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“We Fought Cancer…And Cancer Won”
The headline of an article in Newsweek Magazine said
it all . Richard Nixon declared war on cancer in 1971. Since then, the
federal government, private foundations and companies have spent at least $200
billion in the quest for cures that resulted in an estimated 1.5 million or
more scientific papers. But we are on the losing side of the cancer war.
Cancer was projected to kill
about 230 000 more Americans in 2008, a 69 % increase over 1971. The raw number
is misleading as the population has become older and 50 % larger. Death rates
have fallen, especially for breast cancer in women. Between 1975 and 2005, the death
rate from all cancers dropped by 7.5 %, though this compares unfavourably with
the cardiovascular death rate, which has fallen by 70 % in the same period, thanks
largely to less smoking. New discoveries on cancer pathways, new drugs, new
treatments, and new ways to reduce side effects and suffering and prolong lives
have all been achieved, except for the cure of cancer itself.
The main reason for losing the
cancer war is that basic understanding of the disease continues to elude the
army of cancer researchers who can think of nothing better to do than looking
for yet more genes to attack as cancers develop resistance to new drugs. The
National Cancer Institute admitted that “the biology of more than 100 types of
cancers has proven far more complex than imagined.” Otis Brawley of the
American Cancer Society was quoted saying: “one tumour is smarter than 100
brilliant cancer scientists.”
The issue has come to a head as
the promise of ‘personalized medicine’ in cancer therapy based on genetic
profile of individual patients suffered a serious setback when researchers
found that tumours have more than a hundred gene mutations in coding regions
alone, and not only do individual patients differ from one another, but different
regions within a single tumour also have distinctly different genetic profiles
(see  Personalized
Medicine in Cancer Therapy Fact or Fiction?SiS 54).
That is precisely the picture one would
expect if gene mutations are the effects rather than the causes of cancer;
tumour cells simply mutate their genes to enable them to survive, all too often
at the expense of the patient, thanks to the fluidity of the genome, first
discovered in the late 1970s and abundantly corroborated since the human genome
has been sequenced (see  Living
with the Fluid Genome, ISIS publication).
Cancer an epigenetic disease
I raised the possibility that cancer is an epigenetic
disease in the final chapter of my book  Genetic Engineering Dream or Nightmare,
ISIS publication), first published in 1998. ‘Epigenetic’ implies a change of
the cell or gene expression state in response to the environment that is not
immediately due to alteration in genomic DNA. I cited a paper published in 1992
 by Harry Rubin, Professor Emeritus of cell and developmental biology at
University of California, Berkeley, in the United States, who was among the
first to suggest that cancer is an epigenetic disease when almost everybody
else was assuming cancer was a genetic disease due to mutations in several key
Rubin described experiments
carried out in two laboratories, one using X-rays to induce malignant
transformation, the other using the carcinogen methyl-cholanthrene. Both studies
found that most, if not all exposed cells were altered in some way, so that
their progeny had a higher probability of transformation than untreated cells.
In other words, the entire population of exposed cells showed an
increased probability of transformation to the cancer state, and this increased
probability was inherited in subsequent cell generations. So, if one divided
up the exposed population into several subpopulations, each of them would show
essentially the same frequency of transformation. Moreover, if these were
further subdivided and propagated, the same frequency of transformed cells
arose in all of them. Such high frequencies of transformation are also characteristics
of spontaneous transformations induced by metabolic and other stress on cells
in culture, and are not due to correspondingly high frequencies of mutations.
Still more suggestive was the
observation that clones of cells transformed by X-rays or by metabolic stress
revert to normal when placed under optimal growth conditions. These results are
reminiscent of high rates of reversion in the early stages of malignancy
A team of Russian scientists had been
studying spontaneous transformations of cell lines derived from inbred mice and
rats. The cells produced sarcomas in the mice and rats from which the lines
were established. The researchers found that on culturing cells from the
tumours, they were able to obtain colonies that were fully transformed, partly
transformed or not transformed at all. On six successive recloning of
transformed colonies, the cells persisted in giving rise to all three
kinds of colonies. The non-transformed cells, which have lost their ability to
give rise to tumours in the animals, arose at high frequencies. Commenting on
the results, Rubin wrote : “The question arises…whether the underlying
process in all tumors is fundamentally epigenetic in character. I know of no
experiment that rules out this possibility.”
The strong implication is that mutations are
not the primary cause of transformation. Instead, they may arise after
the crucial transformation of the cellular state, which is the result of
response to physiological stress. It also indicated the possibility that the
transformed state can be reversed (again, thanks to the fluid genome!)
