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Diseases

Cancer — are acidification and weak collagen the key that oncologists are silent about?

Sources: 10 · Article: 13 153 characters

Hubert Czerniak claims that acidification of the body and weakened collagen may promote cancer development and its spread.

  • He also points to the small amount of funding allocated to collagen research.
  • Prof. Klaus F. Kopp links the acidic environment of cancer cells with their growth, but these claims do not prove that oncologists are generally silent about this topic.

What the authors write

Hubert Czerniak

Acidification of the body and weakened collagen structures are presented as factors that may make tumor development easier.

„The first point is acidification of the body, and the second is weakened collagen structures, through which cancer cells can easily infect other healthy tissues, that is, grow. Only a small amount of funding is allocated to research on collagen structures, even though metastases from cancerous tumors are the cause of death for people with cancer.”Pierwszym punktem jest zakwaszenie organizmu, a drugim- osłabione struktury kolagenowe, przez które komórki rakowe łatwo infekują kolejne zdrowe tkanki, czyli rozrastają się. Jedynie niewielkie środki finansowe przeznacza się na badania nad strukturami kolagenowymi, a przecież przerzuty guzów nowotworowych są przyczyną śmierci osób cierpiących na raka.
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Hubert Czerniak

Metastases are presented as a phenomenon that strong collagen can prevent, while poor-quality collagen is said to make cancer spread more easily.

„Similarly, in the case of cancer, the formation of metastases is blocked by strong collagen. If collagen is of poor quality, its structure becomes inconsistent. Uneven surfaces form, where blood cells can gather and create clots, which can then cause thrombotic or embolic events.”Podobnie w przypadku nowotworów – powstawanie przerzutów blokowane jest przez mocny kolagen. Jeżeli kolagen jest słabej jakości, dochodzi do niespójności w jego strukturze. Powstają nierówne powierzchnie, na których mogą gromadzić się krwinki, tworzące zakrzepy, które następnie mogą wywoływać incydenty zakrzepowo/zatorowe.
Kolagen – „klej życia”i zdrowia o potężnejsile działania
Hubert Czerniak

The statement points to the small amount of funding allocated to research on collagen structures.

„Only a small amount of funding is allocated to research on collagen structures, even though metastases from cancerous tumors are the cause of death for people with cancer. The growth of a tumor can cause death in the case of a brain tumor, when the enlarging structure presses on the brain and disrupts its role in controlling vital processes.”Jedynie niewielkie środki finansowe przeznacza się na badania nad strukturami kolagenowymi, a przecież przerzuty guzów nowotworowych są przyczyną śmierci osób cierpiących na raka. Rozwój guza nowotworowego może być przyczyna śmierci w przypadku guza mózgu, gdy powiększająca się struktura uciska na mózg, zaburzając jego pracę sterującą procesami życiowymi.
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Prof. Klaus F. Kopp

The acidic environment of cancer cells is described as promoting their growth, while chronic acidification may possibly promote the development of cancer.

„It is established that in malignant tumors, the cellular environment is distinctly acidic; that is, malignant cells proliferate best in an acidic environment and less well in a basic one (the Otto H. Warburg hypothesis). It is therefore conceivable that a chronically acidic environment promotes so-called carcinogenesis, or the development of cancer, while a basic environment inhibits it.”Gesichert ist, dass bei Malignomen das zelluläre Milieu deutlich sauer ist, d.h. die Malignom-Zelle proliferiert am besten in einer sauren Umgebung und weniger gut in einem basischen Milieu (Otto H. Warburg Hypothese). Daher ist denkbar, dass in einem chronisch sauren Milieu die sog. Carcinogenese, d.h. die Krebsentstehung begünstigt und in einem basischen Milieu gehemmt wird.
Das Bikarbonat-Mangel-Syndrom (BDS): Professor Dr. med. Klaus F. Kopp
Prof. Klaus F. Kopp

The statement links the acidic environment of cancer cells with their growth and suggests that it may weaken the mechanism that removes newly arising cancer cells.

„In malignancies, the cellular environment is rather acidic, and malignant cells proliferate best in an acidic environment (the Otto H. Warburg hypothesis). It can also be assumed that the formation of malignant cells is favored in an acidic environment and inhibited by alkalosis. Observations of vegetarians may support this assumption. Immunosurveillance, which is responsible for eliminating malignant cells, may not function optimally if the environment is acidic.”In malignancies the cellular milieu is rather acid and malignant cell proliferate best in an acidotic surrounding (Otto H. Warburg Hypothesis). It can also be assumed, that the formation of malignant cells is favoured in an acid milieu and is inhibited by alcalosis. Observation from vegetarians may support this assumption. Immunosurveillance which is responsible for the elimination of malignant cells may not function at optimum if the milieu is acidotic.
The Bicarbonate-Deficiency-Syndrome (BDS): Professor Dr. med. Klaus F. Kopp
M. Williamson i N. Moustaid-Moussa i L. Gollahon

The acidic environment outside cancer cells has been linked to their invasiveness and drug resistance.

