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

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Cancer’s energy pathways

Content:

Summary about cancer’s energy pathways

Kræftens forsyningsveje symboliseret ved lyse kurve med forskellige frugt og grøntsager.- i mange farver.

The basic principle: Cancer’s hunger and need for materials:

  • Besides being driven by faulty growth signals, cancer cells also have an insatiable need for physical resources to be able to build new cells. This section focuses on the “energy pathways” that bring fuel (like sugar), building blocks, and oxygen to the tumor.

The strategy: To cut off the supplies:

  • The overviews further down the page show how both diet and various medications/dietary supplements can disrupt these supply routes. The goal is to “starve” the cancer cell, partly through a strategic diet, partly by blocking its access to the resources it depends on, or to prevent it from using its internal survival mechanisms.

Purpose and warning:

  • The purpose is to provide knowledge and inspiration for a conversation with a qualified practitioner.

The overviews are a tool for dialogue and must never be considered a guide for self-treatment.

What is an energy pathway

Kræftens forsyningsveje symboliseret ved foto af en masse røde pebre.

Where signaling pathways are cancer’s information and command system, supply routes are its physical logistics. For a cancer cell to grow and divide, it needs a constant supply of fuel and materials, exactly as a construction site needs cement, bricks, and electricity.

A metabolic approach aims not only to stop the orders to build (the signaling pathways), but also to block the roads so the trucks with materials cannot get through.

Why energy pathways are important

Even if you block the growth signals, a cancer cell can often survive if it still has access to plenty of fuel. By targeting both – the information and the logistics – you create a much more comprehensive and effective blockade, making it harder for the cancer to find detours and develop resistance.

Central energy pathways

Kræftens forsyningsveje symboliseret ved et bundt løg

Below is a list of the most central energy/supply pathways and the strategies aimed at targeting them.

  • Glycolysis: Cancer cells’ primary highway for converting sugar into energy.
  • Glutaminolysis: An alternative highway that uses the amino acid glutamine as fuel.
  • Angiogenesis: The formation of new blood vessels, which supply the tumor with oxygen and nutrients.
  • Fatty acid metabolism: Cancer cells’ ability to create and burn fat.
  • Autophagy: The cancer cell’s internal recycling system and survival mechanism.
  • Inhibition of detoxification enzymes: Strategies to turn off the enzymes cancer cells use to detoxify themselves and resist treatment.

Who is Jane McLelland

Kræftens forsyningsveje symboliseret ved forsiden af Jane McLellands bog

Jane McLelland is a British former physiotherapist who became a well-known patient advocate and author after having survived several aggressive cancer diagnoses herself that were considered terminal.

Her major contribution is not that she discovered the individual signaling or supply pathways. Her “work” is rather having been one of the first to, as a patient, systematically trawl through thousands of scientific studies and systemize the different research areas.

Supply and signaling pathways

She is especially known for her “Metro Map” analogy, where she visualizes cancer’s various supply and signaling pathways as lines in a subway network. Her book, “How to Starve Cancer”, is a guide to how one, via a combination of diet, dietary supplements, and repurposed drugs, can try to block as many of these “lines” as possible at once.

She is thus a central figure in the popularization of the multi-targeted approach for patients.

See also Jane McLelland (how to starve cancer)

Review of the individual energy pathways

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Here follows a more detailed review of each individual energy pathway.

1. Glycolysis (sugar combustion)

Kræftens forsyningsveje symboliseret ved brune sukkerknalldr i en grøn keramikskål

This is the utilization of the Warburg effect in practice. Many cancer cells are extremely dependent on a constant and high supply of sugar (glucose), which they ferment to get quick energy. A “glycolysis inhibitor” is a substance that in one way or another disrupts this process. This can be, for example, by blocking the cell’s ability to absorb sugar or by inhibiting the enzymes necessary for fermentation.

2. Glutaminolysis (glutamine combustion)

Kræftens forsyningsveje symboliseret ved kålhoveder.

When cancer cells lack sugar, or if they need specific building blocks (especially nitrogen), many of them can switch to using the amino acid glutamine as an alternative fuel. Blocking this process (glutaminolysis) removes an important “plan B” for the cancer cell and can make it more vulnerable. (Read more about glutamine, and in which foods it is found, further down the page).

