Remember in 2010, when the National Cancer Institute’s own multi-billion dollar Cancer Genome Atlas Project shocked scientists and researchers across the world by proving that cancer has nothing to do with your genetics? Yeah, it happened.
We are commonly told that cancer is a genetic disease; that if somebody in your family has had cancer you are at increased risk of getting it because “it’s in your genes.” The genetic theory of cancer, also known as ‘the somatic mutations theory’, is taught to doctors and other medical practitioners as if it were fact, but in reality it is just a theory, meaning it’s unproven.
In this article/video/podcast/presentation we’re going to put this theory to the test to find out once-and-for-all if cancer is a genetic disease. As American Nobel prize winner Peyton Rous stated in 1959, “The somatic mutation theory acts like a tranquilizer to those who believe in it.”
Inspiration for this presentation
WHEN I WAS 12 YEARS old my mother died of cancer. We all will face adversity in our lives. The result of that adversity depends on our reaction to it. 20 years after my mom’s death, I realized it was not a tragedy, but an opportunity. She gave me a story to tell that could inspire others and a mind that could solve the problems the world was literally dying to know.
Instead of letting it destroy me, I used the pain inside me as motivation to research and write books on cancer so that no child would have to go through what I did, ever again. As the late Buckminster Fuller once said, “Don’t fight forces, use them.”
The Somatic Mutations Theory of Cancer
The official position of the cancer establishment is that “cancer is a genetic disease,” whereby a specific set of gene mutations cause a single cell to turn irreversibly cancerous and multiply out-of-control, until enough of its mutant clones collectively form a tumor that strives to kill the host.
If this theory is correct, it means that cancer cells are like parasites that must be eradicated at all costs; even if patients are injured or nearly killed in the process.
Weapons of War as Treatments?
It’s this notion, which I call “the angry cancer cell”, that justifies the use of knives, poison injections and ionizing radiation on cancer patients.
If it weren’t for the fear driven into patients by doctors, telling them that they’re going to die if they aren’t rushed into treatment, most people would probably never accept these treatments.
Questioning the genetic theory of Cancer
If cancer really is some kind of monster, entirely foreign to the body and living inside us, then we’re probably doing the right thing by trying to kill the cells during treatment.
However, if cancer is not a murderous mutant cell and these treatments are making the health of patients worse, then we need to know that so we can stop using them. It’s time to question the genetic theory of cancer to find out for certain.
In search of another paradigm that could adequately explain the underlying cause of cancer and why the war on cancer has been such a failure, I stumbled upon a fascinating series of studies that completely contradicted the genetic theory of cancer.
If cancer were a disease of genetic origin, then none of the following observations would have occurred.
Cloned mice from tumor cell DNA
In 2003, a group of scientists from St. Jude Children’s Research Hospital in Memphis, Tennessee took cells from mouse brain tumors, then cloned a mouse using the DNA contained within the brain tumor cell to see if the cloned mouse would harbor cancer.
The study was published in the journal Cancer Research, and what they found was that the cloned brain cancer cells directed normal development both pre- and post-implantation.
Frog Egg Tumor Transplants
In 1969, a group of researchers injected tumor cells from tadpoles into frog eggs to find out the condition of the tadpoles that would emerge from those eggs. The eggs contained “mutant” cancer DNA after the tumor cells were transplanted. Were the tadpoles that emerged cancer-ridden?
From within the eggs emerged healthy, swimming tadpoles – demonstrating once again that mutated cancer DNA can direct normal development.
Mutated genetics, normal behavior
Harry Rubin, Professor Emeritus of Cell and Developmental Biology from the University of California demonstrated in 2006 that cells can have hundreds of mutations and still behave normally within the organism.
The study reports that “The use of a reporter gene in transgenic mice indicates that there are many local mutations and large genomic rearrangements per somatic cell that accumulate with age at different rates per organ and without visible effects.”
Cell Cytoplasm-Swapped Cybrids
Since the 1970’s, scientists have been experimenting with swapping normal cell cytoplasms (containing the energy-producing mitochondria, not DNA) with cancer cell cytoplasms and vice versa. They call the resultant cells ‘cybrids.’ When scientists transplanted normal cell cytoplasms into cancer cells (containing mutated DNA), the cancer cells transformed back into normal cells.[4-8] And when cancer cell cytoplasms were transplanted into normal cells (with normal DNA), the cells turned into cancer cells.
What these findings show is that mutant cancer DNA does not cause cancer and that it’s the mitochondria that appear to dictate carcinogenesis. What better way to resolve the controversies surrounding cancer’s origins than with the biggest and most comprehensive scientific investigation ever conducted on the genetics of cancer?
The Cancer Genome Atlas Project
In 2005, the National Cancer Institute launched a giant multi-national initiative called The Cancer Genome Atlas Project (TCGAP). The goal of the project was to expand human understanding of cancer genetics and to pinpoint a common sequence of genetic mutations that drive carcinogenesis so that new drugs targeting each mutation could be developed. If there ever were a project that could finally either prove or disprove cancer as a genetic disease, this billion-dollar medical behemoth – spanning more than a decade – was it.
Lightning fast sequencing of the cancer genome
As you can imagine, the debut of the project spurred enormous excitement and hope among its many participants and supporters. One of the greatest successes of the project, still underway, has been the accelerated speed at which scientists can fully sequence the genetic code of a cell.