Indeed, long periods of starvation in
bacteria have been known to result in ‘adaptive’ or ‘directed’ non-random
mutations that enable bacteria to survive on new substrates or ones that they
could not metabolize (see [3, 4, 6] To
Mutate or Not to Mutate, SiS 24). British biochemist John Cairns,
who made significant contributions to defining adaptive mutations, had drawn the
parallel between conditions that give rise to adaptive mutations in bacteria
and cancer in mammalian cells .
Recent evidence on epigenetic origin of cancer
More recently, Tatiana Karpinets and Brent Roy at Wright
State University, Dayton, Ohio, in the United States proposed that cells
exposed to stressful environments respond by epigenetic adaptive changes that
result in ‘matched’ mutations arising in the longer term . It is of interest
that the phenomenon parallels a hypothesis of epigenetic evolution Peter
Saunders and I proposed in 1979  (see  Development
and Evolution Revisited, ISIS scientific publication, for a recent review
and evaluation of the hypothesis).
Specifically, Karpinets and Roy proposed that
cells respond to stress by epigenetic changes that hypermethylate (turning
off) tumour-suppressor genes involved in cell cycle arrest, apoptosis
(programmed cell suicide) and DNA repair; hypomethylate (thereby activating)
proto-oncogenes associated with persistent proliferative activity; and globally
demethylate the genome, activating DNA repeats and promoting genome
instability. (Methylation involves adding a methyl-group -CH3 to any cytosine base directly before a guanine base in the
same DNA chain, and has the effect of turning genes off; conversely,
removing the methyl group, or under methylation turns genes on.) As a result of
these epigenetic changes, the cells continue to replicate, activating the processes
related to promotion of replication, and suppressing processes related to
inhibition of proliferation, cell cycle arrest, apoptosis, and DNA repair. Most
of the well-known oncogenes are key regulators in these processes. The
generation of mutations by error-prone DNA replication is not random. Instead
the mutations match the epigenetic alterations .
Hypermethylated genes are known to be predisposed
to all kinds of mutations: point, frameshift, missense, and deletions,
resulting in loss of function. Hypomethylation, on the other hand, predisposes
to chromosomal mutations, rearrangements and aneuploidy, conferring usually a
gain of function. In addition, global demethylation leads to a variety of
mutations through the activation of DNA repeats. In sum, the epigenetic changes
predispose cells to generate adaptive mutations characteristic of tumour cells.
Among the evidence cited in support of
their hypothesis is that the epigenetic changes in cells exposed to stress are
indeed similar to those indicated in premalignant and early stages of cancer
development. For example, many studies have shown early epigenetic silencing of
genes involved in cell cycle arrest and apoptosis, including cyclin-dependent
kinase inhibitors p16, p14, p14, p73, APC,
and DAP-kinase. Early hypomethylation is found for transcription factors
involved in activation of proliferation such as c-myc and c-fos,
and transduction of proliferative and survival signals such as EGFR, and
Karpinets and Roy also pointed out that rodent
cells in culture readily undergo ‘spontaneous’ neoplastic transformations (abnormal
growth that may not may not be malignant). In a primary culture of mouse
embryo cells, a small number of cells survive after apoptosis crisis by forming
immortal cell lines that can overgrow the culture. These cells are primed for
The hypothesis may explain the delayed
effects of environmental factors on cancer development, the latent period
corresponding to epigenetic adaptation (though it does not explain why different
latent periods exist).
A major question raised is what mechanisms
are responsible for the epigenetic ‘reprogramming’ of cells under stress.
Evolution of tumours and adaptive mutations
Chen Ding-Shinn and Wu Chung-I at the Beijing Institute of
Genomics, Chinese Academy of Sciences in China are lead authors in a report
from a team of 44 researchers who analysed the evolution of tumours in a single
case of hepatocellular carcinoma exhaustively . They wanted to know how
many adaptive mutations drive the tumour growth, how strongly each mutation
drives the growth, and what kinds of mutations they are. Cancer mutations are
often divided into drivers - those that contribute directly to tumour formation
- and others that are merely passengers. The team decided to look for answers
in the dynamics of tumour cell proliferation in the patient. They used Next
Generation Sequencing techniques that can generate huge amounts of sequence
data rapidly, with each sequence repeated many times so the frequency of
different variants can be determined and rare variants detected.
