Treatments

Block cancer’s growth pathways

Kræft som metabolisk lidelse symboliseret ved mikroskopi af rosa blomster med gule støvdragere. Der ses et enkelt grønt blad.

Cancer as a metabolic disease

Content:

Summary of cancer as a metabolic disease

What is it

  • Traditionally, cancer has been seen as a purely genetic disease, but modern research—led by, among others, Dr. Thomas Seyfried—indicates that cancer is fundamentally a metabolic disease. The theory is that cancer arises as a result of damage to the cells’ power plants (mitochondria), creating an energy crisis.
  • This approach shifts focus from simply killing cells to targeting the metabolic processes that cancer cells depend on to survive.

The Warburg effect and cell fermentation

  • Over 100 years ago, Otto Warburg discovered that cancer cells have a unique metabolism: they prefer to ferment sugar (fermentation) rather than burn fat using oxygen (cellular respiration). It should be emphasized that cancer cells do not necessarily “lose” the ability to use oxygen. Many cancer cells use both glycolysis and oxidative phosphorylation, and their metabolism can adapt to the environment and energy needs.
  • This discovery was unfortunately largely overlooked for decades but is now widely recognized again.

Treatment Strategies and the Future

  • Treatment focuses on altering the cancer cells’ environment through diet (e.g., keto), fasting, and the use of existing medication for new purposes (repurposed drugs). Examples include Metformin, statins, and anti-parasitic agents like Vermox, which can disrupt the metabolism and cell division of cancer cells or activate the immune system.
  • The goal is a personalized strategy that combines metabolic interventions, preferably with traditional treatment, to increase efficacy.

Cancer as a metabolic disease – general overview

When considering cancer as a metabolic disease, it opens new perspectives on the disease’s development and potential treatment options, including the metabolic pathways (types of metabolism), also called “pathways,” that cancer cells use.

Cancer cells’ unique metabolism

Already 100 years ago, Otto Warburg discovered that the characteristic of cancer is that the cells’ metabolism (energy production) changes from normal fat burning using oxygen (cellular respiration) to fermentation of sugar without using oxygen. However, it should be emphasized that cancer cells do not necessarily “lose” the ability to use oxygen. Many cancer cells use both glycolysis and oxidative phosphorylation, and their metabolism can adapt to the environment and energy needs.

This important discovery was unfortunately completely overlooked in influential circles for the following decades but is now widely recognized again.

The Warburg effect

The Warburg effect is the phenomenon where cancer cells prefer to ferment glucose (thus turning it into lactic acid), even under oxygen-rich conditions (where normal cells would use normal combustion).

Symbiosis with the microenvironment

In addition, cancer cells alter the surrounding tissue to create an environment that supports their energy production for growth and spread. This includes, among other things, increasing blood vessel development and acidity in the tumor environment.

Complexity

Cancer cell metabolism is very complex and varies for different cancer types and can even vary within the same tumor. By identifying the specific metabolic pathways that different cancer cells depend on, one can look for new drugs that block these pathways. This is expected to be effective, at least provided that cancer cells cannot choose another metabolic pathway.

The goal is therefore to try to block all possible pathways for the given cancer type. The importance of broad blocking of cancer cell nutrition is, as mentioned above, due to cancer cells’ ability to change metabolism and thus avoid programmed cell death (apoptosis). They can in this way change/extend the cancer cell’s normal lifespan.

Combination treatments

Metabolic drugs can be combined with traditional cancer treatments such as chemotherapy and radiation to increase effectiveness and reduce side effects.

Combination treatments

By combining metabolic drugs with other types of cancer treatments, one can potentially increase effectiveness and reduce the risk of resistance. To determine which are most effective, biomarker research is used.

See also: Biomarkers for the nerdy at the bottom of the page (scroll down).

Important metabolic pathways for cancer cells

There are many metabolic pathways, and it appears that cancer cells are able to switch pathways so that if one pathway is blocked, they can use one or more of the others to obtain nutrients instead. This means that a broad approach is needed if you want to starve the cancer.

Examples of metabolic pathways

Glycolysis

This is the most well-known of the altered metabolic pathways in cancer cells. Here, glucose is converted to lactic acid, even when sufficient oxygen is available (the aforementioned Warburg effect).