Each cell in our bodies is said to contain around 25,000 genes, and using state-of-the-art technology scientists are now able to churn out the entire genomic sequence of cells with lightning speed. To date, TCGAP has compiled data from more than 10,000 tissue samples from over 30 types of cancer. As far as the origins of cancer are concerned, the results of the project to many of its supporters have been shocking…
Revolutionary Discoveries About The Cancer Genome
- Scientists looked at cancer cells from different people with the same type of tumor and discovered the mutational signatures of cells were so immensely different that they appeared to occur completely at random.[11-13]
- Scientists also looked at the genomes of cells from within the very same tumor, but instead of finding a distinct series of mutations that could explain carcinogenesis, every cell was found to have its own unique set of mutations.[14-18]
- Metastatic cancer cells were also analyzed, and researchers found their genetic defects were completely different than the genetic defects in cells of the original tumor. Time and time again, the story was the same: not a single gene mutation – or any combination of mutations – was found to be absolutely responsible for initiating the disease.[19-23]
The Shocking Results of TCGAP
In 2010, researchers from the University of Washington called the results of the TCGA project “sobering” and conceded, “it is becoming increasingly difficult to envision how it will be possible to develop a realistic number of targeted chemotherapies to be directed against a discrete panel of commonly mutated cancer genes.”
Dr. David Agus of the University of California, the oncologist who treated Steve Jobs, even suggested in a recent speech that cancer is simply too difficult to understand and that we should stop trying.
The multi-billion dollar Cancer Genome Atlas Project, a fascinating milestone in the history of cancer research, has taught us many remarkable things about cancer genetics and confirmed to us unequivocally that, above all, cancer is not a genetic disease.
A Message from the ‘Father of DNA’
After the results of TCGAP, the 81-year-old “father of DNA” himself, James Watson, responded publically by recommending a shift in the focus of cancer research from genetics to metabolism.
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- The Canadian Cancer Society. What is cancer? [Online]. Available: https://www.Cancer.Gov/about-cancer/understanding/what-is-cancer. [March 1st, 2017].
- Li L, connelly MC, wetmore C, curran T, morgan JI. Mouse embryos cloned from brain tumors. Cancer res. 2003;63(11):2733-6.
- Mckinnell RG, deggins BA, labat DD. Transplantation of pluripotential nuclei from triploid frog tumors. Science. 1969;165(3891):394-6.
- Shay JW, werbin H. Cytoplasmic suppression of tumorigenicity in reconstructed mouse cells. Cancer res. 1988;48(4):830-3.
- Israel ba, schaeffer wi. Cytoplasmic suppression of malignancy. In vitro cell dev biol. 1987;23(9):627-32.
- Howell an, sager r. Tumorigenicity and its suppression in cybrids of mouse and chinese hamster cell lines. Proc natl acad sci USA. 1978;75(5):2358-62.
- Shay jw, liu yn, werbin h. Cytoplasmic suppression of tumor progression in reconstituted cells. Somat cell mol genet. 1988;14(4):345-50.
- Giguère l, morais r. On suppression of tumorigenicity in hybrid and cybrid mouse cells. Somatic cell genet. 1981;7(4):457-71.
- Israel BA, schaeffer WI. Cytoplasmic mediation of malignancy. In vitro cell dev biol. 1988;24(5):487-90.
- Rubin H. What keeps cells in tissues behaving normally in the face of myriad mutations?. Bioessays. 2006;28(5):515-24.
- Greenman C, stephens P, smith R, et al. Patterns of somatic mutation in human cancer genomes. Nature. 2007;446(7132):153-8.
- Loeb la. A mutator phenotype in cancer. Cancer res. 2001;61(8):3230-9.
- 13. Parsons dw, jones s, zhang x, et al. An integrated genomic analysis of human glioblastoma multiforme. Science. 2008;321(5897):1807-12.
- Salk JJ, fox EJ, loeb LA. Mutational heterogeneity in human cancers: origin and consequences. Annu rev pathol. 2010;5:51-75.
- Gibbs WW. Untangling the roots of cancer. Sci am. 2003;289(1):56-65.
- Steeg ps. Heterogeneity of drug target expression among metastatic lesions: lessons from a breast cancer autopsy program. Clin cancer res. 2008;14(12):3643-5.
- Wu jm, fackler mj, halushka mk, et al. Heterogeneity of breast cancer metastases: comparison of therapeutic target expression and promoter methylation between primary tumors and their multifocal metastases. Clin cancer res. 2008;14(7):1938-46.
- Gabor miklos gl. The human cancer genome project–one more misstep in the war on cancer. Nat biotechnol. 2005;23(5):535-7.
- Seyfried TN, shelton LM. Cancer as a metabolic disease. Nutr metab (lond). 2010;7:7.
- Stratton MR, et al. The cancer genome. Nature. 2009;458(7239):719.
- Mandinova a, lee sw. The p53 pathway as a target in cancer therapeutics: obstacles and promise. Sci transl med. 2011;3(64):64rv1.
- Gravendeel la, kouwenhoven mc, gevaert o, et al. Intrinsic gene expression profiles of gliomas are a better predictor of survival than histology. Cancer res. 2009;69(23):9065-72.
- Dang l, white dw, gross s, et al. Cancer-associated IDH1 mutations produce 2-hydroxyglutarate. Nature. 2009;462(7274):739-44.
- Agus, D. [Ted]. (2010). David agus: A new strategy in the war against cancer. Available: https://www.Youtube.Com/watch?V=irxgdmsp9gs.[March 1, 2017].