The female patient had chronic hepatitis B
virus infection, and was diagnosed with hepatocellular carcinoma at age 35. A
primary tumour removed in the first surgery was grade II to III (IV being the
most advanced). Fifteen months later a recurrent tumour was removed in the
regenerated liver at the site of the first resection, plus a smaller recurrent
tumour identified at a second site nearby. The team sampled nine different
sections from the three tumours and seven more sections from the adjacent
Selected sections were subjected to exon
(coding sequence) as well as whole-genome sequencing. (Exon or exome sequencing
selectively sequences the coding regions or exons that are translated into
proteins. In the human genome there are some 180 000 exons, constituting about
1 % of the genome ). Among the mutations validated, 24 were amino acid
changes, and 22 were large (> 1 Mb) insertion/deletion copy number variants.
These somatic mutations defined four evolutionary lineages among tumour cells.
Separate evolution and expansion of these lineages were recent and rapid, each
apparently having only one lineage-specific protein-coding mutation. Thus
three coding changes: CCNG1, P62, and an insertion/deletion fusion gene were found
to be tumour-driver mutations. These three mutations affect cell cycle control
and apoptosis, and are functionally distinct from mutations that accumulated
earlier, many of which are involved in inflammation/immunity or cell anchoring.
The early ‘background’ mutations are believed to predispose cells to the
However, the researchers warned that the
results cannot be generalized to other tumours, as each tumour may have its own
repertoire of driving mutations that could be the target of cancer therapy.
Thus, the available evidence suggest that
chronic stress and inflammation may predispose cells epigenetically to
mutations in the stress related genes; but additional changes of mutations in
cell cycle control/cell suicide genes are involved in triggering tumour
formation. This is borne out by the latest research results on cancer
New studies [13, 14] confirm that a
daily intake of low doses (75 mg) aspirin was sufficient to significantly
reduce risk to a range of cancers, especially colorectal cancer, as well as
oesophageal, gastric, biliary (gall bladder) and breast cancer. It also
prevents the distant metastasis of existing cancers. Aspirin is well-known for
its anti-inflammatory properties .
How cancer can be prevented
The root causes of cancer are overwhelmingly environmental,
as generally recognized [16, 17], and hence largely preventable. Yet very
little investment has gone into cancer prevention compared with the hundreds of
billions spent on treatment or potential cures.
In a comprehensive review, Bharat
Aggarwal and his team at University of Texas Houston in the United States documented
that only 5 to 10 % of all cancer cases can be attributed to pre-existing
genetic defects; the remaining 90-95 % of cases are environmental .
Of all cancer-related deaths,
some 25-30 % are due to tobacco, 30-35 % linked to diet (fried foods, red
meat, alcohol), 15-20 % due to infections (especially viral infections), and
the remaining due to radiation (both ionizing and non-ionizing), stress, physical
inactivity, environmental pollutants, etc. Aggarwal’s team suggest that tissue
inflammation is the link between the agents that cause cancer, which can be
addressed by anti-inflammatory agents. They recommend, among other things, to
stop smoking, eat less meat, and drink less alcohol; and instead to eat more
fruits, vegetables and whole grain cereals, all of which are rich in
anti-oxidants that neutralize reactive oxygen species (ROS), pro-inflammatory
agents produced by cells under stress. (The role of ROS will be further
examined in a later report  Cancer a Redox
Disease, SiS 54).
Aggarwal and colleagues highlight
cancer prevention through diet, and provided long mouth-watering lists (with
illustrations) of fruits, vegetables,
spices, condiments and cereals from around the world with the potential to
prevent cancer .
The fruits include apple, apricot, banana,
blackberry, cherry, citrus fruits, dessert date, durian, grapes, guava, Indian
gooseberry, mango, Malay apple, mangosteen, pineapple, and pomegranate.
The vegetables include artichoke, avocado, Brussels
sprouts, broccoli, cabbage, cauliflower,
carrot, daikon (Chinese/Japanese
white radish) kohlrabi, onion,
tomato, turnip, ulluco (a root crop in the Andean region of South America),
watercress, okra, potato, fiddle head
(the tender new leaves of the ostrich fern found along fresh waterways in the
Maritime Provinces of Canada and the United States) , radicchio (Italian red
cabbage), komatsuna (Chinese green leafy vegetable, a
variety of Brassica rapa), salt bush (a salt tolerant plant Atriplex
hortensis used as food since the stone age), winter squash, zucchini,
The spices and condiments are a treasure trove
of turmeric, cardamom, coriander, black
pepper, clove, fennel, rosemary, sesame seed, mustard, licorice,
garlic, ginger, parsley, cinnamon, curry leaves, kalonji, fenugreek,
camphor, pecan, star anise, flax seed, black mustard, pistachio, walnut,
peanut, cashew nut.
