In medical research, the current belief holds that most cancers are caused by exposure to carcinogens, and that carcinogens cause cancer by damaging DNA.
However, a few discoveries and little benefits to the public have been produced by the huge effort and billions of dollars invested by the NIH, private foundations, and pharmaceutical companies in searching for damaged DNA in cancer. This limited success has a simple reason. Most of the cancers’ causes is not damaged DNA.
Hunting for Genetic Mutations and Cancer
A Little background about cancer:
- A gene is an assembly line that generates protein. DNA makes a gene.
- Proteins are cells’ major building blocks
- A mutated gene is assembly line that is modified. Removing an essential part of the assembly line, replacing an important part with junk, etc. are some examples of how a modification can take many forms. In most cases, a mutated gene is considered damaged DNA.
As the word cause has two meanings, the cause of the cancer first refers to carcinogens, such as tobacco, x-ray radiation, asbestos, other chemicals, etc. which are elements in the environment that impact our body. Hundreds of substances are classified as carcinogens today.
The internal element of the body, which is the first to collapse under the attack of the carcinogens, is referred as the other meaning of the word cause. This element is called “Achilles heel.”
That most cancers are caused by exposure to carcinogens, and that carcinogens cause cancer by mutating genes are the current belief in medical research holds. In other words, the structural integrity of our genes is our Achilles heel, and therefore, the first internal element to collapse under the attack of the carcinogens, according to the current belief.
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” as this belief is so ingrained.
Furthermore, the keywords “Mutation” AND “cancer” produced 86,490 papers and 12,238 reviews on PubMed, the search engine for scientific papers in life science. It is a big business as well, the mutation hunting.
Look at 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, the NIH budget allocated to discoveries of genetic mutations, and the number of stories in the media on genetic mutations and their so-called “link” to disease.
Nevertheless, only a few discoveries and little benefits to the public have been produces by this huge effort and billions of dollars. The limited success of this is because the cause of most cancers is not a genetic mutation. The structural integrity of our genes is not our Achilles heels. A typical example of mutation hunting is the story of the BRCA1 gene.
The Mystery of BRCA1
In general, genes produce protein which is cells’ building blocks. Protein’s concentration is tightly regulated. An abnormal concentration of its protein produced by a mutated or physically altered gene can lead to disease.
Mark Skolnick, PhD, discovered the BRCA1 gene (BRCA1 is short for BReast CAncer 1) in 1994. Scientists observed an abnormally low level of the BRCA1 protein in breast cancer tissues when following the discovery. The BRCA1 protein prevents cell replication or a cell cycle suppressor.
Scientists believed that they were on the verge of finding the cause of breast cancer at that time. In breast cancer patients, a defected BRCA1 assembly line, which would explain the decreased production of the protein, and the excessive replication of breast cancer cells in tumors – this is the reason why breast cancer have a mutated BRCA1 gene.
Each year, there are 180,000 cases of breast cancer are diagnosed in the United States. However, there is only less than 5% of the BRCA1 that is mutated in these cases. The assembly line is not defected in more than 95% of breast cancer patients the gene is not mutated. So the mystery is here.
Why are the tumors showing low levels of the BRCA1 protein if the gene is not mutated in the great majority of the breast cancer patients? It is the biggest mysteries in cancer research.
Since the BRCA2 gene is not unique, many normal (perfect shape, non-mutated) genes exhibit a mysterious abnormal (increased or decreased) production of proteins in cancer.
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, abnormal gene expression of normal genes are reported in studies.
“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 deregulated gene(s), suggesting that a genetic alteration is not the initiating event of cancer” – as expressed by 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).
So, what is this event if a genetic alteration (also called genetic mutation or damaged DNA) is not the initiating event of most cancers? And how this event initiated by carcinogens? Find the answers to these questions at www.causeofcancer.org.