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Understanding Cancer

Table of contents

Reading time 10 minutes

Updated – April 13, 2026

Understanding cancer is the foundation for effective, low-side-effect, and comprehensive holistic therapy.

When mechanisms are conceptually understood and tumor-specific facts are known, targeted therapies can be developed that take all aspects into account, from origin and metastasis to new therapeutic approaches.

What is cancer?

Every cell in the body follows a precise set of rules: it grows, divides, takes on its task, and finally dies in an orderly fashion to make way for new, healthy cells. This regulatory mechanism functions smoothly billions of times daily.
If a cell does not follow these rules, cancer arises at that exact moment.

Mutations in the genetic material

Each of our body cells carries the complete blueprint of life in its nucleus, DNA. deoxyribonucleic acid).
Damage to this DNA is called a mutation. Most of the time, the cell recognizes such errors itself and repairs them, or if the repair mechanism fails, it triggers its own programmed cell death (ApoptosisThis prevents degenerate cells from continuing to divide.

For cancer to develop two types of control genes fail at the same time

  • Proto-oncogene
    are mutated into permanently activated growth engines, like a „gas pedal“ that gets stuck and can no longer be released.
  • Tumor suppressor gene
    (e.g., p53, BRCA1/2) normally represent the „brakes“ on cell growth: if they fail, there is no longer any control and the division process accelerates.

Causes of this damage

CategoryExamplesAffected cancer types
ChemicalsTobacco smoke, asbestos, benzene, alcoholLung, Liver, Bladder, Throat
radiationUV light, X-rays, radonSkin cancer, leukemia
OrganicHPV-Virus, Helicobacter pyloriCervical cancer, stomach cancer
Chronic inflammationCrohn's disease, chronic colitisColon cancer
Genetic predispositionBRCA1/2 mutations, Lynch syndromeBreast, ovarian, bowel cancer
SleeveAccumulated mutations over decadesAlmost all types of cancer

Cancer is not a foreign invader like a bacterium or virus, but rather originates from one's own cells.
The challenges: The immune system must learn to distinguish between a „healthy“ self and a „diseased“ self, and therapies must target tumor cells without destroying healthy cells.

Why Cancer Behaves Like You and Me

This is one of the most fascinating—and terrifying—aspects of cancer biology. Although cancer cells have no will, consciousness, or intention, they are always intent on surviving and spreading.

Natural Selection in Miniature

Charles Darwin described how individuals that are best adapted to their environment can survive and reproduce in nature.
Tumor cells do the same: they mutate randomly, and occasionally a mutation arises that gives the cell a survival advantage by allowing it to divide faster, evade the immune system, and even survive despite oxygen deprivation. This cell dominates and passes its characteristics on to all daughter cells.

The evolutionary biologist Athena Aktipis describes cancer aptly as „old code that becomes active again“Survival strategies that were useful in the unicellular original state of life return in a multicellular organism, where they are harmful.

Normal cell behavior is based on cooperation. Each cell refrains from unchecked growth for the good of the whole organism and adheres to the rules.
But the cancer cell reverts to a primal state: grow, divide, survive – no matter the cost.
You don't fight a mistake, but against the fundamental logic of life itself.

Metastasis – Cancer on the Move

The primary tumor, meaning the original cancer at its site of origin, is usually not the actual problem. Over 90 percent of all cancer-related deaths are not due to the primary tumor, but to its spread to other organs: metastases.

How metastasis develops

  • Local Invasion
    Tumor cells produce enzymesMatrix metalloproteinases) which dissolve the surrounding tissue like a solvent and break out of their original matrix.
  • Entry into the blood
    Tumor cells invade blood or lymphatic vessels and circulate as so-called CTCsCirculating Tumor Cellsin the bloodstream.
  • Survival in the bloodstream
    Most tumor cells die there, but the most resilient survive...
  • Settlement
    Surviving cells leave the bloodstream again, invade a foreign organ, and begin to grow, often after years of waiting.

Metastasis begins when cancer cells detach from the primary tumor, invade surrounding tissues, enter the bloodstream or lymphatic system, and then establish new tumors in distant parts of the body. This process can occur at various stages of cancer development, often when the tumor has grown large enough or has acquired the necessary genetic mutations to facilitate invasion and spread.

