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 22-01-2012, 01:55 PM #47 devicenull Senior Member   Join Date: Oct 2011 Location: 127.0.0.1 Posts: 426 Likes: 23 (14 Posts) of cource most of them refuses chemo. Chemo has to do with the theory that a tumor is something that occurs due to oncontrolled cell division and must be killd by poison, burnd etc. But al that is wrong. Mutation theory cannot explain the following phenomena. 1, Of only one mutation causes cancer, the chance for cancers to form is too great. Mutaions require cell devisons. There are 10^12 steam cell devisons per day in the aduld human body. If the point mutation rate is 1.1x10^-8 per cell division and cancer is caused by one point mutation, then the theoretical cancer occurence in everybody would be exceptionally high, 1.1x10^4 point mutations or cancers daily (10^12 steam cell divisionsx1.1.10^-8 point mutation/cell division, meaning everybody would have the chance of 10000 cancer cells to form daily. This is obviously not the case. Therfore, a multiple step mutation cancer theory (mutation-latent-mutation to cancer) and DNA repair theory were developed to match the actual cancer incidence. From another perspective, the chance for cancer is too small if multiple specific mutations cause cancer. If cancer forms from five independent point mutations, the theoretical cancer occurence would be 10^12x(1.1x10^8)^5=1.61x10^-28 daily per person or 10^12x(1.1x10^ 8)^5x365x120=7.05x10^24 for a 120 year old person. It is equilant to the chance of one cancer case in 1.42x10^23 people, meaning no one would get cancer in the world. In clinics, 5~10 specific genetic alternations, ore even 11000 genomic alternations per cell were reported for a sporadic colerectal cancer, leading to the question is mutation the cause ore the result of a cancer? Similarly, if the same gene mutation and same expressed proteins are preveland on a group of cancer patients (e.g, deletions of cdkn2a in bone tumor cell lines, p53 and Rb mutations in small cell lung cancer, or in multiple cancer types (e.g, phosphatase and tensin homo-log aberrations on verious cancer, the chance of random mutatio to cause those cancers simultaneously should be impossible in theory. 2, Mutation theory does not explain the time difference to cause cancer in various organisms. More than 50% Sprague-Dawley rats will develop a spontaneous tumorin 2 years and this occurence is far less than one per million in humans at 2 years old. The doubling times of bone marrow derived steam cells from humans and rats 25,2h and 31,5 hours respectively. The division rate of human cells is not slower than that of rat cells, indicating that the chance for DNA replications mistake in human cells is nit any less than that of a ratĀ“s. From the mutation theory alone, humans have no reason to show mush lower cancer incidence rate than rats with the same DNA replication time. Similary, accumulated mutations cannot explain why the cancer occurences are not correlated with the lifespan among diffrent bioloical species e.g, thousands of old trees without cancer versus a 12 day old Drosophila with cancer, althrough they have the same DNA replication mechanisms and similar enviromental risk that can cause mutations. Furthermore, from the fact that cancer exists in some multicellular organisms but not in others, mutation should not be the necessary premise of cancer since all multicellular organisms have potential mutation risk dureing DNA replications, while cancer only exists in a small proporation of them. 3, Multicellular organism cells from two diffrent species in the same potential mutation enviroment have diffrent outcomes on cancerization. Many schistosome related bladder and prostate cancers are reported, while no cancers can be found in the schistosome itself, althrough it has the same potential risk of mutation from the same cancer enviroment. If schistosomiasis associated bladder cancer is caused by the human p53 mutation, why does the same enviroment never hit the schistosomeĀ“s p53 gene and develop cancer in the schistosome? 4, Cancer recurrence also cannot be explained by the mutation theory. Supposing one live cancer cell survives after surgical, chemo and radiation therapies, another cancer mass with 1x10^12 cells (about 1 kg) can be formed within 80 days if the cell doubling time is 48 h. If all cancer cells are killed by the aboved standard therapies and new cancer cells are produces by the accumulated mutation again, according to the mutation theory, dozens of years will be needed to develop like the first one. However, this does not match the clinical recurrent cases, most breast cancers recur in 5 years. 5, Mutation cannot explain the cancer incidence rate turnaround at very old ages in mice, >800 days, and humans 85 years. If mutation and failures of immunosurveillance or the DNA repair are the cause of cancer, the aging cells in very old babies should have mush more chance in develop cancer. One explanation to this incidence turnaround is the natural selection that allows the less cancer prone population to survive, the survivors at an old age are not susceptible to cancer. However, this mechanism, if it exists, conflicts with why there is no such phenomenon on other aging diseases such as heart disease. natural selection that allows the less cancer prono population to survive, the survivors at an old age are not suspecible to cancer But everything above can be explained if one look at wounds and healing. What sets them apart (diffrent cancer types) can be explaind by epigenetics, but they are al the same. A tumor is a wound that cant heal.