„Increased filopodia were found in metastatic HMECs, driven by extracellular acidosis, contributing to invasiveness (). Extracellular acidosis contributes to tumor drug resistance by providing a protective mechanism that degrades drugs before they are taken up by the cell ().”Increased filipodia was found in metastatic HMECs, driven by extracellular acidosis, contributing to invasiveness (). Extracellular acidosis contributes to the drug resistance of tumors providing a protective mechanism by degrading the drugs before they are taken up by the cell ().
Frontiers | The Molecular Effects of Dietary Acid Load on Metabolic Disease (The Cellular PasaDoble: The Fast-Paced Dance of pH Regulation)
M. Williamson i N. Moustaid-Moussa i L. Gollahon

The acidic external environment is also presented as one in which cancer cells can grow while adapting their activity to it.

„The Warburg effect suggests that cancer cells preferentially grow in an acidic extracellular environment. Tumor cells adapt to and manipulate their environment by continuously expelling acids and protons into the extracellular space (). Metabolic adaptation enables cancer cells to restore intracellular pH balance, allowing them to survive.”The Warburg effect suggests that cancer cells preferentially grow in an acidic extracellular environment. Tumor cells adapt to, and manipulate, their environment by continuously extruding acids and protons into the extracellular space (). Metabolic adaptation facilitates the ability of cancer cells to regain intracellular pH homeostasis, allowing survival.
Frontiers | The Molecular Effects of Dietary Acid Load on Metabolic Disease (The Cellular PasaDoble: The Fast-Paced Dance of pH Regulation)
Prof. Klaus F. Kopp

The statement says that patients undergoing chemotherapy had severe acidosis, and that bicarbonate was used to limit some side effects of treatment.

„The author's scientific experience and measurements have shown that patients undergoing chemotherapy are severely acidotic. Bicarbonate supplementation was able to neutralize and prevent the severe side effects of chemotherapy, such as nephrotoxicity leading to acute kidney failure and dialysis.”Scientific experience and measurements of the author have shown, that patients undergoing chemotherapy are severely acidotic. Supplementation with bicarbonate was able to neutralize and avoid the severe side-effects of chemotherapy, e.g. nephrotoxicity leading to acute renal failure and dialysis.
The Bicarbonate-Deficiency-Syndrome (BDS): Professor Dr. med. Klaus F. Kopp

Research from PubMed · Europe PMC

We selected 5 studies with the best, positive results. This is a selection, not a full review of all research.

Total number of studies on this topic in PubMed: 12.

The review describes how the acidic tumor environment may promote tumor growth, invasion, and metastasis.

Aim of the study: The acidic microenvironment (AME) is a defining metabolic feature of solid tumors that fundamentally reshapes tumor-stroma interactions. Tumor acidosis arises from multiple metabolic processes, including hypoxia-driven glycolysis in poorly vascularized regions, the Warburg Effect (WE) in well-perfused areas, and carbon dioxide accumulation from tumor respiration.

Results: In response, cancer and stromal cells must adapt through the selection of pre-existing phenotypic diversity or acclimate through phenotypic plasticity that enables rapid, non-genetic changes of state. AME influences all stromal components, including fibroblasts, macrophages, extracellular matrix proteins such as collagen and fibronectin, and the broader metabolic habitat, thereby remodeling the tumor niche. Through these adaptive processes, acidosis drives stromal reactivity, niche construction, and reciprocal crosstalk that promote tumor growth, invasion, and metastasis. This review highlights AME as an ecological force governing cancer-stroma symbiosis and proposes mathematical modeling as a systems-level tool to examine the dynamic and nonlinear interactions that shape the tumor ecosystem and its evolution.

Symbiotic cancer cell-stroma crosstalk in the acidic tumor microenvironment. · J Evol Biol 2026
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

In laboratory models, an acidic environment increased enzyme activity and the breakdown of collagen IV, which was linked to tumor invasion.

Aim of the study: One of the noncellular microenvironmental factors that contribute to malignancy in solid tumors is acidic peritumoral pH. We have previously demonstrated that extracellular acidosis leads to the localization of the cysteine protease cathepsin B on the tumor cell membrane and its secretion.

