Thursday, December 14, 2017

Video: Researchers discovered inexpensive cure for cancer in 2007 but no industry support

CTV News, a Canadian news station explores how DCA has been rediscovered as an old drug with a new purpose. News host Lloyd Roberts and Avis Favraro investigate.

www.ctvnews.ca

CTV kept referring to DCA, without saying what DCA is, while frequently pointing at a bottle of corrosive Dichloroacetic Acid. The non-corrosive, perfectly-safe white powder being studied as a cancer treatment is actually called Sodium Dichloracetate.

More details on treatment:
www.youtube.com/watch?v=8uY3bfU3vG4

  • In 2007, Dr. Evangelo Michelakis of the University of Alberta announced the results of a study where rats who had lung, breast and brain cancer were fed DCA. Cancer cells declined by 70% over the course of three weeks while healthy cells were left untouched.
  • Another 2007 study sponsored in part by Harvard Medical School showed the same result for endometrial cancer cells;
  • A 2008 study using DCA in conjunction with radiation on certain kinds of prostate cancer cells determined that “DCA alone produced significant cytotoxic effects” and also made radiation therapy more effective;
  • A 2009 study found that DCA reduced tumor growth in several types of metastatic Breast Cancer cells in both in vitro and animal models
  • A March 2015 study published in the International Journal of Oncology documented the same basic results in human SH-SY5Y neuroblastoma cells.



 
PMH - DCA - Dichloroacetic Treatment from Port Moody Health on Vimeo.




Another simple cancer treatment:



Cancer's Weakest Link

The number one reason cancer is able to grow is excess sticky fibrin, a.k.a. 'snot.' Get rid of the sticky snot that surrounds cancer and the cancer will go away.

The mucus/fibrin that coats all tumor cells is designed to protect them from the body’s immune system

The mucus/fibrin coat is a “Cloaking device” - preventing cancer cells from being recognized by the immune system’s white blood cells (WBCs: macrophages, neutrophils), and thus making them immune to attack by natural killer (NK) cells. Mucus is a glycoprotein (sugar+protein), fibrin is a protein in the blood, which enables blood to clot.

The sticky fibrin coat is ~15 times thicker than the fibrin which surrounds healthy cells – and is revealed by histochemical and microscopic examination.

Egyud LG, Lipinski B. Significance of fibrin formation and dissolution in the pathogenesis and treatment of cancer. Med Hypotheses. 1991 Dec;36(4):336-40.

Massimo Cardinali et al. Interaction of Fibrinogen with Murine Melanoma Cells: Covalent Association with Cell Membranes and Protection against Recognition by Lymphokine-activated Killer Cells. Cancer Res December 15, 1990 50; 8010 Study Link

So how do you get rid of the excess fibrin?  

Click here to read how

Click here for easy recipes


1. Med Hypotheses. 2000 Mar;54(3):456-60.

Resistance of cancer cells to immune recognition and killing.

Lipinski B(1), Egyud LG.

Author information:
(1)Cell Research Incorporated, Chestnut Hill, MA, USA.

Abstract
It is well recognized that, in order for a wound to heal, the fibrin clot must be eliminated by fibrinolytic enzymes. In certain instances, however, fibrin is ineffectively degraded or even not degraded. For example, in pregnancy, the placenta contains a layer of fibrin (Nitabuck's layer) which presents as 'self' to the immune system. Similar situations have been observed in many solid tumors. A hypothesis is presented according to which tumor cells can escape detection and attack by the immune system in most cancer patients. The tumor dons a 'coat' of the host's own protein on its cell surface. The coat is composed of fibrin and of a polymeric form of human serum albumin (HSA) which, by contrast to pure fibrin, is resistant to fibrinolytic degradation. Such a coated tumor appears as 'self' to the immune system, and thus is not detected as a tumor by the immune system (i.e. natural killer cells). When tumors are prepared for in vitro assays against drugs, they are routinely treated with proteolytic enzymes (e.g. pepsin, or chymotrypsin, etc.) which dissolve the protein coat, exposing the tumor cell surface to the drug. Thus, the in vivo existence of a coat on the tumor surface may explain why some drugs have little or no effect in vivo, while the same drugs are active in vitro.

DOI: 10.1054/mehy.1999.0876
PMID: 10783488 [PubMed - indexed for MEDLINE]


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