Glycolysis (sugar splits into ATP and becomes energy) is a faster process than the usual complete oxidative phosphorylation. This gives cancer cells the ability to produce ATP (adenosine triphosphate) quickly, which is a necessary substance to support the rapid growth of cancer cells.

By inhibiting enzymes in the glycolysis process, one can thus limit cancer cells’ energy production and thereby growth.

Glutaminolysis

Cancer cells use glutamine (an amino acid) as both an energy source and to synthesize building blocks for new cells. Glutaminolysis is the process where glutamine is broken down to produce energy and intermediates for use in biosynthesis (formation of, e.g., amino acids).

By preventing the uptake of glutamine, one can limit cancer cells’ access to this important energy source and building block.

Lipid synthesis

Lipid synthesis means that cells produce fat for storage and use, among other things, for growth. Cancer cells often have increased production of fatty acids, which are used to build cell membranes and as energy storage. This is important for maintaining cell membrane integrity (i.e., ensuring the cell membrane’s function to sort/determine what may enter and exit), function as energy storage, and support cell growth.

By inhibiting enzymes involved in lipid synthesis, one can disrupt cell membrane integrity and prevent cell growth.

Pentose phosphate pathway

The pentose phosphate pathway converts glucose into pentose sugars and other substances. This provides building blocks for antioxidants and nucleic acids (DNA and RNA), which are necessary for cell division and to protect the cell from oxidative stress. In addition, ribose-5-phosphate is formed, which is a building block for nucleic acids.

Additional pathways

There are several metabolic pathways that are relevant when attacking cancer cell metabolism, and likely we still have far from a complete picture of how many there are and how best to do it.

There is a lot described in the literature relevant to this issue. See, among others, links below to Jane McLelland’s book:

How to Starve Cancer (Saxo).

The future

Research in metabolic cancer treatment is developing rapidly, and there are high expectations that new drugs will revolutionize cancer treatment. By fully understanding the unique metabolism of cancer cells, more targeted, effective, and less toxic treatments can be developed.

Furthermore, this approach can likely explain the experiences with certain repurposed drugs such as Metformin, which regulates blood sugar, and statins, which regulate cholesterol levels in the blood.

Dr. Thomas Seyfried’s theories on cancer

Warburg’s theories that cancer is primarily a metabolic disease are shared by Dr. Thomas Seyfried, another well-known researcher who has presented the same theory about cancer. His main thesis is also that cancer is fundamentally a metabolic disease rather than a genetic disease, as many other researchers tend to believe.

The key to understanding

This change in metabolism, Seyfried believes, is the key to understanding how cancer cells behave. They divide uncontrollably and ignore the normal signals from the body telling them when to stop dividing.

Otto Warburg and Thomas Seyfried’s theory

Seyfried’s research heavily builds on the work of Otto Warburg, who, as previously mentioned, already in 1931 proposed that cancer cells have a unique form of metabolism. Warburg’s theory has been overlooked for many years, but Seyfried has revived it and added new dimensions.

Implications for treatment

If Seyfried is right, it has major consequences for how we treat cancer. Instead of focusing on killing cancer cells with chemotherapy or radiation, we should perhaps to a much greater extent focus on changing the metabolism of cancer cells. This could, for example, be done through dietary changes (keto diet), fasting, and specific dietary supplements.

Seyfried’s fundamental principles

Cancer as an energy crisis

Seyfried suggests that cancer cells are in a state of chronic energy deficiency. To survive, they adapt their metabolism to primarily use glucose (sugar) as an energy source. This change in metabolism makes it difficult for cancer cells to produce the energy they need to function normally.

The role of mitochondria

Mitochondria are the cells’ power plants. Seyfried believes that mitochondria in cancer cells are damaged and do not function optimally. This contributes to the energy deficiency that cancer cells experience.

Inhibition of normal cell growth

Cancer cells produce substances that inhibit the growth of normal cells. This creates space for cancer cells to grow and spread.

