.Strong preclinical evidence. Many case reports and smaller clinical trials. Lacks large phase III trials.Must be given intravenously for pro-oxidant effect. WARNING: Do not give to patients with G6PD deficiency. Caution with kidney problems.
Ginger (rul til)Root vegetableAnti-inflammatory, anti-nausea.Chemotherapy (against nausea), Curcumin.Good evidence for nausea.Very safe.
IP& & Inositol (rul til)Sugar alcoholImmuno-modulating (increases NK cell activity), chelates iron.Green tea (EGCG).Several preclinical studies.Very safe.
Dandelion (rul til)Herbal extractInduces apoptosis in certain cancer cells.No specific data.Limited, primarily preclinical.Very safe.
Maitake (rul til)Mushroom extractImmuno-modulating (D-Fraction).Chemotherapy (immune support), Vitamin C.Several human studies.Very safe.
Milk thistle (rul til)Herbal extractLiver protective (silymarin), anti-inflammatory.Certain chemotherapies to protect the liver.Good evidence for liver protection.Very safe.
Melatonin (rul til)HormoneOncostatic (inhibits growth), immuno-modulating, antioxidant, improves sleep.Almost all treatments (especially radiotherapy and chemo).Strong evidence from many studies.Very safe.
Modified Citrus Pectin (rul til)FiberInhibits Galectin-3 and thereby metastasis and inflammation.Probiotics, anti-inflammatory substances.Several human studies.Very safe.
N-acetyl-cysteine (NAC) (rul til)Amino acidIncreases the body’s own antioxidant (glutathione).Certain chemotherapies (protects healthy cells).Complex role. Can protect healthy cells.High doses can affect zinc and copper levels.
Omega-3 (Fiskeolie) (rul til)Fatty acidsStrongly anti-inflammatory (competes with omega-6). Can counteract cachexia.Other anti-inflammatory substances.Strong evidence for inflammation and cachexia.Quality (purity, TOTOX value) is crucial.
Pau D’Arco (rul til)Herbal extractDisrupts cancer cells’ energy metabolism and DNA repair (Lapachol).No specific data.Primarily preclinical.Can be toxic. Requires caution.
Probiotics (rul til)Bacterial culturesModulates intestinal flora and thereby the immune system. Can reduce side effects.Immunotherapy, prebiotics (fibers).Very strong and growing evidence, especially in connection with immunotherapy.Strain-specific effect. Choose a broad-spectrum product.
Quercetin (rul til)FlavonoidAnti-inflammatory, antioxidant, inhibits PI3K/Akt.Vitamin C (synergistic antioxidant effect), EGCG.Strong preclinical evidence.Poor bioavailability alone.
Resveratrol (rul til)PolyphenolSirtuin activator, anti-inflammatory.Quercetin, other polyphenols.Strong preclinical evidence.Bioavailability is a challenge.
Selenium (rul til)MineralImportant for antioxidant enzymes and immune function.Vitamin E.Strong evidence for the importance of sufficient levels.Excess is toxic. Must be dosed precisely.
Black Walnut (rul til)Herbal extractPro-oxidative and cytotoxic. Induces apoptosis via ROS formation.Theoretical with other pro-oxidative therapies.Primarily preclinical. Limited human data.WARNING: Potent substance. Use with extreme caution.
Sulforaphane (rul til)Plant substanceHDAC inhibitor, activates Nrf2, targets cancer stem cells.DIM/I3C, Green tea (EGCG).Strong preclinical evidence.Found in broccoli sprouts.
Turkey Tail (rul til)Mushroom extractImmuno-modulating (PSK/PSP).Chemotherapy, radiotherapy (improves immune response).Very strong evidence, especially from Japan.Very safe.
Vitamin C (oralt/ caps/ tabletter) (rul til)VitaminPotent antioxidant. Essential co-factor for immune function (T-cells/NK cells), epigenetic regulation (TET enzymes), and cellular response to hypoxia.Essential nutrient.No evidence for direct anti-cancer effect in oral form.Does not act as a pro-oxidant like IV C. Controversial in high doses during active chemo/radiation.
Vitamin D (rul til)Vitamin/HormoneRegulates cell division and immune function.Vitamin K2.Very strong epidemiological and clinical evidence.Requires blood test for correct dosing.

Overview 2: Here you will find a table for Supplements. This can be used to look up a specific substance and quickly get an overall impression of its mechanism of action, evidence level, and any remarks.

To be continued…

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What you read on I have Cancer (Jeg har Kræft) is not a recommendation. Seek competent guidance.

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Links

General

Danish research: Metabolic control should be a target in cancer treatment (Dagens Medicin, 2023) (Danish Language)

  • Content: Focus on metabolism: Cancer cells alter the body’s metabolism to acquire energy. Goal of the strategy: Research seeks to manipulate metabolic processes to limit cancer cell growth. Benefits for the reader: The strategy aims to stabilize metabolism and reduce the risk of complications.

