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The Cancer Metastases Research Fund is a 501 c (3) non-profit organization.

Your donations are tax deductible in the USA (Tax ID: 87-3870404). 100% of your contributions will go to research.

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What is the Cancer Metastases Research Fund?

After trillions of dollars invested trying to solve the global cancer burden, too little progress has been made, and too few lives have been saved. Standard treatments like chemotherapy and radiation are symptomatic, rarely prevent cancers from spreading, and often result in a poor quality of life in survivors. Newer approaches, like immunotherapy and gene therapy, have proven problematic and are seldom curative, despite the hype surrounding them.

The Cancer Metastases Research Fund (CMRF) builds on years of carcinogenesis research to present an opportunity to explore a new paradigm, one that aims to block primary cancers from spreading (metastases) and potentially prevent them from forming in the first place.

Who are We?

Ijaz S Jamall and Björn LDM Brücher are Fellows of Theodor-Billroth-Academy®, and its International Consortium of Research Excellence (INCORE), the Royal Society of Biology, and Ijaz Jamall the Royal Society of Medicine. In 2014, Jamall and Brücher published a new paradigm of how cancers originate. This was followed by 14 peer-reviewed papers that explain in detail how their paradigm would help prevent cancers and block or reverse the metastases of solid cancers.

Both scientists were elected in 2019 to the European Academy of Science and Arts (EASA, Academia Scientiarum et Artium Europaea) due to their contribution to cancer research.  Among the approximately 2,000 members of the Academy worldwide, there are 34 Nobel Prize Laureates. Known EASA members (Nobel Prize and year) are Michail Gorbatschow (Nobel Peace Prize 1990), Sir Richard Timothy Hunt (Physiology/Medicine 2001), Harald zur Hausen (Physiology/Medicine 2008), Thomas Südhof (Physiology/Medicine 2013), Fraser Stoddart (Chemistry 2016), and Emmanuelle Charpentier (Chemistry 2020). Jamall and Brücher are among a handful of scholars who deal with issues relevant to cancer research in an interdisciplinary and cross-border manner.

Dr Ijaz Jamall received his B.S. in Toxicology from St. John’s University in New York. He obtained his Ph.D. from the University of Cincinnati College of Medicine, and was hired as an Assistant Professor at St. John’s University. He was granted tenure and promoted to Associate Professor. Jamall also held the rank of Associate Clinical Professor (Volunteer Clinical Faculty) at the University of California-Davis School of Medicine in Internal Medicine. Since 2007, Dr. Jamall has served pro bono as the Clinical Research Director for the Xeroderma Pigmentosum Family Support Group in the USA. This is a genetic disease where children develop skin cancers from exposure to sunlight as their DNA repair enzymes are defective. Dr. Jamall has been studying the role of inflammation and fibrosis in diseases for decades. He ranks in the 97th percentile of all scientists worldwide ( His focus, in collaboration with Dr. Brücher, has been in oncology with an emphasis on the roles of inflammation and fibrosis in cancer and how these processes affect the initiation and progression of most cancers and promote metastases.

Professor Björn Brücher received his medical degree (MD) from Johannes Gutenberg University Mainz and completed residencies at University of Oxford and Bradford College. He earned his Ph.D. in 2001 in clinical and molecular biology from the TUM and the Helmholtz Centre in Munich in 2003. He did a stint at the MD Anderson Cancer Center, in Houston, Texas, USA. Brücher led the cancer surgery team at the University Hospital in Tübingen from 2007 to 2012. In 2008, he was appointed Professor of Surgery, founded the Theodor Billroth Academy and co-founded in 2013 its international consortium for scientific excellence (INCORE). Professor Brücher received numerous national and international awards including the Karl-Heinrich-Bauer Cancer Research Award and the prestigious Theodor-Billroth-Award by the Austrian Society of Surgery. He is a Fellow of the American College of Surgeons (F.A.C.S.), and a Fellow of the Royal College of Surgeons of England (F.R.C.S. Engl.). In 2012 he received honorary membership of the Israeli Society of Surgical Oncology (ISSO). Professor Brücher serves as ambassador of the European Association of Cancer Research (EACR) since 2013 and as one of the Leading Physicians of the World – “Top Surgical Oncologist, Cancer Patient Care & Research Specialist” by ‘The International Association of Oncologists’ in 2014. He was invited as an expert of the American Joint Cancer Committee (AJCC) for the new cancer classification system. He is a founder and Editor in Chief of 4open, an open access journal. He now serves as Deputy Chair at the Department of Surgery, Carl-Thiem-Klinikum in Cottbus, Germany. Brücher serves the entire spectrum of general and cancer surgery and is an expert in the field of tumors of the digestive tract and in research on carcinogenesis and metastases.

The Problem

The Cancer Metastases Research Fund was created in recognition of some troubling realities about the long-labeled “war on cancer.” Despite trillions of dollars invested over the past 50+ years into cancer research, cancer remains one of the leading causes of death worldwide. Although we can now prevent a small fraction of cancers, such as HPV-caused cervical cancer and hepatitis B-caused liver cancer with vaccines, we don’t know how to prevent the formation of most cancers, nor do we know how to keep them from spreading to other parts of the body – the deadly process we know as metastasis.