Treatment

Ketogenic diet

Seyfried suggests that a ketogenic diet can be an effective treatment against cancer. By limiting carbohydrate intake and increasing fat intake, the body is forced to use fat as an energy source instead of glucose. This can make it more difficult for cancer cells to survive, as they are dependent on glucose.

See also: Ketogenic diet and LCHF

Other metabolic measures

In addition to the ketogenic diet, Seyfried also suggests other metabolic interventions, such as fasting and specific dietary supplements that can help combat cancer.

Specific dietary supplements

Seyfried mentions potential benefits of certain dietary supplements when combined with a ketogenic diet. Some of the dietary supplements mentioned in connection with Seyfried’s work include (there are more than these):

Anti-parasite agents

Why anti-parasite agents can have an effect on cancer cells:

Analogous (related) biological processes:

Metabolism

Both cancer cells and some parasites have high metabolic activity to grow and divide quickly. Agents such as Fenbendazole, Vermox, and Plaquenil can affect specific metabolic pathways that are important for both cancer cells and parasites.

Protein synthesis

Both cancer cells and parasites produce a range of proteins necessary for their survival and spread. Some of these proteins may have analogous structures or functions, and therefore agents that inhibit protein synthesis in parasites may also affect cancer cells.

Cell division

Both cancer cells and parasites divide rapidly, and agents that disrupt cell division can have an effect on both.

Indirect effects

Microenvironment

Parasites can affect the microenvironment where cancer cells are located. By removing parasites, one can change this microenvironment and make it less favorable for cancer cell growth.

Activation of the immune system

Some parasites have an ability to stimulate and activate our immune system in a way that makes it more effective at fighting diseases, including cancer cells. Anti-parasite agents can thus, paradoxically, strengthen this immune response and thus indirectly have a cancer-inhibiting effect.

Awakening dormant immune cells

Cancer cells are skilled at “shutting down” our immune system. Parasites can help “awaken” these dormant immune cells so they can recognize and attack cancer cells again.

Is parasite infection good?

Why do we take antiparasitic agents, but research parasites for cancer treatment?

This is not a contradiction. Researchers are trying to exploit the positive aspects of parasites without exposing people to the negative consequences of an infection. This can be done by:

Isolating the active substances

Researchers are trying to isolate the specific substances in parasites that have a positive effect on the immune system and develop drugs based on these substances.

Genetically modified parasites

Work is being done to develop genetically modified parasites that only have the desired properties and do not cause disease.

Combination treatment

Parasites can potentially be used in combination with existing cancer treatments to increase effectiveness.

While we wait

The result of this research lies somewhere in the future. Personally, I don’t dare to wait for it, so I have chosen repurposed drugs in the form of Vermox (in combination with other repurposed drugs).

Note

It is important to have a nuanced understanding of parasites. While some parasites may have positive effects on our health, most parasites are harmful and can cause serious diseases. Research in this area is still in its infancy, and it is important to be critical of the information you find.

Conclusion

Viewing cancer as a metabolic disease has revolutionized our understanding of the disease and opened up new and promising treatment options. Although there are still many challenges to overcome, this approach is an important step toward more effective and less toxic cancer treatments.

Thomas Seyfried’s theory is still controversial, and there are many researchers who do not share his viewpoint. But his work has led to a new and exciting debate about the origin and treatment of cancer.

Personally, I find the theory of cancer as a metabolic disease particularly plausible. The fact alone that many proponents of this theory have lived in good health for many years with their cancer diagnosis is convincing.

However, this is a general overview of metabolic pathways in cancer. It is important to note that cancer is a complex disease, and the metabolic changes can vary greatly between different cancer types and even within the same tumor.

See also: Dietary supplements grouped by effect

See also: Nutrition and Diet

See also: Symptoms

To menu

Links

[1] Expert says ketogenic diet ‘prevents’ and ‘destroys’ cancer – best foods to eat (Get Surrey)

  • Content: How a ketogenic diet can help prevent and combat cancer by starving cancer cells of glucose.

[2] Video: Dr. Thomas Seyfried reveals: Cancer is a Metabolic Disease, not Genetic! (Dr. Thomas Seyfried Charity Channel, YouTube)

  • Content: Seyfried explains his metabolic theory of cancer and how diet can be used as treatment.