Repurposed drugs

1. Benzimidazoles (Mebendazole/ Fenbendazole)

Adrenal cancer:

  • Link 10: Repurposing existing therapies for adrenal cancer (ESMO Open, 2023)
    • Content: A scientific abstract describing a method for identifying existing, approved drugs that can be repurposed against adrenal cancer. The study uses genetic analysis to pinpoint medications that can potentially target the disease’s specific vulnerabilities.

Bladder and ureteral cancer:

Brain cancer:

Multiple myeloma & kidney cancer:

Prostate cancer:

  • Link 15: Benzimidazole as Novel Therapy for Hormone-Refractory Prostate Cancer (dtic.mil, 2011)
    • Content: Report showing that Benzimidazole treatment prolongs survival in mice with prostate cancer metastases and inhibits the growth of prostate cancer cells. This supports the drug’s role as an anti-metastatic agent by inhibiting microtubules (the cell’s skeleton).
  • Link 16: Benzimidazole and its derivatives as cancer therapeutics (National Institutes of Health, 2022)
    • Content: Review article describing the bioactivity of Benzimidazoles as potent anticancer agents. The article validates that the compounds work by inhibiting microtubules (the cell’s skeleton) and inducing cell death, which is the core strategy against metastatic prostate cancer.

Back to: Overview table for Repurposed drugs

1.A Celecoxib

Binyrebarkkræft:

Bladder and ureteral cancer:

Multiple myeloma:

Kidney cancer:

Back to: Overview table for Repurposed drugs

2. Desloratadine

Back to: Overview table for Repurposed drugs

3. Dipyridamole

  • Link 1: Dipyridamole prevents triple-negative breast-cancer progression (Clinical & Experimental Metastasis, 2013)
    • Relevance: A strong preclinical study showing how dipyridamole inhibits both the growth of the primary tumor and the formation of metastases in a model of triple-negative breast cancer, partly by influencing the immune environment in the tumor.
  • Link 2: Reverse screening approach to identify potential anti-cancer targets of dipyridamole (PubMed, 2016)
    • Relevance: Researchers used computer models to uncover why the drug Dipyridamole (DIP) enhances the effect of chemotherapy like 5-fluorouracil (5-FU). The study predicts that Dipyridamole works by blocking the enzyme (DPD) that normally breaks down chemotherapy. This could explain why chemotherapy becomes more effective and has fewer side effects.

Skin cancer:

Back to: Overview table for Repurposed drugs

4. Disulfiram (Antabus)

Adrenal cancer:

Bladder and urinary tract cancer:

Pancreatic cancer:

  • Link 10: Disulfiram: A novel repurposed drug for cancer therapy (MedNexus, 2024)
    • Content: A recent 2024 review article summarizing the mechanisms by which Disulfiram (in combination with copper) combats cancer. The article focuses particularly on the drug’s ability to create oxidative stress (ROS) inside cancer cells, thereby inhibiting their growth.

Brain cancer:

  • Link 10A: Disulfiram: A novel repurposed drug for cancer therapy (PMC, 2024)
    • Content: A scientific review describing disulfiram’s mechanisms against cancer, including the ability to target cancer stem cells, inhibit NF-κB, and reverse resistance to chemotherapy. The article highlights the drug’s potential as a repurposed drug.
  • Link 11: Disulfiram in glioma: Literature review of drug repurposing (Frontiers in Pharmacology, 2022)
    • Content: A scientific review describing disulfiram’s potential against gliomas. The article focuses on the drug’s ability to overcome resistance and target cancer stem cells, making it a promising candidate for repurposing.

Bone cancer:

Multiple myeloma:

Kidney cancer:

Back to: Overview table for Repurposed drugs

5. Doxycycline

Adrenal cancer:

Blood cancer:

  • Link 14: Targeting mitochondrial metabolism in acute myeloid leukemia (PubMed, 2022)
    • Content: A study analyzing the importance of cancer cell energy factories (mitochondria) for the survival of leukemia stem cells. The research supports the strategy of using agents like Doxycycline to inhibit mitochondrial protein synthesis and thereby remove the energy supply for the most aggressive cells.

Brain cancer:

  • Link 15: Anti-Tumor Effect of Doxycycline on Glioblastoma Cells (ResearchGate, 2007)
    • Content: A recent study investigating doxycycline’s effect on glioblastoma cells. The results confirm that the drug acts as an inhibitor of matrix metalloproteinases (MMPs), which is crucial for preventing cancer cells from invading surrounding brain tissue.
  • Link 16: Matrix Metalloproteinases in Glioma: Drivers of Invasion (MDPI, 2025)
    • Content: A recent review article identifying matrix metalloproteinases (MMP) as central drivers for invasion in glioma. The text discusses doxycycline’s role as an MMP inhibitor in the attempt to slow this spread.

