THE METABOLIC BASIS OF CANCER. Something the I STARTED and which I get NO credit for AND it is being plagiarized as we speak. It is now THE accepted model and replaces the GENETIC BASIS. A little MIR (Soviet Publisher) book “Leukemia Following the Atomic Bomb on Nagasaki” described how patients who had been exposed to the radiation experienced a period of severe anemia before developing Leukemia. Dogma would suggest that the drop in red blood cell (RBC) count was a result of direct exposure to the radiation, ie that the RBCs had been killed by it. However, red blood cells lose there nucleus and are just a non living bag of hemoglobin. So I reasoned that the radiation had wiped out the bodies antioxidants and there ability to mop up free radicals of oxygen, so that lowering the RBC was a protective measure, but one that inadvertently created severe hypoxia AND THAT IT WAS THE HYPOXIA (oxygen starvation) THAT LEAD TO THE LEUKEMIA. MY FIRST CANCER CONFERENCE. The first Cancer conference I attended about 20 years ago was a joint Lorne (Vic Aust) AACR (American Association of Cancer Research) conference. A lecture on the second day was about a bowel cancer in which the number one tumor repressor p53 was mutated, presumably the reason for the tumor, and it secreted a prostaglandin PGF2. Now I knew that PGF2 constricted or narrowed blood vessels supplying the gastrointestinal tract and suddenly I had a different spin on the sequence of events. At question time I suggested that hypoxia or oxygen starvation was the cause of the bowel cancer, not the mutations in the p53 tumor repressor. I suggested that the mutations in the p53 were a RESULT of the hypoxia. As I said this tumor secreted a prostaglandin PGF2 which is a vasoconstrictor. Adrenalin activates PGF2 in the gastro-intestinal tract in response to fight or flight, stress in other words. My theory went like this. Stress>adrenalin>PGF2>vasoconstriction>HYPOXIA>p53 mutation>CANCER. At the end of the symposium a chap approached me and suggested that this was a very interesting idea as he was working on the same cells. It turned out that he was the AACR convener. I saw him later and explained to him what is called the RAS pathway by which adrenalin works. He said, You must be a very good biochemist I was nonplussed by this as I didnt thing my suggestion was anything extraordinary and I replied that Im not a biochemist, Im an electronic technician, this is just a hobby for me. He looked dumbfounded as if I was taking the Mickey out of him and didnt say anything, then took off. I didnt run into him again for the rest of the Conference. The following year when I went to pay the Conference secretary for everything, registration, all meals and accommodation she whispered as she handed me my bag, Dont worry Noddy, it all been taken care off ($750}. I was gobsmacked as there was no explanation as to why. The same thing happened for the following two years the gradually tapered off. I know now. You see my answer that day involved endocrinology, biochemistry, hematology, oncology, molecular biology etc. all of which I had studied BECAUSE I DIDNT KNOW THAT I WASNT SUPPOSED TO HYPOXIA 2. All of the delegates are molecular biologist looking for GENES to blame, then design the appropriate drug. It is pure commerce and that blinds totally. This, plus Dawkinist dogma, makes it IMPOSSIBLE to understand cancer, let alone find a cure. How could the delegates POSSIBLY admit that an amateur scientist had worked something out that the entire global community of cancer researchers couldnt. Yet taking the multidisciplinary approach made it easy, hence my amazement at the response to my suggestion. These conferences are run by private enterprise and they are not gonna give away thousands of dollars to some amateur out the goodness of their hearts. Now I know this sounds incredibly mean spirited, but I really am grateful. At the last conference I attended there were two lectures on the discovery of the HIF (hypoxia inducable factor) proteins and their associated genes. No kudos for me, however. If I had said “I suggested that years ago” I would have been howled down. THE WARBURG EFFECT. The Warburg effect refers to a characteristic in which cancer cells use less and less oxygen as they become more malignant. Cancer researchers use the term but it has fallen into misuse as cancer is seem more and more as simply a stuff up. I use a LOT as it is pivotal to my theories on cancer. A few months ago I decided to check the history of what Warburg did to arrive at his conclusion. I ALMOST FELL OFF THE CHAIR AT WHAT I READ. Fifty years ago Otto Warburg discovered that when normal cells in a Petri dish were deprived of oxygen they transformed into cancer cells. Thats it, nothing else, just deprived of oxygen, no carcinogens and no promoters. So this has been known for FIFTY years yet all of those 500 delegates at my first Cancer conference, half from the biggest cancer research organisation in the world, didnt know about it. If I had known that day I would NOT have suggested it and the genes might not have been found. But then its not my job to know. HYPOXIA can be caused by a number of things, primarily vasoconstriction. Vasoconstriction to the gastro intestinal tract, resulting from persistent stress, means malabsorption of nutrients such as IRON needed for red blood cells to transport OXYGEN. Now add gunked up blood vessels (arteriosclerosis) due to glucose and cholesterol forming plaques and thus even worse hypoxia. HYPOXIA 3 HIFs IN CANCER PROGRESSION. (Semenza. PDF) This is from an excellent paper on hypoxia, with several exceptions. The text in brackets is mine. HIFs play key roles in many crucial aspects of cancer biology including 1. angiogenesis, (the growth of blood vessels to accommodate the growth of a tumour) 2. stem cell maintenance, (preventing the cell from fully differentiating to a mature cell going onto terminal differentiation, ie apoptosis or cell suicide) 3. metabolic reprogramming (from oxidative metabolism to non oxidative fermentation of glucose), 4. autocrine growth factor signalling (self signalling rather than paracrine {from cells next door}, juxtacrine {close by}, or endocrine {distant} signalling, 5. epithelial-mesenchymal transition (not limited to a single or monolayer of cells, eg those lining a milk duct), 6. invasion (of surrounding tissue), 7. metastasis (cells moving into nearby bloodvessels then circulating to set up a secondary tumor at a a distant site), and 8. resistance to radiation therapy and chemotherapy. AMAZING!!! ALL attributes of CANCER, built into every cell in response to HYPOXIA. WHY? Why dont cancer researchers ask this question? This and a lot of other factors suggest wild type cancer. There is one very important word missing in this paper. DEDIFFERENTIATION of the cancer cell, going BACKWARDS, retracing the steps that it took during embryogenesis. Older books eg my Ocology are full of the word. It is not questioned. It is a word that has fallen into almost total misuse, maybe for the very reason that is might suggest Larmarkism, ie back all the way to the germ line and THAT is heresy. ( This blindness seems to coincide with the rise of Richard Dawkins). Thus the stem cells referred to might have arisen from fully differentiated cells that have dediffentiated in response to hypoxia. Instead of the paper suggesting addressing the CAUSES of the hyoxia, ie stress and arteriosclerosis it instead suggests different sites whereby the action of HIFs might be blocked by a drug.
Posted on: Thu, 01 Jan 2015 23:30:19 +0000
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