[3] Book: Cancer as a Metabolic Disease (By Thomas Seyfried)

  • Content: Seyfried’s comprehensive book on the metabolic theory of cancer.

[4] Thomas Seyfried’s Metabolic Theory of Cancer and How The Paleo Diet Could Help Curtail the Disease (The Paleo Diet)

  • Content: How metabolic theory connects to dietary approaches like the Paleo diet.

[5] Targeting the Mitochondrial-Stem Cell Connection in Cancer (Journal of Orthomolecular Medicine)

  • Content: Research on how mitochondrial dysfunction contributes to cancer.

[6] Treatment: A Hybrid Orthomolecular Protocol (Journal of Orthomolecular Medicine)

  • Content: Combining metabolic approaches with orthomolecular medicine for cancer treatment.

[7] How breast cancer goes hungry (Cold Spring Harbor Laboratory)

  • Content: How metabolic targeting can starve breast cancer cells.

[8] Cancer as a metabolic disease (IOM)

  • Content: Danish article on metabolic approaches to cancer treatment.

[9] How to Starve Cancer (Jane McLelland’s website)

  • Content: Jane McLelland’s resources on metabolic cancer treatment.

[10] Insulin resistance plays an important role in cancer (Science News.dk)

  • Content: How insulin resistance is linked to cancer development.

[11] Research group leader: Chronically elevated insulin can drive cancer risk in severe obesity (Onkologisk Tidsskrift)

  • Content: The connection between insulin levels and cancer risk.

[12] Metabolism of primary high-grade serous ovarian carcinoma (HGSOC) cells under limited glutamine or glucose availability (PubMed)

  • Content: How ovarian cancer cells adapt metabolically under nutrient deprivation.

[13] The Warburg Effect: How Does it Benefit Cancer Cells? (PubMed, 2017)

  • Content: Detailed explanation of the Warburg effect and its role in cancer.

[14] The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (PubMed)

  • Content: How mitochondrial metabolism affects cancer progression.

[15] On the Origin of the Warburg Effect in Cancer Cells: Controlling Cancer as a Metabolic Disease (Asian Pacific Journal of Cancer Biology)

  • Content: Origins and implications of the Warburg effect in cancer.

[16] Metabolic Signature of Warburg Effect in Cancer: An Effective and Obligatory Interplay between Nutrient Transporters and Catabolic/Anabolic Pathways to Promote Tumor Growth (MDPI)

  • Content: How cancer cells reprogram their metabolism for growth.

[17] Function of intramitochondrial melatonin and its association with Warburg metabolism (PubMed, 2025)

  • Content: How melatonin can reduce abnormal energy metabolism in cancer cells by restoring pyruvate entry into mitochondria.

Page created: August 31, 2024

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What you read on I Have Cancer is not a recommendation. Seek competent guidance.

Cancer as a Metabolic Disease – Pathways – Nerdy

Content:

New cancer drugs with metabolic targeting

Now researchers have found a new way to fight cancer cells. They have discovered that when cancer cells can no longer get glutamine, they find another pathway to get the nutrients they need—a new pathway. But researchers can block both the direct pathway and the new ones that cancer cells can use. This can cause cancer cells to starve to death.

Why is this so important?

Because many cancer types, especially when they spread to the brain, are very difficult to treat. By researching how to best block cancer cells’ pathways, researchers hope to develop new and more effective treatments.

Glucose transporter inhibitors

What is it

Glucose transporters are proteins in our cell membranes with an important task. They transport glucose (grape sugar) from the blood into the cells. Glucose is our cells’ primary energy source, and therefore these transporters are crucial for our body to function optimally.

Glucose transporter inhibitors, as the name suggests, are substances that block or reduce the activity of these transporters. By doing this, one can reduce glucose uptake in the cells.

Why inhibit glucose transporters

Cancer

Many cancer cells have an increased need for glucose to grow and divide. By inhibiting glucose transporters in cancer cells, one can potentially slow their growth.

Examples of glucose transporter inhibitors

  • SGLT2 inhibitors: These drugs inhibit a specific type of glucose transporter found in the kidneys. By inhibiting this transporter, more glucose is excreted in the urine, leading to lower blood sugar levels. SGLT2 inhibitors are used in the treatment of type 2 diabetes.

