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You‟ve probably heard the concept that cancer is a genetic disease.

The idea 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.

Today 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.”
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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 “Don’t fight forces, use them.”
pain inside me as motivation to research ~Buckminster Fuller
and write books on cancer so that no
child would have to go through what I
did, ever again.
Based on the book

This presentation is based on the book Cancer: The Metabolic Disease Unravelled by
Mark Sloan.
The Somatic Mutations Theory of Cancer
- The Mainstream Theory of Cancer - -

The official position of the cancer establishment is that “cancer is a genetic disease,”[1]
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
• 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, The study was published in the journal
Tennessee took cells from mouse brain Cancer Research, and what they found
tumors, then cloned a mouse using the DNA was that the cloned brain cancer cells
contained within the brain tumor cell to see directed normal development both pre-
if the cloned mouse would harbor cancer. and post-implantation.

Reference 2
(Li L, et al. 2003)
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

• Were the tadpoles that emerged


• From within the eggs emerged healthy,
swimming tadpoles - demonstrating once again
that mutated cancer DNA can direct normal

Reference 3
(McKinnell RG, et al. 1969)
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

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.”
Reference 10
(Rubin H. 2006)
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.‟

References 4-8
When scientists transplanted normal cell
cytoplasms into cancer cells (containing
mutated DNA), the cancer cells transformed
back into normal cells.

Reference 9
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 appears to dictate carcinogenesis.
Solving the controversy
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

• 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 genomic sequencing
• 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…
Discoveries about Cancer cell genetics
Different people, same type of tumor
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. [References 11-13]

Difference cells of the same tumor

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. [References 14-18]

Metastatic cells vs original tumor

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. [References 19-23]
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.” [Reference 14]

• 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. [Reference 24]

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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Check out the Show Notes

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please share it with someone you love.
The Canadian Cancer Society. What is cancer? [Online]. Available: https://www.Cancer.Gov/about-cancer/understanding/what-is-cancer.
[March 1st, 2017].

2. Li L, connelly MC, wetmore C, curran T, morgan JI. Mouse embryos cloned from brain tumors. Cancer res. 2003;63(11):2733-6.

3. Mckinnell RG, deggins BA, labat DD. Transplantation of pluripotential nuclei from triploid frog tumors. Science. 1969;165(3891):394-6.

4. Shay JW, werbin H. Cytoplasmic suppression of tumorigenicity in reconstructed mouse cells. Cancer res. 1988;48(4):830-3.

5. Israel ba, schaeffer wi. Cytoplasmic suppression of malignancy. In vitro cell dev biol. 1987;23(9):627-32.

6. Howell an, sager r. Tumorigenicity and its suppression in cybrids of mouse and chinese hamster cell lines. Proc natl acad sci USA.

7. Shay jw, liu yn, werbin h. Cytoplasmic suppression of tumor progression in reconstituted cells. Somat cell mol genet. 1988;14(4):345-50.

8. Giguère l, morais r. On suppression of tumorigenicity in hybrid and cybrid mouse cells. Somatic cell genet. 1981;7(4):457-71.

9. Israel BA, schaeffer WI. Cytoplasmic mediation of malignancy. In vitro cell dev biol. 1988;24(5):487-90.

10. Rubin H. What keeps cells in tissues behaving normally in the face of myriad mutations?. Bioessays. 2006;28(5):515-24.

11. Greenman C, stephens P, smith R, et al. Patterns of somatic mutation in human cancer genomes. Nature. 2007;446(7132):153-8.

12. Loeb la. A mutator phenotype in cancer. Cancer res. 2001;61(8):3230-9.
References 2
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14. Salk JJ, fox EJ, loeb LA. Mutational heterogeneity in human cancers: origin and consequences. Annu rev pathol. 2010;5:51-75.

15. Gibbs WW. Untangling the roots of cancer. Sci am. 2003;289(1):56-65.

16. Steeg ps. Heterogeneity of drug target expression among metastatic lesions: lessons from a breast cancer autopsy program. Clin cancer res. 2008;14(12):3643-

17. 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.

18. Gabor miklos gl. The human cancer genome project--one more misstep in the war on cancer. Nat biotechnol. 2005;23(5):535-7.

19. Seyfried TN, shelton LM. Cancer as a metabolic disease. Nutr metab (lond). 2010;7:7.

20. Stratton MR, et al. The cancer genome. Nature. 2009;458(7239):719.

21. Mandinova a, lee sw. The p53 pathway as a target in cancer therapeutics: obstacles and promise. Sci transl med. 2011;3(64):64rv1.

22. Gravendeel la, kouwenhoven mc, gevaert o, et al. Intrinsic gene expression profiles of gliomas are a better predictor of survival than histology. Cancer res.

23. Dang l, white dw, gross s, et al. Cancer-associated IDH1 mutations produce 2-hydroxyglutarate. Nature. 2009;462(7274):739-44.

24. 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].