Major Discovery: How Carcinogens Cause Cancer
The current belief in medical research holds that most cancers
are caused by exposure to carcinogens, and that carcinogens
cause cancer by damaging DNA. However, the huge effort and
billions of dollars invested by the NIH, private foundations,
and pharmaceutical companies in searching for damaged DNA
in cancer has produced few discoveries and little benefits
to the public. The reason for this limited success is very
simple. The cause of most cancers is not damaged DNA.
(PRWEB) May 27, 2006 -- The current belief in medical research
holds that most cancers are caused by exposure to carcinogens,
and that carcinogens cause cancer by damaging DNA. However,
the huge effort and billions of dollars invested by the NIH,
private foundations, and pharmaceutical companies in searching
for damaged DNA in cancer has produced few discoveries and
little benefits to the public. The reason for this limited
success is very simple. The cause of most cancers is not damaged
DNA.
Hunting for Genetic Mutations and Cancer.
A little background:
1. What is a gene? A gene is an assembly line that produces
a protein. A gene is made out of DNA.
2. What are proteins? Proteins are the major building blocks
of cells.
3. What is a mutated gene? A mutated gene is a modified assembly
line. A modification can take many forms, such as removing
an essential part of the assembly line, replacing an important
part with junk, etc. Very rarely a mutation is beneficial
to the organism (X-Men, Evolution, Lance Armstrong?). In all
other cases, a mutated gene is considered damaged DNA.
Current belief:
What is the cause of cancer? The word cause has two meanings.
The first refers to the elements in the environment which
impact our body, for instance, tobacco, x-ray radiation, asbestos,
other chemicals, etc. These elements are called carcinogens.
Today, hundreds of substances are classified as carcinogens.
The other meaning of the word cause refers to the internal
element of the body, which is the first to collapse under
the attack of the carcinogens. Let's call this element our
"Achilles heel."
The current belief in medical research holds that most cancers
are caused by exposure to carcinogens, and that carcinogens
cause cancer by mutating genes. In other words, according
to the current belief, the structural integrity of our genes
is our Achilles heel, and therefore, the first internal element
to collapse under the attack of the carcinogens. This belief
is so ingrained that the National Human Genome Research Institute
(NHGRI), an institute at the NIH, recently stated that "all
cancers are based on genetic mutations in body cells."
Moreover, a search on PubMed, the search engine for scientific
papers in life science, with the keywords "Mutation"
AND "cancer" produced 86,490 papers and 12,238 reviews.
Mutation hunting is also a big business. Look at the NIH budget
allocated to discoveries of genetic mutations, the number
of biotech companies chasing genetic mutations, the magnitude
of the licensing agreements between biotech and pharmaceutical
companies aimed to utilize newly discovered genetic mutations,
and the number of stories in the media on genetic mutations
and their so-called "link" to disease. However,
this huge effort and billions of dollars has produced few
discoveries and little benefits to the public. The reason
for this limited success is simple. The cause of most cancers
is not a genetic mutation. Our Achilles heel is not the structural
integrity of our genes.
The story of the BRCA1 gene is a typical example of mutation
hunting.
The Mystery of BRCA1
Genes, in general, produce proteins, which are the building
blocks of cells. The concentration of proteins is tightly
regulated. A mutated or physically altered gene produces an
abnormal concentration of its protein, which may lead to disease.
In 1994, Mark Skolnick, PhD, discovered the BRCA1 gene (BRCA1
is short for BReast CAncer 1). Following the discovery, scientists
observed an abnormally low level of the BRCA1 protein in breast
cancer tissues. The BRCA1 protein is a cell cycle suppressor,
which means that the protein prevents cell replication. This
observation created a lot of excitement. At the time, scientists
believed that they were on the verge of finding the cause
of breast cancer. The reasoning was that breast cancer patients
must have a mutated BRCA1 gene, that is, a defected BRCA1
assembly line, which would explain the decreased production
of the protein, and the excessive replication of breast cancer
cells in tumors.
In the United States, 180,000 cases of breast cancer are diagnosed
each year. However, the BRCA1 gene is mutated in less than
5% of these cases. In more than 95% of breast cancer patients
the gene is not mutated, the assembly line is not defected.
So here is the mystery. If the gene is not mutated in the
great majority of the breast cancer patients, why are the
tumors showing low levels of the BRCA1 protein? Today, this
is one of the biggest mysteries in cancer research.
The BRCA1 gene is not unique. Many normal (perfect shape,
non-mutated) genes exhibit a mysterious abnormal (increased
or decreased) production of proteins in cancer. Moreover,
studies also report abnormal gene expression of normal genes
in other diseases, such as atherosclerosis, obesity, osteoarthritis,
type II diabetes, alopecia, type I diabetes, multiple sclerosis,
asthma, lupus, thyroiditis, inflammatory bowel disease, rheumatoid
arthritis, psoriasis, atopic dermatitis, and graft versus
host disease.
According to Dr. Raxit J. Jariwalla in his European Journal
of Cancer paper: (Jariwalla RJ. Microcompetition and the origin
of cancer. Eur J Cancer. 2005 Jan;41(1):15-9): "The prevalent
view of the nature of cancer holds that it is a complex genetic
process resulting from the progressive accumulation of mutations
in specific cellular genes, such as proto-oncogenes or tumor-suppressor
genes, leading to perturbations in processes involving signal
transduction, cell cycle regulation, and/or apoptosis. Genetic
instability in tumors has been known for decades, however,
the role of genomic instability in causing and promoting tumor
growth remains controversial. Furthermore, although many studies
report abnormal gene expression in cancer cells, often, no
mutations or chemical modifications are observed around the
locus of the dysregulated gene(s), suggesting that a genetic
alteration is not the initiating event of cancer."
So, if a genetic alteration (also called genetic mutation
or damaged DNA) is not the initiating event of most cancers,
what is this event? And how do carcinogens produce this initiating
event? You can find the answers to these questions at http://www.causeofcancer.org/
John S. Boyd, Ph.D.
The Center for the Biology of Chronic Disease (see http://www.cbcd.net/),
and causeofcancer.org (see http://www.causeofcancer.org/),
Rochester, NY. We are a 501(c)3 not-for-profit organization
that specializes in researching the biology of chronic disease,
which means the original disruption that causes a chronic
disease, and the sequence of events that lead from the original
disruption to the development of clinical symptoms. We hope
that once the biology is clear, pharmaceutical and biotech
companies will be able to formulate drugs that reverse the
effects of the disruption, and therefore cure the disease,
or even block the original disruption, and therefore prevent
the disease from developing in healthy individuals.
Company Name: CENTER FOR THE BIOLOGY OF CHRONIC DISEASE
Website: http://www.causeofcancer.org