Dietary supplements with similar effects

Although there are no direct inhibitors, certain substances in foods and dietary supplements can indirectly affect glucose metabolism. Examples include:

  • Chromium: This mineral is involved in insulin function and can help the body maintain normal blood sugar levels.
  • B vitamins: Some B vitamins play a role in energy production and can indirectly affect glucose metabolism.
  • Alpha-lipoic acid: This antioxidant can help improve insulin sensitivity.

How they work

These drugs prevent cancer cells from absorbing glucose, their primary energy source.

Examples

GLUT1 inhibitors

Benefits

By limiting glucose supply, cancer cells are forced to use alternative energy sources, which can slow their growth.

Challenges

Normal cells also use glucose, so there is a risk of side effects.

Hexokinase inhibitors

What is it

Hexokinase is a central enzyme in the glycolytic process, where glucose is converted into energy. In cancer cells, hexokinase is often overexpressed, contributing to the so-called Warburg effect. Therefore, hexokinase inhibitors are an interesting target for cancer treatment.

Examples of hexokinase inhibitors:

3-Bromopyruvate

This compound is one of the most studied hexokinase inhibitors. It works by binding to hexokinase and preventing it from functioning properly.

2-Deoxyglucose

This substance is a glucose analog that can inhibit hexokinase. When cancer cells absorb 2-deoxyglucose, they get trapped in an inactive state, as 2-deoxyglucose cannot be metabolized further.

Dietary supplements with similar effects

Several natural compounds, such as:

Hexokinase inhibitors and cancer treatment

Specific for cancer cells

Since hexokinase is overexpressed in many cancer cells, inhibitors of this enzyme can potentially kill cancer cells without harming normal cells.

How they work

Hexokinase is the first enzyme in glycolysis. By inhibiting this enzyme, the first phase of glucose conversion to energy is blocked.

Benefits

Direct attack on the Warburg effect.

Fatal genetic interaction

Combining hexokinase inhibitors with other drugs can exploit lethal synergy, where a combination of two drugs kills cancer cells but not normal cells.

Selectivity

A major challenge is to develop hexokinase inhibitors that are specific to cancer cells and do not affect normal cell metabolism.

Challenges

Hexokinase exists in different isoforms, and specific inhibition of the cancer cell-specific isoform can be challenging.

mTOR inhibitors

What is it

mTOR stands for “mammalian target of rapamycin.” It is a protein that plays a central role in regulating growth, cell division, and survival. When mTOR is hyperactive, it can contribute to the development of various diseases, including cancer.

Effect

mTOR is a central protein that regulates cell growth, proliferation, and survival. By inhibiting mTOR, one can limit cancer cell growth and division.

Benefits
Broad-spectrum effect on several different cancer types.

mTOR inhibitors are drugs that specifically block the activity of mTOR.

By inhibiting mTOR, one can:

Inhibit cell growth

This can be useful in treating cancer, where unregulated cell growth is a hallmark.

Reduce inflammation

mTOR also plays a role in inflammatory processes. By inhibiting mTOR, one can reduce inflammation.

Protect against neurodegenerative diseases

Some studies suggest that mTOR inhibitors may be beneficial in treating neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

How mTOR inhibitors work

mTOR inhibitors work by binding to the mTOR protein and preventing it from sending signals that stimulate cell growth and survival. This leads to cancer cells dying and inflammation being reduced.

Use of mTOR inhibitors

mTOR inhibitors are used in cancer primarily to treat:

Certain types of cancer

For example, renal cell carcinoma, neuroendocrine tumors, and some types of lymphoma.

Examples of mTOR inhibitors

  • Sirolimus (Rapamycin): One of the first mTOR inhibitors developed.
  • Everolimus: Another mTOR inhibitor used to treat various cancer types.
  • Metformin: A well-known mTOR inhibitor primarily used for type 2 diabetes.
    Content: Common diabetes medication with potential anti-cancer properties through mTOR inhibition.