Whole grain cereals include rice,
wheat, oats, rye, barley, maize, jowar (sorghum), pearl millet, proso millet, foxtail
millet, little millet, barnyard millet, kidney bean, soybean,
mung bean, black bean, pigeon pea, green pea, scarlet
runner bean, black beluga, and
all the varieties of Spanish
pardina (lentil), brown, green, green eston, ivory white, multicolored blend,
petite crimson, petite golden, and red
What Aggarwal and colleagues failed to mention
is the importance of eating organically produced food, which are known to
contain more cancer-fighting antioxidants as well as other beneficial nutrients
while being free of cancer-causing pesticides and polluting chemical
fertilizers, and are also what we need for mitigating and adapting to climate
change ( Food
Futures Now: *Organic *Sustainable *Fossil Fuel Free , ISIS publication).
dr.ravindra. Comment left 4th April 2012 15:03:59 enlightened article...
Dr. Michael Godfrey Comment left 4th April 2012 19:07:37 The biologist Bruce Lipton was teaching epigenetics before the word was coined. He famously stated that the nucleus was merely a gonad for cell reproduction and the membrane was all-important as it responded to the environment. Environmental medicine is still regarded as fringe and predictably devoid of financial support by the game-players. However, this article reinforces what we have suspected for some time namely, that cancer results from a toxic and nutrient deficient environment. Change the latter and the cell can revert to normal. Thomas Tallberg in Helsinki at the Bio-Immunology Institute did this with malignant melanoma of the retina last century.
Todd Millions Comment left 8th April 2012 08:08:58 Caveat on the Asprin as a preventative-
The pills are buffered and stuck together with starch.Usually loop hole labeled with the-'may contain'.So you can just bet its corn starch contaminated with unstabe and highly toxicBt insert insecticide mods.Same with the vit C powders and tablets.As well as all baking powders.In the case of ASA-you may wish too try experiments with willow bark teas as an alternative.Caveat-try small weak doses too test and when your gut gets queasy-STOP at that level,which varies fron species and time of harvest.
Stephanie Seneff Comment left 9th April 2012 07:07:18
Very interesting article, and I agree wholeheartedly with much of it. However, I believe that cancer is basically a metabolic disease, where the trigger for the cells to become immortal is tied to a need to dispose of excess serum glucose, fructose and methylglyoxal. Where I disagree is the dietary recommendations for avoiding cancer. The key factor here is dietary sugars, as well as carbohydrates, which are readily converted to sugar. Cancers form a useful function in converting massive amounts of sugar to lactate via aerobic glycolysis. Red meats, on the other hand, are an important source of sulfur-containing amino acids, especially taurine, which is only present in animal-based foods. Low serum taurine is associated with many cancers. Sulfur plays a key role in detoxifying environmental toxins, and sulfur deficiency therefore plays a key role in inducing cancer.
Alison Bleaney Comment left 9th April 2012 09:09:07 Makes perfect sense...it is the 'soup' around the cell that signals stress or non-stress...whatever that 'stress' may be that initiates this/these processes.
Dr. Townley Comment left 9th August 2012 10:10:58 I agree with dr.ravindra. Very enlightening, you should read My work
KAFUI ANKU KAETOZENA (ND) Comment left 6th December 2013 09:09:25 This article is very inspiring and I shall site it in my future discourse. I however disagree with the notion that the cause of cancer has eluded the army of cancer researchers. There is no iota of doubt in my mind! They know exactly what the causes of cancer are. To suggest otherwise is akin to saying that the researchers don't have ears; don't have eyes; don't have families; don't eat or breath; they don't walk on the same streets as all of us; they are hermits! What anybody will term an illusion is actually the control mechanism of the pharmaceutical industry! They control most of the funding of the research works on cancer! Cancer has become a big business just like the vaccines! A multi-trillion industry! It is crass capitalism! There are dozens of people curing cancer naturally; but have been hounded out of oblivion.
kyrani eade Comment left 7th April 2014 15:03:04 I have found that cancer is really about stem cell mediated immunity that is erroneously ignited in the body due to mistaken perceptions. Once the person has an aha experience their body will begin spontaneous remission. The genetic changes are deliberate (adaptive / epigenetic)both in creating cancer cells -what I call barrier and resistance cells- and in returning those cells back to being fully functional, fully specialized cells of whatever tissues they belong to. And the excesses are removed by apoptosis. It all has to do with immunity. The process can be hurried up by what I call mental prescriptions.
Here is where I explain in ordinary language because my audience are lay people.
I have even reached the level of avoiding cancer by "stage-managing" my biology.