New Cancer Theory by two US Scientists in peer-reviewed Cancer Journal
Reporter: Aviva Lev-Ari, PhD, RN
UPDATED on 6/25/2014
A New Understanding of the Cause of Cancer
Genetics are important but not the reason for everything
SOURCE
http://www.theepochtimes.com/n3/753288-a-new-understanding-of-the-cause-of-cancer/?photo=2
This view was first suggested in 1928 and has held pretty fast in the minds of the medical and scientific communities for some 85 years, despite the fact that this mutation theory has been proven true for less than 10 percent of cancers.
With some cancers, even fewer mutations are associated with their development. For example, only about 1 percent of gastric cancers are caused by mutations, and only 3–5 percent of colon cancers. For breast cancer patients with the BRCA gene, only about 8 percent are caused by mutations of this gene. (Angelina Jolie copycats contemplating extreme preventive medicine take note.)
“Cancer is thought of as being triggered in 5–10 percent of cases by mutations; 15 percent by infections; with the remaining 80 percent deemed to be sporadic, a euphemism for having an ‘unknown cause,’” said Dr. Björn L.D.M. Brücher, one of the authors of a paper that presents a new hypothesis of the genesis for the majority of cancers.
Dr. Brücher is a professor of surgery and medical director at the Bon Secours Cancer Institute in Richmond, Va. The other author of the paper, Dr. Ijaz S. Jamall, is the president and principal scientist with Risk-Based Decisions, Inc., in Sacramento, Calif.
However, despite the fact that we don’t know what causes 80 percent of cancers, the majority of funding for cancer research goes toward studying mutations instead of other causes, the authors say.
Dr. Brücher used the analogy that the mutations are like apples we’ve found in a car and just assumed they grew there.
A New Cancer Paradigm
Could cancer also be caused by chronic inflammation, just like arthritis and heart disease?
Although Dr. Brücher and Dr. Jamall have known each other for many years, and have long been exposed to new ideas about cancer through work with the Theodor Billroth Academy, an international research organization that is more open-minded than most, the researchers say they never planned on developing a new cancer hypothesis. It came to them out of a degree of frustration.
“There was so little progress in clinical oncology [cancer research] where every new drug approved by the FDA to treat this or that cancer extended the life of cancer patients by a few weeks or a few months, but were being touted as ‘huge successes or breakthroughs,’ when it in fact has little impact,” Dr. Brücher said in a telephone interview.
The new cancer hypothesis provides the missing explanation, as the authors see it, for the origin of the majority of cancers. The paradigm takes into consideration biochemical and physiological processes, including communication between cells, as well as cell-signaling information.
The new paradigm is summarized in a sequence of six steps:
“(1) A pathogenic stimulus (biological or chemical) leads at first to a normal reaction seen in wound healing, namely, inflammation. When the inflammatory stimulus is too great or too prolonged, the healing process is unsuccessful, and that results in (2) chronic inflammation.
“That’s just the beginning. When chronic inflammation persists, (3) fibrosis [thickening and scarring of the connective tissue,] develops. The fibrosis, with its ongoing alteration of the cellular microenvironment is different and creates (4) a precancerous niche, resulting in a chronically stressed cellular matrix. In such a situation, the organism deploys (5) a chronic stress escape strategy. But if this attempt fails to resolve the precancerous state, then (6) a normal cell is transformed into a cancerous cell.”
Supporting Evidence
Dr. Brücher and Dr. Jamall say that observations in both the plant and animal kingdoms support their hypothesis. The following are some examples:
• The discovery that the bacteria H. pylori, which infects two-thirds of the world population, is a major cause of gastric cancer.
• The finding that viruses such as the Epstein-Barr virus can cause lymphoma.
• The identification of human papilloma virus in cervical cancers (the viral infection is a precondition for about 75 percent of human cervical cancers).
• Hepatitis B and C infections, which raise the risk of contracting liver cancer, suggest that certain infectious agents play a prominent role in non-hereditary cancers.