Dietary supplements with mTOR-inhibiting effects

  • Resveratrol: Found in grape skins and other berries. Studies suggest that resveratrol may have an inhibitory effect on mTOR.
  • Curcumin: The active compound in turmeric. Curcumin has shown promising results in reducing inflammation and may potentially affect mTOR.
  • EGCG (epigallocatechin gallate): A powerful antioxidant found in green tea. EGCG has shown anti-cancer properties and may potentially inhibit mTOR.
  • Fish oil: Omega-3 fatty acids in fish oil may have anti-inflammatory properties and potentially affect mTOR.

Challenges

Can have systemic side effects, as mTOR plays an important role in many normal cells.

Fatty Acid Synthase (FAS) inhibitors

What is it
Fatty Acid Synthase (FAS) is an enzyme that plays a central role in the production of fatty acids in our body. Fatty acids are building blocks for cell membranes and are necessary for many biological processes.

FAS inhibitors are substances that block or reduce the activity of this enzyme. By inhibiting FAS, one can reduce the production of fatty acids, which can have several consequences for cells, especially cancer cells.

How they work

FAS is a key enzyme in fatty acid synthesis. By inhibiting FAS, one can limit cancer cells’ ability to produce lipid membranes necessary for cell growth.

Benefits

Can be effective against cancer types with high fatty acid synthesis.

Why are FAS inhibitors interesting?

Many cancer cells have increased FAS activity compared to normal cells. By inhibiting FAS, one can prevent cancer cells from building the fatty acids they need to grow and divide.

How FAS inhibitors work

FAS inhibitors work by binding to the FAS enzyme and preventing it from catalyzing the chemical reactions necessary to produce fatty acids. This leads to an accumulation of intermediate products in the process and can ultimately lead to cell death.

Potential side effects and challenges:

Non-specific effects

Since fatty acids are essential for many cellular processes, inhibiting FAS can also affect normal cells.

Resistance

Cancer cells can develop resistance to FAS inhibitors.

Liver toxicity

Some FAS inhibitors can be harmful to the liver.

Examples of FAS inhibitors

  • Cerulenin: A natural substance that has been used in research but has limited clinical use due to toxicity.
  • Orlistat: Originally developed as a weight loss medication, but has also shown to inhibit FAS.

Dietary supplements with similar effects

Although there are no direct FAS inhibitors as dietary supplements, there are several substances found naturally in foods and supplements that have shown potential to affect fatty acid synthesis:

  • Resveratrol: Found in grape skins and other berries. Resveratrol has shown anti-inflammatory and anti-cancer properties, and some studies suggest it may affect fatty acid synthesis.
  • Curcumin: The active compound in turmeric. Curcumin has a range of health benefits and may potentially affect fatty acid synthesis.
  • Green tea extract: Contains EGCG, a powerful antioxidant that may have a range of health benefits, including potentially affecting fatty acid synthesis.
  • Fish oil: Contains omega-3 fatty acids, which are important for many bodily functions. Some studies suggest that omega-3 fatty acids may have a modulating effect on fatty acid synthesis.

Challenges

FAS also has important functions in normal cells, so there is a risk of side effects.

Glutaminolysis inhibitors

What is it

Glutaminolysis is a biochemical process where the amino acid glutamine is broken down. Glutamine is one of the most common amino acids in the body and plays an important role in many biological processes, including cell growth and energy metabolism.

Glutaminolysis inhibitors are substances that block or reduce the speed of this breakdown process. By inhibiting glutaminolysis, one can affect a number of cellular processes, making these substances interesting in research and potentially also therapeutic.

How they work

By inhibiting enzymes involved in glutaminolysis, one can limit cancer cells’ access to this important energy source and building block.

Benefits

Can be effective against cancer types with high glutamine dependency.

Interesting in cancer treatment

Cancer treatment

Many cancer cells have an increased need for glutamine to maintain their rapid growth. By inhibiting glutaminolysis, one can weaken cancer cells’ energy production and thus inhibit their growth.

How glutaminolysis inhibitors work

Glutaminolysis inhibitors work by blocking the enzymes involved in the breakdown of glutamine. This can happen in different ways, e.g., by binding to the enzyme and preventing it from functioning, or by preventing the enzyme from accessing its substrate (glutamine).