Metastasis is not a random process, but is triggered by stress. When the tumor comes under pressure, it sends out „scouts“ (it fears dying and wants to stay alive), which is why it:

  • Oxygen deficiency (hypoxia)
    grows faster than its blood supply, which is why cells that don't get enough oxygen activate escape programs and migrate.
  • Immune assault
    evades the attacking immune system and allows cells to seek refuge elsewhere. Those that survive are the most resistant and therefore even harder to attack.
  • Nutrient deficiency
    seeks out „better“ niches in the body to escape the lack of nutrients.
  • Therapy stress
    rapidly triggers metastatic outbreaks when it is in existential distress due to aggressive chemotherapy.

Tumor cells behave like an organism under pressure: the stronger the attack (e.g., chemo, immune system, nutrient deprivation), the stronger the impulse for survival-essential spread (metastasis).
This explains why the type and intensity of therapy are crucial.

Chemotherapy – Curse and Blessing

Chemotherapy has been the most powerful tool in cancer medicine for decades. It saves lives, but it also has a biologically explainable Achilles' heel that remained underestimated in classical oncology for a long time.

How does classical chemotherapy work?

Chemotherapeutic drugs target a specific characteristic that distinguishes tumor cells from healthy cells: they divide uncontrollably and rapidly.
Chemotherapy agents preferentially kill rapidly dividing cells.
However, many healthy cells in the body also divide rapidly, such as in bone marrow, intestinal lining, hair follicles, and immune cells, which is the cause of well-known chemo side effects, such as hair loss, nausea, and immunodeficiency.

The Problem of Selection

The critical biological flaw in the classical approach lies in its own logic: Maximum dose to kill as many tumor cells as possible. That sounds sensible, but it doesn't take into account the previously described evolutionary dynamics.

  • In the tumor, there is always a small minority of cells that are naturally more resistant.
  • High-dose chemo kills all sensitive cells; only the resistant ones survive.
  • Now competition is missing, which allows resistant cells to spread unimpeded.
  • The next tumor consists almost entirely of resistant cells, making it harder to treat than ever.

Researchers call this effect „Competitive Release“The competition between sensitive and resistant cells, which is eliminated by therapy, leading to an advantage for the resistant cells.

For some cancers, such as testicular tumors, lymphomas, and leukemias, chemotherapy is curative.
The primary problem is its use in advanced solid tumors with maximum-dose protocols, as selection effects often outweigh the intended benefit here.

Fasting as a biological enhancer

One of the most surprising findings in recent cancer research: Short fasting periods of about 9 hours before and during chemotherapy can significantly increase the effectiveness of the treatment while protecting healthy cells.

The Principle - Differential Stress Resistance

It sounds contradictory at first. The researcher Valter Longo (University of Southern California) has described it in contrast as:

Healthy cell during fasting
– switches to standby mode
– cell division stops
activates repair programs
becomes less sensitive to chemotoxic agents
– recovers quickly after fasting		Tumor cells during fasting
can't stop growing
– remains active and willing to divide
– has no protection mode
– becomes even more vulnerable for chemo
– cannot compensate for fasting stress

This asymmetrical effect is scientifically proven. In the randomized Phase 2 study DIRECT (de Groot, Longo et al., Nature Communications 2020) with 131 breast cancer patients, it was shown that:
An FMD (Fasting-Mimicking Diet – calorie-reduced plant-based diet), which puts the body into fasting mode, increased the probability of complete or extensive tumor destruction from 90-100% threefold to fourfold compared to a normal diet.

source:

What happens after fasting – when healthy cells „wake up“?

Healthy cells wake up after nutrient intake, while tumor cells were damaged by chemotherapy and recover more slowly. During this time window, the body has its advantage and can reactivate its strengthened immune system:

  • Immune rejuvenation
    Fasting induces autophagy, where cells break down old, dysfunctional immune cells, leading to the creation of new, fresh cells after refeeding. T-cells and NK cells (natural killer cells), which can react more aggressively to tumor cells.
  • Normalization of the environment
    IGF-1 (a growth hormone) and insulin levels decrease, both of which are conducive to inhibiting tumor growth because autophagy is promoted. After fasting, these values remain temporarily low.
  • No more stress signal
    Healthy cells no longer send out stress signals that could cause tumor cells to metastasize.