Bone cancer:

  • Link 17: Doxycycline inhibits the progression of metastases in early-stage osteosarcoma (Europe PMC, 2022)
    • Content: A study documenting Doxycycline’s ability to inhibit the spread of osteosarcoma. The article describes how the drug downregulates the enzymes (MMP) and growth factors (VEGF) that cancer cells use to invade tissue and form blood vessels, confirming its potential to slow disease progression.

Multiple myeloma:

Kidney cancer:

Back to: Overview table for Repurposed drugs

6. Aspirin – Low dose Aspirin

Pancreatic cancer:

Gallbladder and biliary tract cancer:

  • Link 11: Aspirin and Statin Use and the Risk of Gallbladder Cancer (ResearchGate, 2025)
    • Content: A recent study evaluating the association between statin use and the risk of gallbladder cancer. Results show that statins (especially in combination with aspirin) are associated with a greatly reduced risk of developing the disease, supporting their potential to inhibit cancer development in the biliary tract.

Gastric cancer:

  • Link 12: Aspirin use associated with a decreased risk of gastric cancer (PubMed/Cancer Epidemiology, 2025)
    • Content: A recent 2025 study supporting aspirin’s role in the prevention and treatment of gastric cancer. Results show a significant decreased risk of the disease, supporting the theory of aspirin’s anti-inflammatory and anticancer effects in the stomach.

Multiple myeloma:

  • Link 13: Regular Aspirin Use and Mortality in Multiple Myeloma (National Institutes of Health, 2021)
    • Content: A scientific article investigating the effect of aspirin in multiple myeloma patients. The study highlights that blood-thinning treatment is crucial for patients receiving immunomodulatory drugs (e.g., lenalidomide), as these increase the risk of blood clots. Simultaneously, data points to an association between aspirin use and reduced mortality.

Colorectal cancer:

  • Link 14: Low-Dose Aspirin for PI3K-Altered Localized Colorectal Cancer (New England Journal of Medicine, 2025)
    • Content: A clinical study investigating the effect of low-dose aspirin in colorectal cancer patients. Results indicate that aspirin reduces the risk of recurrence, especially in patients with genetic alterations in the PI3K signaling pathway, supporting targeted use of the drug.

Back to: Overview table for Repurposed drugs

7. Hydroxychloroquine

Bladder and urinary tract cancer:

Prostate cancer:

Gallbladder and biliary tract cancer:

Glioblastoma:

Adrenal cancer:

  • Link 17: Modulation of Autophagy in Adrenal Tumors (National Institutes of Health, 2022)
    • Content: A scientific investigation documenting how the standard treatment Mitotane activates autophagy in adrenal tumors. The article describes this “self-eating” process as a survival mechanism for cancer cells and that blocking autophagy can therefore be a strategy to increase treatment effectiveness.

Pancreatic cancer:

  • Link 18: Autophagy: a novel target in order to overcome drug resistance in cancer (National Institutes of Health, 2025)
    • Content: A recent scientific review confirming the strategy of using autophagy inhibitors (like Hydroxychloroquine) to break down cancer cell defenses. The article concludes that this blockade is crucial for overcoming the resistance cancer cells often develop against chemotherapy, thereby making standard treatment effective again.

Brain cancer:

Multiple myeloma:

Kidney cancer:

  • Link 21: Therapeutic Targeting of Autophagy for Renal Cell Carcinoma (MDPI, 2020)
    • Content: A scientific article investigating autophagy as a therapeutic target in kidney cancer. The article explains how inhibiting autophagy blocks a central recycling process cancer cells exploit to survive stress, making them more susceptible to treatment.

Salivary gland and nasal cancer

  • Link 22: Autophagy and salivary gland cancer: A putative target for therapeutic intervention (National Institutes of Health, 2020)
    • Content: A scientific review focusing on autophagy (the cell’s recycling system) in salivary gland cancer. The article supports the strategy of manipulating this process (e.g., with hydroxychloroquine) to make cancer cells vulnerable to treatment, as they often rely on autophagy to survive.

Ovarian cancer:

  • Link 23: Targeting autophagy to overcome drug resistance in ovarian cancer (Journal of Hematology & Oncology, 2020)
    • Content: A scientific review focusing on autophagy (the cell’s recycling system) as a key factor in resistance in ovarian cancer. The article supports the strategy of using chloroquine/hydroxychloroquine to block this survival mechanism and thereby make cancer cells vulnerable to treatment again.

Eye cancer:

  • Link 24: The Role of Autophagy in Human Uveal Melanoma and Targeted Therapy (National Institutes of Health, 2024)
    • Content: A scientific review investigating the role of autophagy in ocular melanoma. The article describes how cancer cells use this process to survive stress and how targeted inhibition can be an effective strategy for slowing the disease.

Back to: Overview table for Repurposed drugs

8. Ivermectin

Adrenal cancer:

  • Link 5: Blocking the WNT/\beta-catenin pathway in cancer treatment and drug resistance (ScienceDirect, 2024)
    • Content: A scientific article reviewing strategies for blocking the Wnt signaling pathway in cancer treatment. The study highlights that Ivermectin effectively inhibits this signaling pathway, reducing cancer cells’ ability to spread and counteracting the mechanisms driving tumor growth.