Cancers today are widely believed to occur as the result of mutated genes and the body’s inability to stop the aberrant cell growth, leading to cancer’s rampant invasion of other cells and potential spread. Thus far, only some 5%-8% of all solid cancers have been shown to have a genetic origin. An additional 10% are known to be caused by viruses, but the remaining 80+% are termed “sporadic” which simply means we do not know what causes these cancers. How can we treat these cancers if we do not know what causes them?

Cancer Hypothesis (Epistemology of the origin of cancer)

Based on observations and experimental findings in plants, animals, and humans, we proposed a new paradigm for the origin of most cancers. It involves a six-step pathway:

Pathogenic stimulus. Cancers begin with a biological or chemical stimulus that leads to inflammation, in response to which the affected tissue takes defensive measures to heal.   When the inflammation cannot be resolved, this leads to chronic inflammation.

Chronic Inflammation. Inflammation is usually a normal process during healing and usually resolves itself when an infection is over or an injury is repaired. This healing process is unsuccessful when the stimulus and inflammation are too great or too prolonged and the inflammation becomes chronic. Here, the disruption that occur in biochemical and physiological processes are complex, but this same complexity provides many opportunities to block some of these pathways. If chronic inflammation persists, it can cause fibrosis.

Fibrosis. Fibrosis is a process similar to scar formation where cells called fibroblasts grow and form thick fibrous tissue. A product of collagen accumulation with remodeling of healthy tissue by incessant inflammation, fibrosis drastically changes the cellular microenvironment affected and results in formation of the precancerous niche.

Pre-cancerous Niche (PCN). This can be thought of as a kind of nest of collagen and elastin fibers that is a product of an altered cellular environment (fibrosis) and accompanying changes in the levels of biochemical signaling molecules can lead to a precancerous state.

Chronic Stress Escape Strategy (CSES). In response to the disruption, the human body employs a chronic stress escape strategy to return cellular functions to normal (a process called homeostasis). If successful, cancer does not develop. If the body’s attempts to escape this situation prove ineffective, then the affected cells may transition into cancer cells.

Normal Cell to Cancer Cell Transition (NCCCT). If the chronic stress escape strategy fails, the cells will transition from healthy to malignant, a process mediated by enzymes and a host of consequent signaling abnormalities.

Our Hope

The Cancer Metastasis Research Fund will support studies of the development and spread of cancer. Our goal is to transform cancer research from a symptom-orientated approach to a cause-based approach. By this, it is not only the intent to buy time for patients but to block the very mechanisms that lead to cancer progression, and even its very formation. Our hope is to develop affordable therapies that make the scourge of cancer and its metastasis a thing of the past.

The Cancer Metastases Research Fund is a 501 c (3) non-profit organization.

Your donations are tax deductible in the USA (Tax ID: 87-3870404). 100% of your contributions will go to research.

Open Access Peer-Reviewed Cancer Paradigm Publications

CONCEPT 1 (defined 2012, realized 2014-2016)

  1. (2014) Epistemology of the origin of cancer: a new paradigm, BMC Cancer 14(186), 1-15.
    Website / DOI:
  2. (2014) Cell-Cell communication in tumor microenvironment, carcinogenesis and anticancer treatment, Cell Physiol Biochem 34(2), 213-243.
    Website / DOI:
  3. (2014) Imagine a World without Cancer, BMC Cancer 14(186), 1-8.
    Website / DOI:
  4. (2016)‎ Somatic Mutation Theory: Why it’s Wrong for Most Cancers, Cell Physiol Biochem 38(5), 1-18.
    Website / DOI:
  5. (2016) Genomics, microRNA, epigenetics, and proteomics for future diagnosis, treatment and monitoring response in upper GI cancers. Clin Transl Med 5(1), 1-16.
    Website / DOI

    CONCEPT 3 (defined 2012, realized 2019) Key Summaries

  6. (2019) Prelude and Premise to the Special Issue, 4open 2(6), 1-8.
  7. (2019) Undervalued ubiquitous proteins, 4open 2(7), 1-13.
  8. (2019) Chronic inflammation evoked by pathogenic stimulus during carcinogenesis, 4open 2(8), 1-22.
  9. (2019) Eicosanoids in carcinogenesis, 4open 2(9), 1-34.
  10. (2019) Microbiome and morbid obesity increase pathogenic stimulus diversity, 4open 2(10), 1-16.
  11. (2019) Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation, 4open 2(11), 1-21.
  12. (2019) Metformin alters signaling homeostasis, 4open 2(12), 1-17.
  13. (2019) NF-κB signaling and crosstalk in carcinogenesis, 4open 2(13), 1-35.
  14. (2019) Transition from normal to cancerous cell by precancerous niche (PCN) induced chronic cell-matrix stress, 4open 2(14), 1-31.
  15. (2019) Synopsis: Special Issue, 4open 2(28), 1-30.
    CONCEPT 4 (defined 2012, realized 2022)
  16. (2022) Physics Essentials Enable Deeper Understanding in Signaling and Crosstalk of the Carcinogenesis Paradigm “Epistemology of the Origin of Cancer”, Cell Physiol Biochem 56(5). 546-572.

Key Summaries