Results: At pHe 6.8, there were increases in pericellular active cysteine cathepsins and in the degradation of dye-quenched collagen IV, which was partially blocked by a cathepsin B inhibitor. Imaging probes for active cysteine cathepsins localized to tumors in vivo. The amount of bound probe decreased in tumors in bicarbonate-treated mice, a treatment previously shown to increase peritumoral pHe and reduce local tumor invasion. Our results are consistent with the acid-mediated invasion hypothesis and with a role for cathepsin B in promoting the degradation of a basement membrane protein substrate, namely type IV collagen, in an acidic peritumoral environment.

Acid-mediated tumor proteolysis: contribution of cysteine cathepsins. · Neoplasia 2013
Money for the studygovernment, public institutions · NCI NIH HHS, National Institutes of Health, National Institute of Child Health and Human Development
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyanimal study

“Not stated” does not mean nobody paid — the database does not always record it.

In a study of pancreatic cancer cells, adaptation to an acidic environment increased some traits associated with cancer aggressiveness.

Aim of the study: Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive malignancy with minimal treatment options and a global rise in prevalence. PDAC is characterized by frequent driver mutations including KRAS and TP53 (p53), and a dense, acidic tumor microenvironment (TME).

Results: Akt and Transforming growth factor-β (TGFβ) signaling, as well as expression of the Na+/H+ exchanger NHE1, were increased by acid adaptation. Whereas Akt inhibition decreased spheroid growth regardless of treatment and genotype, stimulation with TGFβI increased growth of WT control spheroids, and inhibition of TGFβ signaling tended to limit growth only under acidic conditions. Our results indicate that complex crosstalk between tumor acidosis, ECM composition, and genotype contributes to PDAC development. The findings may guide future strategies for acidosis-targeted therapies.

Crosstalk between tumor acidosis, p53 and extracellular matrix regulates pancreatic cancer aggressiveness. · Int J Cancer 2023
Money for the studygovernment, public institutions · Danish Cancer Society, Novo Nordisk Foundation, European Union
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studylaboratory study (on cells)

“Not stated” does not mean nobody paid — the database does not always record it.

The study suggests that precancerous cells may produce collagen that helps them survive acidic conditions.

Aim of the study: Growing tumors are dynamic and nonlinear ecosystems, in which cancer cells adapt to their local microenvironment, and these adaptations further modify the environment, causing more changes. From early intraductal neoplasms to disseminated metastatic disease, several levels of evolutionary adaptation and selection occur.

Results: Subsequent experiments in 3D culture, spinning-disk microscopy, and second-harmonic generation microscopy of DCIS lesions in patient samples are consistent with these findings. A collagen production assay using acid-adapted cells in vitro showed that the induction mechanism involves the RAS and SMAD pathways. Secretome analyses show increased expression of ECM-remodeling enzymes such as TGM2 and LOXL2, which cross-link collagen. These data strongly indicate that acidosis in early cancers induces collagen production by cancer cells and support the hypothesis that this adaptation initiates a tumor-permissive microenvironment that promotes the survival and growth of early cancers.

Collagen production and niche engineering: A novel strategy for cancer cells to survive acidosis in DCIS and evolve. · Evol Appl 2020
Money for the studygovernment, public institutions · NCI NIH HHS
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studylaboratory study (on cells)

“Not stated” does not mean nobody paid — the database does not always record it.

The review indicates that remodeling of the collagen network may make it easier for cancer cells to invade.

Aim of the study: The tumor microenvironment (TME) is composed of various cell types embedded in an altered extracellular matrix (ECM). The ECM not only provides support for tumor cells but also regulates cell-cell and cell-matrix interactions.

Results: Collagen network reorganization facilitates tumor cell invasion. Proteoglycan expression and location are modified in the TME and affect cell invasion and metastatic dissemination. ECM macromolecule degradation by proteases may induce the release of angiogenic growth factors, as well as proteoglycan-derived or ECM protein fragments called matrikines or matricryptins. This review focuses on current knowledge and new insights into ECM alterations, degradation, and reticulation through cross-linking enzymes, as well as the role of ECM fragments in controlling cancer progression and their potential use as biomarkers in cancer diagnosis and prognosis.

Tumor Microenvironment: Extracellular Matrix Alterations Influence Tumor Progression. · Front Oncol 2020
Money for the studygovernment, public institutions · Centre National de la Recherche Scientifique (UMR 7369), University of Reims Champagne-Ardenne, Region Grand-Est
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

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