3. Angiogenesis (blood vessel formation)

Kræftens forsyningsveje symboliseret ved nærbillede af en gruppe tomater.

A tumor cannot grow larger than a pinhead before it needs its own blood supply to deliver oxygen and nutrients. The process where a tumor stimulates the formation of new blood vessels is called angiogenesis. “Anti-angiogenic” substances work by inhibiting this process and thereby “starving” the tumor of oxygen and nutrients.

Comment:

There is a close relationship between the VEGF signaling pathway and Angiogenesis, which is described under Energy pathways. The difference is:

  • Angiogenesis: is the actual process of building the new blood vessels as a result of the order. It is a physical energy/supply pathway.
  • VEGF signaling pathway: is the order itself or the “order form” that the cancer cell sends out. It is a signal/information pathway.

See also Block cancer’s signaling pathways

4. Fatty acid metabolism

Kræftens forsyningsveje symboliseret ved forskellige typer oliven.

Cancer cells need fats (lipids) to build new cell membranes when they divide rapidly. Many cancers have an upregulated ability to produce fatty acids themselves. Substances that inhibit this (e.g., by blocking the Mevalonate pathway) can therefore slow down cancer growth.

5. Autophagy (cellular “self-eating”)

Kræftens forsyningsveje symboliseret ved et par artiskokker.

This is the cancer cell’s built-in “survival kit”. When attacked by e.g. chemotherapy, it can begin to “eat” and recycle its own, non-essential parts to obtain energy and survive the attack. An “autophagy inhibitor” blocks this survival mechanism and makes the cancer cell more vulnerable to the primary treatment.

6. Inhibition of detoxification enzymes (e.g. ALDH)

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Some of the most resistant cancer cells (the so-called cancer stem cells) survive treatment because they have a high level of special “detoxification enzymes” like ALDH (aldehyde dehydrogenase). These enzymes act as an internal shield that can neutralize chemotherapy before it has time to work.

An “ALDH inhibitor” like Disulfiram is a substance that specifically turns off this shield and thus makes the most stubborn cancer stem cells vulnerable to treatment.

An important property of Disulfiram is that it can cross the blood-brain barrier, making it theoretically relevant for the treatment of brain tumors and metastases in the brain.

The role of diet

Kræftens forsyningsveje symboliseret ved fletkurve fyldt med grøntsager, herunder bønner, hvidløg, artiskok mfl.

Besides blocking specific pathways with medications and dietary supplements, the most fundamental way to affect cancer’s energy/supply pathways is via the diet.

The purpose is to create a systemic (body-wide) environment that is limitedly hospitable for cancer cells. Two main strategies are particularly well-described in this context:

Ketogenic diet and glycolysis

  • A ketogenic diet (very few carbohydrates, high fat content) is the most direct way to intervene in the glycolysis supply pathway.
  • By minimizing the intake of sugar and carbohydrates, one “starves” the cancer cells that are heavily dependent on glucose as their primary fuel. At the same time, the diet lowers the level of the growth-promoting hormone insulin, which affects several of the signaling pathways described above.
  • Dr. Thomas Seyfried, among others, is a strong advocate of this approach as a complementary cancer treatment.

See also Metabolic principles in cancer treatment

Fasting and calorie restriction

  • Periods of fasting or a general restriction of calorie intake can activate the body’s “emergency brake” – the AMPK signaling pathway. As described on the page about cancer’s signaling pathways, an activation of AMPK leads to an inhibition of growth-promoting pathways like mTOR. This creates a state of metabolic stress for the cancer cells and can make them more vulnerable to other treatments.

Jane McLellands ‘starve cancer’ principles

  • The approach popularized by Jane McLelland is more specific regarding certain food items and aims to remove the primary “building blocks” and “growth promoters”.
  • This typically involves a diet that excludes sugar, dairy products, and meat from four-legged animals, and which has a low content of the growth-promoting amino acid glutamine.
  • The focus is instead on a wide variety of vegetables, berries, and healthy fats.

See also Diet that starves cancer.

Focus on glutamine

Glutamine is the most common amino acid (one of the building blocks of proteins) in the body. While it is crucial for many normal functions, especially in the gut and immune system, many aggressive cancer cells are also extremely “dependent” on it.

