Dr. Weeks’ Comment: This research paper linking inflammation and cancer, accompanied by her comment, was sent by a highly respected lady who owns a cancer care clinic. She writes:
Note the date: late December of 2007 (6 years ago~) , and a close reading of the article indicates that the link between inflammation and the spread of cancer had been known and acknowledged for about five years, THEN. Do the math, and you realize the NCI has been aware of the link for 11 years now. But have they cautioned against radiation therapy, and the inflammation caused by it? Hell, no, the bastards–they don’t want to be attacked by the hordes of radiologists whose bread and butter would be under attack.
This article published in Science Daily in 2007 should have been major headlines and well covered by the media–which ignored it. Why? Because of Big Pharma’s advertising budgets, that largesse is dispensed directly to the media outlets. Anyway, when I was in nurses’ training, human psychology I and II were required subjects, and the non-science related elective I chose was Marketing & Salesmanship. Now even a dim-bulb patient has enough sense to realize that if the spread of cancer is now known to be triggered by inflammation, then obviously the most powerful anti-inflammatory known to man (with zero liver toxicity!) might well at least retard the rate of disease progression, if not block it entirely. The manufacturers of SOUL dare not openly make the claim, but if given the information below, the patient can connect the dots and come to the logical conclusion that SOUL can quell inflammation and thereby prevent the spread of the malignancy, even if more tools are required to reverse it into remission.
Subject: Cancer TRAIL leads to inflammation
Cell-death Receptor Links Cancer Susceptibility And Inflammation
ScienceDaily (Dec. 31, 2007) ”” For over 10 years, Wafik S. El-Deiry, MD, PhD, Professor of Medicine, Genetics, and Pharmacology at the University of Pennsylvania School of Medicine, has been pursuing a cancer-targeting molecule called TRAIL and its molecular partners. TRAIL is normally produced by immune cells and curtails tumor spread by binding to a specialized receptor on a tumor’s surface.
“However, in cancer patients who often have suppressed immunity, and for reasons we still don’t understand, there isn’t enough TRAIL being produced, so tumors are not suppressed,” explains El-Deiry, who is also Co-Program Leader of the Radiation Biology Program for the Abramson Cancer Center at Penn.
Most recently, El-Deiry and colleagues demonstrated for the first time a link between TRAIL’s receptor and cancer susceptibility. Unexpectedly, they also found a connection — via Trail — between inflammation and cancer susceptibility.
Mice engineered without the TRAIL receptor on their cells versus healthy controls developed larger and more tumors in their livers and other organs after being challenged with a chemical carcinogen or radiation. The team also bred TRAIL receptor knock-out mice with mice genetically engineered to get B-cell lymphomas that metastasize to the liver. Their offspring displayed more liver tumors compared to controls. “This is the first direct in vivo evidence that loss of the tumor death-inducing TRAIL receptor confers cancer susceptibility,” says El-Deiry.
When intact, TRAIL and its receptor decrease the influx of inflammatory cells and molecules that can lead to cancer. New models of cancer have suggested a link between inflammation and cancer in the last five years, and El-Deiry is in the early stages of trying to understand this connection with respect to the TRAIL pathway.
For example, in this study, the mice without the TRAIL receptor that were irradiated developed chronic pneumonia, an inflammatory response, as well tumors, evidence pointing to the connection between cancer and inflammation via TRAIL. “One benefit of this work is that it provides a new and unanticipated model implicating a TRAIL pathway deficiency in the chronic toxicity of radiation therapy,” he notes. Inflammation is a common late and serious side-effect of radiation treatment in people.
El-Deiry and his team are now looking within tumor tissue for inflammatory molecules as clues to how cancer and inflammation are coupled. “Our work with TRAIL and its receptor in mouse models represents a new way to look at cancer susceptibility and its potential therapy in humans as well as new ways to decrease debilitating radiation side-effects experienced by cancer patients,” says El-Deiry.
This research was reported online December 13, 2007 in the Journal of Clinical Investigation in advance of the January 2008 print issue. Co-authors in addition to El-Deiry are Niklas Finnberg from Penn and Andres J.P. Klein-Szanto from Fox Chase Cancer Center, Philadelphia. This research was funded in part by the National Cancer Institute.