Potential side effects and challenges

Non-specific effects

Since glutamine is such an important amino acid for many cells in the body, inhibiting glutaminolysis can also affect normal cells.

Resistance

Cancer cells can develop resistance to glutaminolysis inhibitors.

Liver toxicity

Some glutaminolysis inhibitors can be harmful to the liver.

Examples of glutaminolysis inhibitors

  • L-asparaginase: An enzyme that breaks down asparagine, another amino acid, but which can also affect glutamine metabolism.
  • 6-diazo-5-oxo-L-norleucin (DON): A synthetic substance that is a potent inhibitor of glutamine synthetase.

Dietary supplements with some effect

Although there are no direct inhibitors, certain substances in foods and dietary supplements can indirectly affect glutamine metabolism. Examples include:

  • Amino acids: Consuming amino acids such as L-glutamine or L-asparagine can affect the balance between different amino acids in the body and thus indirectly affect glutaminolysis.
  • Antioxidants: Substances like vitamin C, E, and selenium can help protect cells from oxidative stress, which may be relevant in connection with cancer and other diseases where glutamine metabolism is disrupted.
  • Herbal extracts: Some herbal extracts, such as green tea extract or curcumin, have shown potential to affect various cellular processes, including cell growth and metabolism.

Challenges

Glutamine is also important for normal cells, so there is a risk of systemic side effects.

Blocking pathways

Here is a chart for blocking pathways, a concept that, among others, Jane McLelland works with to prevent nutrients from reaching the cancer. Here it is shown for glioblastoma, prepared by Ulrik Hedrich Munk. Under each repurposed drug and dietary supplement, you can see the mechanism of action.
To the chart

Combination treatments

A promising strategy is to combine metabolic drugs with other types of cancer treatments, such as chemotherapy, radiation therapy, or immunotherapy. This can increase effectiveness and reduce the risk of resistance.

Conclusion

Research in metabolic targeting of cancer is developing rapidly, and there are high expectations that these new drugs will revolutionize cancer treatment. By understanding the unique metabolism of cancer cells, we can develop more effective and less toxic treatments.

See also: Dietary supplements grouped by effect

See also: Nutrition and Diet

See also: Symptoms

To be continued…

(to menu)

Links

[18] Sensitivity determination and resistance (antibiotics for systemic use) (Medicin.dk)

  • Content: How antibiotic resistance mechanisms can inform cancer treatment strategies.

[19] Cancer as a Metabolic Disease, The Right Way (Carsten Vagn Hansen, DSOM)

  • Content: Danish medical perspective on metabolic cancer treatment.

[20] MicroRNA – small genes with great potential (Videnskab.dk)

  • Content: How microRNAs can be used as biomarkers and therapeutic targets in cancer.

[21] What is a biomarker? (Biotech Academy)

  • Content: Explanation of biomarkers and their role in personalized cancer treatment.

[22] Testing biomarkers in cancer treatment (Kræft og Livet)

  • Content: How biomarker testing guides treatment decisions.

[23] Scientists Discover Unexpected Link Between Diet And Lung Cancer Risk (Science Alert)

  • Content: Research on dietary factors affecting cancer risk.

[24] Sensitivity determination and resistance (antibiotics for systemic use) (Medicin.dk)

  • Content: How antibiotic resistance mechanisms can inform cancer treatment strategies.

[25] MicroRNA – small genes with great potential (Videnskab.dk)

  • Content: How microRNAs can be used as biomarkers and therapeutic targets in cancer.

[26] What is a biomarker? (Biotech Academy)

  • Content: Explanation of biomarkers and their role in personalized cancer treatment.

[27] Testing biomarkers in cancer treatment (Kræft og Livet)

  • Content: How biomarker testing guides treatment decisions.

[28] Scientists Discover Unexpected Link Between Diet And Lung Cancer Risk (Science Alert)

  • Content: Research on dietary factors affecting cancer risk.

[29] Video: The Cancer Doctor: “This Common Food Is Making Cancer Worse!” (The Diary Of A CEO, interview with professor Dr. Thomas Seyfried, YouTube, 2024)

  • Content: Seyfried discusses how common foods may worsen cancer and the importance of metabolic approaches.