Cancer cells not only use sugar but also glutamine as an alternative fuel and as a critical source of the building blocks they need to make new cancer cells.

Limiting the intake of glutamine-rich foods is therefore a central part of certain metabolic strategies aimed at targeting cancer’s “glutaminolysis” supply pathway. This also applies to Jane McLelland’s: Starve cancer diet.

Glutamine is found in the highest concentrations in protein-rich foods. Foods that are often limited or excluded in a low-glutamine approach include:

  • Dairy products: Especially cheese, milk, and protein powder based on casein or whey.
  • Red meat: Beef, veal, and pork.
  • Soy and tofu.
  • Wheat, corn, and certain legumes like beans and lentils.
  • Bone broth and gelatin.

However, be careful that you do not get too little protein, as it will reduce your muscle mass.

(For my own part, I had to give up this part of the strategy, as I could not eat enough to maintain my muscle mass, and therefore became increasingly weak. This completely corrected itself when I started eating an increased amount of meat and dairy products again – as well as protein bars with no added sugar).

Conclusion

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Understanding and targeting cancer’s energy and supply pathways – its access to fuel like sugar and glutamine, and its ability to build new infrastructure like blood vessels – is a fundamental part of a modern, metabolic strategy – and of the principles that Jane McLelland has greatly contributed to developing.

As this page shows, by combining conscious dietary choices with a range of substances (repurposed drugs and dietary supplements), one can try to disrupt these logistical chains. The most effective approach, however, is often achieved through a combined effort, where one both cuts off the physical supplies (described here) and at the same time blocks the growth orders sent via cancer’s signaling pathways.

Since cancer cells are often good at finding detours, a combination of substances that target several different signaling pathways simultaneously is often the most promising approach.

This knowledge serves as a foundation for a qualified dialogue with a practitioner about possible supplementary strategies.

Warning

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This is in no way a call for self-treatment. Experimenting with treatment on your own, without professional guidance, can be ineffective and potentially dangerous.

Content:

Strategies grouped by energy/ supply pathway

This overview groups relevant substances according to which energy pathway they primarily affect.

1. Glycolysis inhibitors (blocks sugar combustion)

Kræftens forsyningsveje symboliseret ved brune sukkerknalldr i en grøn keramikskål
  • Metformin (via mitochondrial inhibition and AMPK activation)
  • Berberine (via AMPK activation)
  • Benzimidazoles (inhibits glucose uptake directly)
  • Doxycycline (via mitochondrial inhibition)
  • Hydroxychloroquine (via disruption of lysosomes/autophagy)
  • Curcumin (inhibits several glycolytic enzymes)
  • EGCG (Green tea) (inhibits several glycolytic enzymes)
  • Vitamin D (can modulate glycolytic enzymes)
  • Statins (indirect effect via the Mevalonate pathway)
  • Alpha-lipoic acid (ALA) (inhibits the enzyme pyruvate dehydrogenase)
  • Artemisinin (can inhibit key enzymes like hexokinase)
  • Probiotics (via production of SCFA, which affects metabolism)
  • Quercetin (inhibits glucose uptake)
  • Resveratrol (via SIRT1 activation)
  • Black Walnut (Juglone) (inhibits several glycolytic enzymes)
  • Sulforaphane (inhibits several glycolytic enzymes)

2. Glutaminolysis inhibitors (blocks glutamine combustion)

Kræftens forsyningsveje symboliseret ved kålhoveder.
  • Curcumin (potent, inhibits the enzyme glutaminase)
  • EGCG (Green tea) (inhibits the enzyme glutamate dehydrogenase)
  • Metformin (indirect effect via altered metabolism)
  • Doxycycline (via mitochondrial inhibition)
  • Probiotics (can affect glutamine availability in the gut)
  • Berberine (inhibits glutamine uptake)
  • Quercetin (inhibits glutamine uptake)