Bladder and ureteral cancer:

Skin cancer:

  • Link 7: Ivermectin as an Alternative Anticancer Agent: A Review of Current Evidence (MDPI, 2025)
    • Content: A scientific review investigating Ivermectin’s potential as an alternative cancer treatment. The article highlights the drug’s ability to inhibit cancer growth and spread by affecting several central signaling pathways, including the Wnt pathway, supporting its use as a cytotoxic agent.

Uterine cancer:

Multiple myeloma:

Kidney cancer:

Back to: Overview table for Repurposed drugs

9. Low-dose Naltrexone (LDN)

Back to: Overview table for Repurposed drugs

0. Mebendazole – See Benzomidazole

0. Melatonin – See Supplements

10. Metformin

Prostate cancer:

Anal cancer:

  • Link 23: Metabolic Reprogramming in Cancer: Role of HPV 16 Variants (PMC, 2021)
    • Content: A scientific review article describing how HPV 16 proteins E6 and E7 (the primary cause of anal cancer) promote cancer cells’ metabolic reorganization (the Warburg effect) to meet their energy needs.

Adrenal cancer:

Blood cancer:

Bladder and urinary tract cancer:

Gallbladder and biliary tract cancer:

Glioblastoma:

  • Link 29: Metformin as Potential Therapy for High-Grade Glioma (NIH, 2020)
    • Content: Review article validating Metformin’s (1) Main Strategy against GBM. The article confirms that the drug inhibits the PI3K/Akt/mTOR growth pathway and can improve survival in patients with high-grade gliomas.

Pancreatic cancer:

  • Link 30: From basics to clinics: New opportunities for metformin in pancreatic cancer (ScienceDirect, 2025)
    • Content: A recent scientific article investigating the link between metabolic diseases and pancreatic cancer. The article reviews the latest knowledge from both basic research and clinical trials to identify new opportunities for using Metformin as treatment, focusing particularly on its ability to affect cancer metabolism.
  • Link 31: Metformin and pancreatic neuroendocrine tumors: A systematic review and meta-analysis (World Journal of Gastroenterology, 2024)
    • Content: Analysis investigating the effect of the diabetes medication Metformin on pancreatic neuroendocrine tumors (PNETs). The study concludes that metformin may have a protective effect and potentially improve survival by inhibiting growth signals like mTOR, making it a promising supplemental strategy.

Head and neck cancer:

Brain cancer:

Skin cancer:

  • Link 35: Metformin – A New Frontier in Skin Cancer Pharmacotherapy (ResearchGate, 2025)
    • Content: A scientific review analyzing Metformin’s potential as treatment against skin cancer. The article concludes the drug can have a broad effect by inhibiting central cancer signaling pathways (like PI3K/Akt/mTOR) and disrupting cancer cells’ energy supply (mitochondria), supporting its potential as an effective metabolic treatment.

Cervical cancer:

  • Link 36: Potential Mechanisms of Metformin-Induced Apoptosis in HeLa Cells (MDPI, 2023)
    • Content: A scientific article investigating metformin’s direct ability to combat cervical cancer cells (HeLa). The study concludes that metformin works by inhibiting cancer cell division and promoting programmed cell death (apoptosis), supporting the drug’s potential as a standalone treatment.

Gastric cancer:

  • Link 37: A New Inhibitor of the Wnt Signaling Pathway in Cancer (ResearchGate, 2023)
    • Content: A study documenting how metformin inhibits growth and spread in cancer cells. The article focuses on the drug’s ability to block the Wnt signaling pathway and regulate cell energy metabolism via AMPK activation, confirming its potential as a metabolic treatment.

Multiple myeloma:

Kidney cancer:

  • Link 40: Metformin Induces Different Responses in Clear Cell Renal Cell Carcinoma (ResearchGate, 2019)
    • Content: A scientific study investigating metformin’s effect on kidney cancer. Results show that metformin dampens the specific protein that functions as cancer cells’ “oxygen sensor.” When this protein is suppressed, cancer cells lose their primary survival mechanism and ability to grow.

Colorectal cancer:

  • Link 41: Metformin’s multifaceted role in colorectal cancer (Springer, 2025)
    • Content: A scientific article elucidating metformin’s multifaceted role in colorectal cancer. The article describes how the drug can suppress resistance in cancer stem cells to treatment, which is crucial for preventing relapse and spread (metastasis).

Uterine cancer:

  • Link 42: Metformin and endometrial cancer: an updated meta-analysis of case-control studies (Archives of Medical Science, 2024)
    • Content: A comprehensive analysis confirming metformin’s protective effect against uterine cancer. The study shows a clear association where metformin use is linked to a decreased risk of the disease, supporting the strategy of regulating blood sugar and insulin to inhibit cancer growth.