Next Steps
The next necessary step is knowing the enemy and providing a more complete explanation for how cancer begins and how it develops.
“If … this hypothesis is plausible, then the majority of findings in the genetics of cancer so far reported in the literature are either late events or sideshows that could have occurred after the development of a precancerous niche,” Dr. Brücher said.
In other words, researchers need to start looking for the tree that grew the apples and where it stands.
At one or more of the steps spelled out in the new paradigm, conditions could be modified to prevent or, at a bare minimum, slow down the progression of many cancers.
“Given that most cancers are diseases of old age, it’s not necessarily beneficial from the patient’s quality of life choices to kill every cancer cell to succeed. By merely slowing or inhibiting the progression of the disease, dramatic public health benefits can be obtained and with less dread on the part of the patient,” Dr. Brücher said.
Personal Connection
The author’s older brother, Thomas Edward Grundvig, died of lymphoma cancer on June 16 after a four-year battle against the disease. With his life extended a couple extra years by new pioneering technology at Sloan Kettering in New York City, Tom succumbed to the cancer that was a direct result of being diagnosed with Crohn’s disease in 1990.
While Crohn’s disease is genetic for many, it was not present in any of the previous 10 generations on either side of his Norwegian families. The disease came to Tom after spending a decade working in highway construction in the 1970s, being exposed to leaded gasoline. He was 63 years old.
James Grundvig is the CEO of Cloudnician LLC, a mobile-cloud startup with big data pull, and a contributing writer to Epoch Times.
SOURCE
http://www.theepochtimes.com/n3/753288-a-new-understanding-of-the-cause-of-cancer/?photo=2
Epistemology of the origin of cancer: a new paradigm
BMC Cancer 2014, 14:331 doi:10.1186/1471-2407-14-331
Published: 10 May 2014
Fulltext
http://www.biomedcentral.com/1471-2407/14/331
PDF:
http://www.biomedcentral.com/content/pdf/1471-2407-14-331.pdf
Abstract (provisional)
Background
Carcinogenesis is widely thought to originate from somatic mutations and an inhibition of growth suppressors, followed by cell proliferation, tissue invasion, and risk of metastasis. Fewer than 10% of all cancers are hereditary; the ratio in gastric (1%), colorectal (3-5%) and breast (8%) cancers is even less. Cancers caused by infection are thought to constitute some 15% of the non-hereditary cancers. Those remaining, 70 to 80%, are called “sporadic,” because they are essentially of unknown etiology. We propose a new paradigm for the origin of the majority of cancers.
Presentation of hypothesis: Our paradigm postulates that cancer originates following a sequence of events that include (1) a pathogenic stimulus (biological or chemical) followed by (2) chronic inflammation, from which develops (3) fibrosis with associated changes in the cellular microenvironment. From these changes a (4) pre-cancerous niche develops, which triggers the deployment of (5) a chronic stress escape strategy, and when this fails to resolve, (6) a transition of a normal cell to a cancer cell occurs. If we are correct, this paradigm would suggest that the majority of the findings in cancer genetics so far reported are either late events or are epiphenomena that occur after the appearance of the pre-cancerous niche.
Testing the hypothesis
If, based on experimental and clinical findings presented here, this hypothesis is plausible, then the majority of findings in the genetics of cancer so far reported in the literature are late events or epiphenomena that could have occurred after the development of a PCN. Our model would make clear the need to establish preventive measures long before a cancer becomes clinically apparent. Future research should focus on the intermediate steps of our proposed sequence of events, which will enhance our understanding of the nature of carcinogenesis. Findings on inflammation and fibrosis would be given their warranted importance, with research in anticancer therapies focusing on suppressing the PCN state with very early intervention to detect and quantify any subclinical inflammatory change and to treat all levels of chronic inflammation and prevent fibrotic changes, and so avoid the transition from a normal cell to a cancer cell.