3. Anti-angiogenesis (blocks blood vessel formation)

Kræftens forsyningsveje symboliseret ved nærbillede af en gruppe tomater.
  • Propranolol (blocks stress signaling that drives angiogenesis)
  • Metformin (inhibits VEGF signaling via AMPK)
  • Statins (inhibits the Mevalonate pathway, which is necessary for vascular proteins)
  • Doxycycline (inhibits MMP enzymes that are necessary for blood vessel formation)
  • Curcumin (very potent, inhibits e.g. VEGF)
  • Vitamin D (direct anti-angiogenesis effect)
  • EGCG (Green tea) (inhibits VEGF signaling)
  • Aspirin (anti-inflammatory effect)
  • Milk Thistle (Silymarin) (inhibits VEGF signaling)
  • Melatonin (inhibits HIF-1α and VEGF)
  • Apigenin (inhibits HIF-1α and VEGF)
  • Boswellia (inhibits several pro-angiogenic factors)
  • Turkey Tail (via immune modulation)
  • Modified Citrus Pectin (MCP) (via inhibition of Galectin-3)
  • IP6 & Inositol (inhibits VEGF signaling)
  • Quercetin (inhibits VEGF signaling)
  • Resveratrol (inhibits VEGF signaling)
  • DIM / I3C (inhibits HIF-1α and VEGF)

4. Fatty acid metabolism inhibitors

Kræftens forsyningsveje symboliseret ved forskellige typer oliven.
  • Statins (very potent inhibitor of the Mevalonate pathway/cholesterol synthesis)
  • Sirolimus/Everolimus (mTOR inhibitors, as mTOR controls lipid synthesis)
  • Metformin (via AMPK activation)
  • Berberine (via AMPK activation)
  • Vitamin D (is an important regulator of lipid metabolism)
  • Alpha-lipoic acid (ALA) (regulates fatty acid oxidation)
  • EGCG (Green tea) (is a known FASN inhibitor (Fatty Acid Synthase))
  • Curcumin (modulates several enzymes in lipid metabolism)
  • Propranolol (affects lipid metabolism)
  • Hydroxychloroquine (affects lipid droplet autophagy)

5. Autophagy inhibitors (blocks the cell’s “self-eating”)

Kræftens forsyningsveje symboliseret ved et par artiskokker.

Note: Many substances below are modulators; only a few are pure inhibitors

  • Hydroxychloroquine (potent and well-researched late-stage inhibitor)
  • Vitamin D (is an important modulator of autophagy)
  • N-acetyl-cysteine (NAC) (modulating and context-dependent effect)
  • Desloratadine (induces lysosomal cell death, which disrupts the process)
  • Curcumin (modulating and context-dependent effect)
  • Resveratrol (modulating and context-dependent effect)
  • EGCG (Green tea) (modulating and context-dependent effect)
  • Probiotics (modulating effect)
  • Turkey Tail (modulating effect)
  • Modified Citrus Pectin (MCP) (modulating effect)
  • Aspirin (induces autophagy in certain contexts, but can disrupt it)

6. Inhibition of detoxification enzymes

  • Disulfiram (inhibits the ALDH enzyme in cancer stem cells)
  • Sulforaphane (optimizes the different steps in the body’s detoxification function)
  • N-acetyl-cysteine (NAC) (as a precursor to glutathione, central in phase II)
  • Probiotics (the gut flora is crucial for the body’s overall detoxification)
  • EGCG (Green tea) (inhibits certain CYP enzymes)
  • Milk Thistle (Silymarin) (affects the liver’s detoxification pathways)
  • Quercetin (inhibits certain CYP enzymes)

Concluding remark

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These lists illustrate how a single medication/dietary supplement in several cases can disrupt several of cancer’s logistical chains at once – e.g. by both inhibiting sugar combustion and the formation of new blood vessels.

The overview can be used as inspiration to put together a broad strategy aimed at creating a “resource crisis” for the cancer cells.

The list can be used as a tool to understand how one, together with a qualified practitioner, can potentially put together a strategy that attacks the cancer’s vulnerabilities from several different angles.

See also Dietary supplements and Chemotherapy – how does it work

Links

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Page created: June 15, 2025

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What you read on I have Cancer 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:

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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:

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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)

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3. Apigenin

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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

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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

Back to: Overview table for Repurposed drugs

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

Back to: Overview table for Repurposed drugs

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:

Back to: Overview table for Repurposed drugs

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.