Salivary gland and nasal cancer:

Vulvar and vaginal cancer:

Ovarian cancer:

  • Link 46: Metformin and ovarian cancer: the evidence (Annals of Translational Medicine, 2020)
    • Content: A scientific review gathering evidence for metformin’s effect in ovarian cancer. The article concludes the drug has clear effects making cancer cells more sensitive to treatment and that it functions as an effective inhibitor of new blood vessel formation (angiogenesis).

Eye cancer:

  • Link 47: Effects of metformin on retinoblastoma growth in vitro and in vivo (National Institutes of Health, 2014)
    • Content: A study documenting metformin’s effect on retinoblastoma (childhood eye cancer). It shows the drug can slow cell division and inhibit cancer growth in both cell studies and animal models, supporting its potential as a metabolic treatment.
  • Link 48: Metformin and glioma: Targeting metabolic dysregulation for enhanced therapeutic outcomes (Science Direct, 2025)
    • Content: A scientific review investigating metformin’s potential as treatment for neural tumors. The article describes how the drug targets metabolic dysregulation and inhibits growth pathways, mechanisms transferable to other cancers of the nervous system such as retinoblastoma in the eye.

Back to: Overview table for Repurposed drugs

11. Propranolol

Adrenal cancer:

  • Link 7: Neurobiology of Cancer: The Role of \beta-Adrenergic Receptor Signaling in Cancer (MDPI, 2020)
    • Content: A scientific review article mapping how the body’s stress signals (beta-adrenergic signaling) directly promote new blood vessel formation (angiogenesis) and tumor growth. Since the adrenal gland is the center of the stress system, the study supports the relevance of blocking these signals with propranolol to slow disease progression.

Skin cancer:

  • Link 8: Does propranolol have a role in cancer treatment? (Springer, 2025)
    • Content: A scientific article reviewing evidence that the beta-blocker propranolol can improve the outcome of cancer treatment. The article highlights the drug appears to be able to decrease the risk of relapse, supporting the strategy of dampening stress signals and inhibiting mechanisms driving cancer growth.

Kidney cancer:

  • Link 9: Blockade of beta-adrenergic receptors reduces cancer growth and metastasis (Nature, 2022)
    • Content: A scientific article describing how beta-blockers (specifically propranolol) dampen the body’s stress signals. The study explains the treatment thereby reduces the tumor’s ability to form new blood vessels (angiogenesis) and alters the tumor microenvironment so the immune system can better fight cancer cells.

Prostate cancer:

Back to: Overview table for Repurposed drugs

12. Statins

Adrenal cancer:

Blood cancer:

  • Link 19: Impact of statin use on survival and adverse events in patients (BMC Cancer, 2025)
    • Content: A systematic review and meta-analysis investigating the effect of statins on survival in cancer patients. The study gathers the latest evidence and indicates statin use may have a positive effect on survival rates in various cancers, including blood cancer, supporting potential as supplemental treatment.

Prostate cancer:

  • Link 20: Prostate Cancer and the Mevalonate Pathway (PubMed, 2024)
    • Content: Review article describing how dysregulation of lipid metabolism (fat metabolism) is a survival strategy for prostate cancer. The article validates that Statins work by inhibiting the Mevalonate pathway, thereby disrupting cell growth and signaling.

Glioblastoma:

Pancreatic cancer:

Head and neck cancer:

Brain cancer:

  • Link 24: Investigation into the synergistic effect of atorvastatin (Spandidos Publications, 2025)
    • Content: An investigation describing how atorvastatin can act synergistically with other treatments against glioblastoma. Results indicate statins may contribute to improved survival by affecting tumor cell growth conditions.

Skin cancer:

Bone cancer:

  • Link 26: New insights into the therapeutic potentials of statins in cancer therapy (Frontiers, 2023)
    • Content: A scientific article from 2023 highlighting statins’ potential to prevent spread to the bones (skeletal metastases). The study shows how statin treatment can inhibit specific markers on cancer stem cells, making it harder for cancer to establish itself in bone tissue.

Gastric cancer:

Multiple myeloma:

Kidney cancer:

  • Link 29: Statin use and kidney cancer survival outcomes (Cancer Treatment Reviews, 2017)
    • Content: A scientific meta-analysis reviewing data from several studies. The conclusion is that statin use (cholesterol-lowering medication) is significantly associated with better survival in kidney cancer patients, regarding both cancer-specific and overall survival.

Colorectal cancer:

  • Link 30: Statins and colorectal cancer: A systematic review (PubMed, 2020)
    • Content: A systematic review showing statin use is associated with better survival in colorectal cancer. The article points out statins can inhibit spread (metastasis) and make cancer cells more sensitive to other treatments.

Uterine cancer:

  • Link 31: Association between statin use and the risk, prognosis of gynecologic cancers (European Journal of Obstetrics and Gynecology, 2022)
    • Content: A systematic review and meta-analysis investigating the association between statin use and the prognosis of gynecological cancers. Results show statin use is associated with lower mortality, supporting the strategy of inhibiting cancer growth by blocking the Mevalonate pathway.