Adaptive Therapy – Paradigm Shift

Robert Gatenby, Researchers at Moffitt Cancer Center in Tampa (Florida), a heretical question arose: What if the goal wasn't to destroy the tumor, but to control it?

Not to exterminate the enemy, but to rule them.

In classical strategy, one fights with maximum force until the tumor is defeated or resistant cells take over. Gatenby suggests something else: The tumor cells are granted the state of a stable, controlled tumor, in a manageable equilibrium.

The logic behind it: Sensitive and resistant cancer cells compete for resources within the tumor. Sensitive cells are more numerous and fitter, as long as they are not eradicated (by high-dose chemotherapy pulses). If you pause a lower-dose chemotherapy treatment when the tumor shrinks, sensitive cells remain alive and keep the resistant ones in check. The tumor remains, but has no incentive to grow and is thus under control.

Clinical Study Results – Moffitt Cancer Center
In a pilot study (Nature Communications 2017 and eLife 2022 (NCT02415621)) with 17 patients with metastatic prostate cancer, Abiraterone (a hormone therapy drug) not given continuously, but only when the Public Service Announcement-value (a tumor marker) increased, paused when it sufficiently decreased.
After more than six years of observation, the convincing result:

  • Median Time to Progression
    33.5 months (vs. 14.3 months with standard therapy)
  • Cumulative drug dose
    um about 60% reduced
  • Advantage
    Every patient in the control group benefited from the adaptive therapy according to the model.

Sources:

The Evolutionary Double Bind – Research 2026

Another groundbreaking discovery from Moffitt Cancer Center from February 2026
When cancer cells develop resistance to radiation therapy, they change their surface. This makes them vulnerable to natural killer cells (NK) is highly vulnerable to the immune system. Resistance to one therapy makes it vulnerable to another. This strategy is called an „evolutionary double bind.“.

Metronomic chemotherapy

Another alternative to the maximum dose approach: low-dose, continuous chemotherapy, the so-called. metronomic chemotherapy.
Instead of high doses at long intervals (which grant the tumor regeneration breaks), a drug is administered permanently in small amounts.

The mode of action is different here: the tumor cells themselves are not primarily attacked, but rather the blood vessels that supply the tumor.
These endothelial cells are genetically more stable than tumor cells, as they develop hardly any resistance. At the same time, metronomic chemo activates the immune system, instead of damaging and suppressing it like high-dose chemo.

 High-dose chemotherapy (MTD)Metronomic chemo
doseMaximum tolerable1/10 to 1/3 of the MTD
RhythmEvery 2–4 weeks, then a breakDaily or several times a week
Main goalTumor cells directlyTumor blood vessels + immunomodulation
Resistance riskHigh (Selection)Significantly lower
Side effectsHeavy to severeMostly mild
Metastasis riskCan be elevatedIn studies, reduced

source:

Which clinics offer metronomic chemotherapy?

The following are exclusively non-private clinics. The reason:

All German hospitals with statutory health insurance accreditation are legally obliged to publish annual quality reports., whose statements are more reliable in case of doubt than marketing statements on the websites of private practices or clinics. 

In these public reports, objective data can be found on Treatment frequency (Number of cases per year) and interdisciplinary collaboration determine crucial indicators of a clinic's expertise. Additionally, for those with public health insurance, access to modern therapy standards, scientific studies and specialized outpatient clinics in these facilities directly and without additional cost.