Page created: August 31, 2024

❤

What you read on I Have Cancer is not a recommendation. Seek competent guidance.

Cancer as a Metabolic Disease – Biomarkers – Nerdy

Content:

What is a biomarker

A biomarker is a measurable indicator of a biological process. In relation to cancer, it can be a molecule, a cell, or a genetic trait associated with a specific cancer disease or response to treatment.

Why are biomarkers important

Early detection
Some biomarkers can be detected in the blood or other fluids before there are visible symptoms of cancer.

Risk assessment
Biomarkers can help identify people at high risk of developing cancer.

Diagnosis
Biomarkers can confirm a cancer diagnosis and help classify the cancer type.

Prognosis
Biomarkers can provide information about how aggressive a cancer is and how it is likely to develop.

Treatment choice
Biomarkers can help choose the most effective treatment for an individual patient.

Biomarkers in cancer

Tumor markers

Substances produced by cancer cells that can be measured in the blood, such as PSA (prostate-specific antigen).

Genetic mutations

Changes in genes that may be associated with an increased risk of cancer or resistance to treatment.

Proteins

Specific proteins that are overexpressed or underexpressed in cancer cells.

MicroRNA

Small RNA molecules that can regulate gene expression and be involved in cancer development.

Resistance mechanisms in cancer cells

Why does resistance occur?
Cancer cells are genetically unstable and can quickly develop mutations that make them resistant to treatment. This can be due to several factors, including:

Changes in target molecules
Cancer cells can develop mutations in the molecules that a drug is targeted at.

Efflux pumps

Efflux pumps are like small, built-in pumps in a cell that can actively pump various substances, including cancer drugs, out of the cell. It is like a kind of ejection mechanism that helps the cancer cell protect itself from harmful substances. Cancer cells can thus pump drugs out of the cell.

Activation of alternative signaling pathways

Cancer cells can find new ways to survive and proliferate.

Consequences of resistance
Resistance to cancer treatment can lead to relapse and reduced survival.

Strategies to overcome resistance

Combination treatment
By combining different types of treatment, one can reduce the risk of resistance.

New targets

Researchers are working to identify new molecular targets within cancer cell metabolism and signaling pathways.

Personalized medicine

By analyzing a patient’s tumor at the molecular level, one can identify the specific mechanisms behind resistance and thus tailor the treatment.

Biomarkers and resistance

Biomarkers can help us understand why some patients develop resistance to treatment. By identifying biomarkers associated with resistance, we can develop new strategies to overcome this challenge.

Conclusion

Biomarkers have proven to be an indispensable tool in the fight against cancer. By identifying specific molecular changes in cancer cells, we can develop more targeted and effective treatments. Efflux pumps are an example of a mechanism that can limit the effect of cancer treatment, but by combining different treatment strategies and developing new drugs, we can overcome this challenge. The future of cancer treatment lies in individualizing treatment based on the patient’s unique biological profile.

See also: Dietary supplements grouped by effect

See also: Nutrition and Diet

See also: Symptoms

(to menu)

Links

[24] Sensitivity determination and resistance (antibiotics for systemic use) (Medicin.dk)

  • Content: How antibiotic resistance mechanisms can inform cancer treatment strategies.

[25] MicroRNA – small genes with great potential (Videnskab.dk)

  • Content: How microRNAs can be used as biomarkers and therapeutic targets in cancer.

[26] What is a biomarker? (Biotech Academy)

  • Content: Explanation of biomarkers and their role in personalized cancer treatment.

[27] Testing biomarkers in cancer treatment (Kræft og Livet)

  • Content: How biomarker testing guides treatment decisions.

[28] Scientists Discover Unexpected Link Between Diet And Lung Cancer Risk (Science Alert)

  • Content: Research on dietary factors affecting cancer risk.

[29] Video: The Cancer Doctor: “This Common Food Is Making Cancer Worse!” (The Diary Of A CEO, interview with professor Dr. Thomas Seyfried, YouTube, 2024)

  • Content: Seyfried discusses how common foods may worsen cancer and the importance of metabolic approaches.

Page created: August 31, 2024

❤

What you read on I Have Cancer is not a recommendation. Seek competent guidance.