Ovarian cancer:

  • Link 32: Association between statin use and the risk, prognosis of gynecologic cancers (European Journal of Obstetrics and Gynecology, 2022)
    • Content: A systematic review and meta-analysis investigating the association between statin use and the prognosis of gynecological cancers. Results show statin use is associated with lower mortality, supporting the strategy of inhibiting cancer growth by blocking the Mevalonate pathway.

Eye cancer:

Back to: Overview table for Repurposed drugs

Vermox – See Benzimidazoles

Supplements

1. AHCC (Active Hexose Correlated Compound)

Cervical cancer:

Vulvar and vaginal cancer:

  • Link 6: AHCC, a mushroom culture extract to boost immune defence (Nature, (2022))
    • Content: An article from the prestigious journal Nature describing AHCC’s potential as an immune-supporting supplement. The article focuses on how the extract can help the immune system fight Human Papillomavirus (HPV), the primary cause of cellular changes in the vulva and vagina.

Back to: Overview table for Repurposed drugs

2. Alfa-lipoic acid (ALA)

Back to: Overview table for Repurposed drugs

3. Apigenin

Back to: Overview table for Repurposed drugs

4. Artemisinin / Artesunat

Blood cancer:

  • Link 8: Dihydroartemisinin-induced ferroptosis in acute myeloid leukemia (Nature, 2023)
    • Content: A study published in Nature documenting how an artemisinin derivative (DHA) effectively kills acute myeloid leukemia (AML) cells. The study confirms the mechanism is ferroptosis (iron-dependent cell death) and that the treatment specifically targets cancer cells’ reliance on iron, supporting its potential as a targeted metabolic strategy.

Head and neck cancer:

  • Link 9: Advances in ferroptosis in head and neck cancer (Spandidos Publications, 2024)
    • Content: A scientific review describing how artemisinin and its derivatives can trigger ferroptosis (iron-dependent cell death) in head and neck cancer cells. The article explains how this mechanism can be used to overcome resistance to other treatments.

Cervical cancer:

  • Link 10: Artemisinin and Its Derivatives as Potential Anticancer Agents (MDPI, 2024)
    • Content: A comprehensive scientific review from 2024 mapping artemisinin’s potential against various cancers. The article describes in detail how the substance induces cell death via oxidative stress and ferroptosis, confirming its effectiveness against resistant cell lines, making it a relevant strategy.

Lung and liver cancer:

Lymphoma:

  • Link 12: Targeting BCL-2 in B-cell malignancies and overcoming resistance (Nature, 2020)
    • Content: An authoritative review article confirming that BCL-2 family inhibition is a rational therapeutic strategy for lymphomas and other B-cell malignancies. The article discusses how BCL-2 dependent conditions (e.g., Follicular Lymphoma) are treated by restoring the cell’s ability to die (apoptosis).

Prostate cancer:

Glioblastoma:

Salivary gland and nasal cancer:

  • Link 15: Natural products targeting ferroptosis pathways in cancer (Spandidos Publications, 2024)
    • Content: A scientific review from 2024 describing how natural substances like artemisinin can trigger ferroptosis (iron-dependent cell death). The article specifically highlights the effect on nasopharyngeal cancer cells, supporting the strategy of using this mechanism to kill cancer cells otherwise resistant.

Vulvar and vaginal cancer:

  • Link 16: Artemisinin Suppressed Melanoma Recurrence and Metastasis (International Journal of Biological Sciences, 2025)
    • Content: A scientific study documenting artemisinin’s ability to suppress recurrence and spread (metastasis) of melanoma. Results support the substance’s potential as a strategy against aggressive cancers where risk of spread is high.

Back to: Overview table for Repurposed drugs

5. Astragalus

Back to: Overview table for Repurposed drugs

6. Berberine

Adrenocortical cancer:

  • Link 12: Berberine inhibits androgen synthesis by interaction with aldo-keto reductase 1C3 (National Institutes of Health, 2015)
    • Content: A scientific study documenting that berberine inhibits the formation of hormones (androgens). The results show that the substance reduces hormone production in a dose-dependent manner, supporting the strategy of using berberine to suppress functional tumors that produce excess hormones.

Bladder cancer and ureteral cancer:

Pancreatic cancer:

Gallbladder and biliary tract cancer:

Brain cancer:

Uterine cancer:

  • Link 18: Berberine inhibits the development of endometrial cancer (PubMed, 2022)
    • Content: A scientific study documenting that berberine can inhibit the development of uterine cancer. The results show the substance works by blocking specific signaling pathways involved in inflammation (COX-2), confirming its potential to slow cancer growth.

Multiple myeloma/bone marrow cancer:

Kidney cancer:

  • Link 20: Coptidis rhizoma and berberine as anti-cancer drugs (ScienceDirect, 2025)
    • Content: A scientific article documenting berberine’s ability to inhibit invasion and migration in kidney cancer cells. The study describes how the substance works by downregulating METTL3 expression, which is crucial for reducing the cancer cells’ ability to spread and form metastases.