  • UKE Hamburg – University Cancer Center (UCCH)
    II. Medical Clinic – East Building 43, Ground Floor or O24
    Martinistraße 52 – 20246 Hamburg
    +49 (0) 40 7410-52960
    a.darimont@uke.de
  • St. Georg Clinic
    Rosenheimer Straße 6-8 – 83043 Bad Aibling
    +49 (0) 80 61-398-0
    info@clinicum-stgeorg.de
  • University Hospital Regensburg (UKR)
    Franz-Josef-Strauß-Allee 11 – 93053 Regensburg
    +49 (0) 941 944-00941 / +49 (0) 941 944-4488
    info@ukr.de

Sleeping metastases – awaken and eliminate

One of the most dangerous and simultaneously fascinating phenomena in cancer biology: metastatic cells often migrate to distant organs years or decades before their clinical appearance and remain dormant there.Tumor sleep or dormancybarely share, slow down their metabolism, and thus make themselves invisible and unattainable for most therapies.

This explains why some patients are considered „cured“ but develop metastases ten years later.

What keeps her in her sleep – what wakes her up?

While sleeping, she
an intact immune system
– an unfavorable microenvironment
(the environment of a tumor cell)
– missing growth signal
– lack of blood supply  		They are awakened by
– Immunosuppression (Stress, Age)
chronic inflammation
– surgical procedures
– some chemotherapies  

Trigger apoptosis in sleeping cells

Apoptosis, programmed cell death, functions perfectly in healthy cells. Cancer cells have learned to bypass this protective mechanism. It is particularly strongly blocked in dormant metastatic cells. Science now knows the exact molecular locks and is searching for keys:

BCL-2/BAX Balance – Mitochondrial Death Switch

Every cell contains proteins that induce deathBAX – Associated X, Apoptosis Regulator, BAK - BCL2 Homologous Antagonist/Killer) and those who want to prevent it (BCL-2 – B-cell lymphoma 2, BCL-xL - B-cell lymphoma-X large).
In healthy cells, balance prevails. In cancer cells, especially dormant ones, survival proteins dominate.BCL-2clearly.
Active ingredients, which BCL-2 inhibit, tilt this balance towards apoptosis. The drug Venetoclax is already clinically approved and works exactly like that.

TRAIL-Way – the external death knell

The immune system can also instruct cancer cells to die from the outside, using the signaling molecule TRAIL (Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand), which binds to specific „death receptors“ on the cell surface, thereby triggering the apoptosis cascade.
Dormant cells often downregulate these receptors, but can be reactivated by so-called. Sensitizer they can be made accessible again by intervening in intracellular signaling pathways. Key classes of these sensitizers include signaling pathway inhibitors, potassium channel inhibitors, and Bcl-2 inhibitors.

Autophagy Inhibition - Turning Off the Power to the Sleeper

Dormant cancer cells use autophagy, cellular self-digestion, as an energy source while in a resting state. Inhibiting this process causes them to lose their most important survival strategy and become susceptible to apoptosis. Chloroquine (a well-known antimalarial drug) is being investigated in combination with other therapies.

source:

Medicinal mushrooms and natural substances as adjuvant active ingredients

This is where Huaier mushroom and Reishi come into play, two traditional medicinal mushrooms that were long scoffed at in Western medicine but have now demonstrated well-documented molecular mechanisms of action.

Huaier (Trametes robiniophila Murr)

Huaier is a sand-beige mushroom that has been used in traditional Chinese medicine for over 1,600 years. While the Chinese drug regulatory authority has approved it as a cancer medication, it holds the status of a dietary supplement in the EU. What's behind this?

  • BCL-2/BAX axis
    Huaier extract lowers BCL-2 (Survival signal) and increased BAX (Death signal), exactly the same mechanism that the drug Venetoclax uses. Additionally, Caspase-3 activates the execution enzyme of cell death.
  • p53 activation
    Huaier activated p53, the most important tumor suppressor gene that initiates cell self-destruction.
  • Immunomodulation
    Huaier increases CD4+ T cells Surface marker CD-4) and NK cells, both main weapons of the immune system against tumor cells.
  • Anti-metastasis
    Huaier inhibits the enzymes (matrix metalloproteinases) that break down tissue, thus creating space for tumor cells to spread.
  • Anti-angiogenesis
    Huaier inhibits the formation of new blood vessels towards the tumor, thereby weakening its lifeline.