Implication of the hypothesis: The paradigm proposed here, if proven, spells out a sequence of steps, one or more of which could be interdicted or modulated early in carcinogenesis to prevent or, at a minimum, slow down the progression of many cancers.
SOURCE
http://www.biomedcentral.com/1471-2407/14/331/abstract
Click to access 1471-2407-14-331.pdf
Epistemology of the Origin of Cancer: A New Paradigm
From: “Theodor-Billroth-Academy® (TBA®) Germany – USA” <info@theodor-billroth-akademie.de>
Reply-To: <info@theodor-billroth-akademie.de>
Date: Sun, 11 May 2014 13:43:17 +0000
Subject: New Cancer Theory by two US scientists in peer-reviewed Cancer Journal
FOR IMMEDIATE RELEASE
May, 11th 2014
US SCIENTISTS PROPOSE A NEW PARADIGM FOR THE ORIGIN OF CANCER
Two US scientists have developed a new hypothesis for the origin of cancer. Their work has just been published in the peer-reviewed journal, BMC Cancer, entitled
“Epistemology of the Origin of Cancer: A New Paradigm”.
Until recently it is thought that the percentage rates of all cancers are triggered (1) in 5 to 10% of all cancers by somatic mutations (hereditary cancers), (2) in 10-15% of cancers by infection and (3) in some 80% of all cancers “sporadic cancers”, the cause remains unknown.
Both authors point out that mutagenic changes, as triggers for cancer, were first suggested in 1928. While being thought to be valid for some 5 to 10% of cancers, the mutation theory leaves the origin of the remaining 80% of cancers still unexplained. Their new hypothesis suggests that in the majority of cancers mutagenic changes are either epiphenomena or later events that occur during carcinogenesis.
The US scientists propose a new paradigm for the origin of the majority of cancers that takes into consideration the biochemical processes, physiological processes including cell-cell communication and signaling information which can be summarized in a sequence of six steps. These are:
(1) A pathogenic stimulus that leads to inflammation in response to which the affected tissue takes defensive measures to heal and, when unsuccessful, results in (2) chronic inflammation. When chronic inflammation persists (3) fibrosis develops. The fibrosis, with its ongoing remodeling of the cellular microenvironment, creates (4) a precancerous niche. In such a situation the organism employs (5) a chronic stress escape strategy and if this attempt fails to resolve the precancerous state, (6) a normal cell becomes a cancerous cell.
Observations from research in the plant and animal kingdoms, in cell culture, and from clinical studies reveal that the transition of a cell of one type to one of another type is a routine and normal biological process, which in the case of cancer is subverted.
The authors propose that, after 85 years of searching for genetic sources it is time to shift to a new paradigm and suggest concentrating research efforts on the nearly 80% of cancer cases which are still of “unknown etiology.” In so doing the authors state,
“The paradigm proposed here, if proven, spells out a sequence of steps, one or more of which could be interdicted or modulated early in carcinogenesis to prevent or, at a minimum, delay the progression of many cancers.”
The scientist’s affiliations are from the following global/individual Academic Centers /Countries/States (Cities):
1
THEODOR-BILLROTH-ACADEMY® (TBA®), Germany – USA
2
INCORE, International Consortium of Research Excellence of the TBA®, Germany – USA
3
Bon Secours Cancer Institute, Richmond, Virginia, USA
4
Risk-Based Decisions, Inc., Sacramento, California, USA
If this is of interest to you, please find attached the weblink of the manuscript as well as the PDF file of the proposed new paradigm for your convenience.
http://www.biomedcentral.com/1471-2407/14/331
With best regards
Theodor-Billroth-Academy® (TBA®)
PS:
The Theodor-Billroth-Academy® (TBA®) provides this press release without a signature and/or a name. It is the philosophy of the TBA® to concentrate on the content of research rather than on individual names. This release is not confidential. Anyone should free to forward it.
sent from Theodor-Billroth-Academy® (TBA®) Germany – USA