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7. Boswellia (Frankincense)

Brain cancer:

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8. Cat’s Claw (Uncaria tomentosa)

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9. Coenzym Q10

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10. Curcumin

Adrenocortical cancer

Bladder cancer and urinary tract cancer

Pancreatic cancer

  • Link 31: Insights into curcumin’s anticancer activity in pancreatic cancer (ScienceDirect, 2025)
    • Content: A new scientific investigation highlighting curcumin’s potential against pancreatic cancer. The article focuses specifically on how the substance regulates the tumor microenvironment and inhibits the activation of cells that form dense scar tissue (stroma), reducing the tumor’s aggressiveness and ability to spread.

Gallbladder and biliary tract cancer

  • Link 32: Revisiting Curcumin in Cancer Therapy: Recent Insights into Molecular Mechanisms (PubMed Central, 2025)
    • Content: A comprehensive review from 2025 mapping curcumin’s mechanisms of action against cancer. The article highlights how the substance can specifically inhibit growth signals (Wnt/β-catenin, mTOR) and induce cell death in biliary tract cancer cells, as well as suppress the inflammation that often drives the disease.

Brain cancer

  • Link 33: Potential of Curcumin and Its Analogs in Glioblastoma Treatment (MDPI, 2025)
    • Content: A review article describing curcumin’s ability to inhibit growth, migration, and invasion in brain tumors through regulation of oxidative stress and signaling pathways. Results support the use of curcumin as part of the strategy against aggressive forms of brain cancer.
  • Link 34: Regulation of the Notch signaling pathway by natural products (ScienceDirect, 2023)
    • Content: A review of how natural substances like curcumin regulate the Notch signaling pathway in various cancers. The article describes the specific mechanisms by which the substance can block this pathway and thus inhibit tumor development.

Head and oral cancer

  • Link 35: Role of curcumin in selected head and neck lesions (ScienceDirect, 2022)
    • Content: A scientific article summarizing knowledge about curcumin’s effect on diseases in the head and neck region, including squamous cell carcinoma. It describes how the substance can inhibit tumor growth and reduce inflammation in the mucous membranes, supporting its use in this context.

Bone cancer

  • Link 36: Curcumin suppresses metastasis, invasion, and proliferation (Sage Journals, 2024)
    • Content: A 2024 study documenting curcumin’s ability to inhibit the spread (metastasis) and growth of bone cancer cells. The article describes how the substance works by downregulating specific signaling pathways (EGFR/Src) that otherwise drive the cancer’s development and ability to invade new tissue.

Cervical cancer

  • Link 37: Basic research on curcumin in cervical cancer (ScienceDirect, 2023)
    • Content: A scientific article analyzing curcumin’s effects against cervical cancer. It highlights that the substance works by inducing programmed cell death (apoptosis) and inhibiting tumor cell division, confirming its potential as part of the treatment.

Stomach cancer

Multiple myeloma/bone marrow cancer

Kidney cancer

Colon cancer

  • Link 41: Curcumin and its anti‐colorectal cancer potential (Wiley Online Library, 2024)
    • Content: A scientific review mapping curcumin’s potential against colon cancer. The article describes how the substance can fight cancer cells by affecting a wide range of signaling pathways governing cell growth and survival, confirming its broad mechanism of action.

Salivary gland and nasal cancer

  • Link 42: Curcumin derivative C210 induces Epstein–Barr virus lytic reactivation (Nature, 2024)
    • Content: A scientific study demonstrating how curcumin-based substances can force latent Epstein-Barr virus to become active again. This mechanism causes cancer cells in the nasopharynx to die as they cannot survive the viral activation, supporting a specific antiviral strategy against the cancer.

Ovarian cancer

Vulvar and vaginal cancer

  • Link 44: Curcumin nanoemulsion suppresses HPV oncogenes and induces apoptosis (Virology Journal, 2025)
    • Content: A study documenting curcumin’s ability to suppress carcinogenic HPV genes and induce cell death (apoptosis). The results confirm that the substance effectively targets the virus-driven mechanisms central to the development of cancer in the lower genitals.

Eye cancer

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11. DIM/ I3C (Indole-3-Carbinol)

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12. EGCG (Green tea)

Adrenocortical cancer

  • Link 11: Plant Natural Compounds in the Treatment of ACT and adrenocortical cancer (Wiley Online Library, 2021)
    • Content: A scientific review article examining the effect of natural plant compounds against adrenocortical cancer. The article discusses the potential of substances like EGCG to inhibit both tumor growth and the overproduction of hormones (steroidogenesis) characteristic of functional tumors.