Clinical Evidence for Huaier:
Systematic Review (2023, PubMed): Of 39 clinical studies with 12 different mushroom preparations, Huaier was the only preparation to show a clear survival advantage, in two liver cancer studies and one breast cancer study.

source:

Reishi (Ganoderma lucidum)

Reishi has been known in East Asia for millennia as the „mushroom of immortality.“ Recent research has identified its molecular fingerprint:

  • Mitochondrial pathway
    How Huaier attacks Reishi BCL-2/BCL-xL-Proteins and increases BAX/BCL-2-ratio and promotes cell death.
  • NF-κB inhibition
    NF-κB is a central survival switch in tumor cells. Reishi effectively inhibits it, making tumor cells more susceptible to apoptosis.
  • MMP-9 inhibition
    Reishi reduces MMP-9, an enzyme that tumor cells need for invasion and metastasis.
  • Selectivity
    Reishi does not damage healthy cells (e.g., breast epithelium) in studies; only tumor cells showed reduced viability.

source:

Overview of Further Adjuvant Natural Products

SubstancesourceMechanism of actionEvidence
QuercetinOnions, capers, applesInhibit PI3K/AKT, BCL-2↓, BAX↑, Caspase-3↑Pre-clinically strong
CurcuminTurmericNF-κB↓, mTOR↓, p53 activationWell pre-clinical, bioavailability problematic
EGCGGreen teaPI3K/AKT/mTOR↓, Apoptosis InductionPreclinically proven
BerbetinBarberry plantAMPK activation, mTOR↓, mitochondrial pathwayGrowing clinical data
ArtemisinMugwort (TCM)ROS induction, ferroptosis inducer, NF-κB↓Preclinically very active
PSK (Polysaccharide-K)Corilous mushroomImmunomodulation, T-cell activationClinically proven (Adjuvant gastric cancer)

Intelligent overall strategy instead of attack

All the insights presented in this guide come together to paint a picture: The classic approach—maximizing attacks on an evolutionarily adaptable adversary—is often not the wisest strategy. The more modern perspective treats cancer as a dynamic system that must be intelligently managed if one wishes to overcome it.

The new paradigm emerges from a fundamental shift in understanding. It challenges established norms and opens up novel possibilities. This transformation redefines our approach to complex systems and their interdependencies. Ultimately, it paves the way for innovative solutions and a more integrated perspective.
1. Not destroy, but control
Adaptive therapy keeps sensitive tumor cells alive to keep resistant ones in check.

2. Don't attack, but change the conditions
– FMD, metronomic therapy, and metabolic interventions alter the tumor microenvironment without triggering massive selection pressure.

3. The Immune System as the Mightiest Weapon
– Immunotherapy, immune rejuvenation through fasting, and NK cell activation by medicinal mushrooms are more effective in the long term than external chemotoxic agents.

4. Do not awaken dormant metastases
– but to maintain the conditions that allow them to sleep:
a strong immune system, low inflammation, and IGF-1 levels.

Practical framework – what makes sense as an adjuvant?

All natural substances and dietary approaches described here are complementary measures. They do not replace medical treatment, but can be useful as supportive therapy when coordinated with the treating oncologist.

  • FMD cycles
    (3-5 days of calorie reduction before chemotherapy) to protect healthy cells and increase tumor sensitivity
    DIRECT study shows 3–4 times higher remission rates
  • Huaier granules
    BCL-2 inhibition, immunomodulation, anti-metastasis
  • Reishi extract
    BCL-2/BCL-xL inhibition, NF-κB blockade, selectively toxic to tumor cells
  • EGCG (Green Tea Extract) + Quercetin
    Synergistic effect on the PI3K/AKT/mTOR pathway
  • Ketogenic or Low-Glycemic Diet
    Permanently lowers IGF-1 and insulin, unfavorably altering the metabolic environment for tumor cells without triggering acute stress
  • Regular exercise
    Lowers IGF-1, reduces chronic inflammation, strengthens NK cell activity, one of the best-documented adjuvant effects ever.

This guide summarizes the state of research as of 2025/2026. It is for informational purposes only and does not replace medical advice. All therapeutic decisions should be discussed with a qualified oncologist, as should the aforementioned adjuvant measures, such as medicinal mushrooms, FMD, and dietary interventions, to avoid potential interactions with ongoing therapies.

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