Neck and oral cancer

Brain cancer

Cervical cancer

Kidney cancer

Vulvar and vaginal cancer

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13. High-dose Vitamin C (IV)

Lung cancer:

  • Link 6:Vitamin C Inhibited Pulmonary Metastasis through Activating Nrf2/HO-1 Pathway (NIH, Molecular Nutrition & Food Research, 2024)
    • Content: A scientific study investigating vitamin C’s ability to stop the spread of cancer to the lungs (lung metastases). The results show that treatment (both as injection and oral intake) activates specific signaling pathways (Nrf2/HO-1 and p53), which cause cancer cells to undergo apoptosis and prevent them from migrating, while sparing healthy cells.

Uterine cancer:

Adrenocortical cancer:

  • Link 8:Targeting cancer vulnerabilities with high-dose vitamin C (National Institutes of Health, 2019)
    • Content: A scientific review article describing how high doses of vitamin C exploit specific weaknesses in cancer cells. The article explains that the treatment targets the cells’ oxygen sensors (HIF) and disrupts their sugar metabolism, stressing aggressive cancer cells that are heavily dependent on these mechanisms to survive.

Blood cancer:

  • Link 9:Vitamin C and D supplementation in acute myeloid leukemia (National Institutes of Health, 2023)
    • Content: A clinical study from 2023 investigating the effect of vitamin C and D supplementation in patients with acute myeloid leukemia (AML) during intensive chemotherapy. The results indicate that the supplements are safe and may have a positive influence on treatment outcomes.

Colon cancer:

Gastrointestinal cancer:

Kidney cancer:

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14. Ginger

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15. IP6 & Inositol

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16. Dandelion root

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17. Maitake (Grifola frondosa)

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18. Milk thistle (Silymarin/ Silybin)

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19. Melatonin

Glioblastoma:

Skin cancer:

  • Link 22: Melatonin: a natural guardian in cancer treatment (PubMed Central, 2025)
    • Content: A scientific review highlighting how melatonin can inhibit cell growth, block the formation of new blood vessels, and promote cell death in tumors, while also enhancing the effect of other treatments.

Bone cancer:

Stomach cancer:

  • Link 24: Melatonin: a natural guardian in cancer treatment (Frontiers, 2025)
    • Content: A comprehensive article describing melatonin’s potential as a “natural guardian” in cancer treatment, including its ability to promote cell death in gastrointestinal tumors.

Uterine cancer:

Ovarian cancer:

  • Link 26: Melatonin: a natural guardian in cancer treatment (PubMed Central, 2025)
    • Content: A new scientific article from 2025 highlighting how melatonin can reduce the tumor burden in ovarian cancer by inhibiting central signaling pathways (such as AKT and \beta-catenin).

Eye cancer:

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20. Modified citrus pectin (MCP)

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21. N-acetyl-cysteine (NAC)

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22. Omega-3 (Fish oil)

Adrenocortical cancer:

Brain cancer:

Multiple myeloma/bone marrow cancer:

Kidney cancer:

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23. Pau D’Arco

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24. Probiotics

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25. Quercetin

Stomach cancer:

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26. Resveratrol

Stomach cancer:

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27. Selenium

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28. Black walnut (Juglone)

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29. Sulforaphane

Adrenocortical cancer:

Bladder cancer and urinary tract cancer:

Glioblastoma:

Multiple myeloma/bone marrow cancer:

Kidney cancer:

Prostate cancer:

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30. Turkey Tail (Coriolus versicolor)

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31. Vitamin C i.v. / Vitamin C oral

Adrenocortical cancer:

Blood cancer:

Colon cancer:

Kidney cancer:

32. Vitamin D

Skin cancer:

Blood cancer:

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Page created: 10.06.25, last revised: 01.12.25

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What you read on Jeg har Kræft is not a recommendation. Seek competent guidance.

About the Author & Professional Background

Portrætfoto af Hanne til forsiden.

This article has been prepared and validated by the undersigned, Hanne Kjær Uhlig. I am a registered nurse (1975, with clinical experience until 2013) and hold an M.Arch. (1983, specializing in industrial design), and I taught at DTU (Technical University of Denmark) for a number of years.

Following the loss of my mother to cancer in 2000 and my own cancer diagnosis in 2024, I founded this non-profit information site “Jeg har Kræft” (I Have Cancer).

The goal is to use my analytical and academic approach to bring clarity, safety, and scientific evidence to the field of integrative, complementary, and alternative cancer treatment. At the same time, my healthcare experience is utilized to make the articles patient-centered and relevant.

Article characteristics:

  • Clinical and personal background: Created from a combination of decades of experience as a nurse and personal experiences as both a patient and a relative.
  • Scientific methodology: The content is based on systematic research of medical databases and clinical trials. The articles are consistently supported by source references under Links.
  • Independent non-profit project: Operations are funded through voluntary donations and memberships through the Support Association Jeg har Kræft. The site is completely independent of commercial manufacturer interests and works solely to improve the quality of life for cancer patients.
  • The board of directors of the support association consists of:

Community: Join the Facebook group: Jeg har Kræft – Hvad kan jeg gøre? Danish Language only.

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What you read on Jeg har Kræft is not a recommendation. Seek professional guidance.