Colorectal Cancer

While smoking, obesity, and a poor diet play a contributory role in the development of colorectal cancer, it has been estimated that up to 30% of such cancers are genetically linked. Colorectal cancer is the fourth most common cancer, and the average risk that an individual will develop colorectal cancer in their lifetime is 6%. Individuals with a first-degree relative with colorectal cancer are twice as likely to develop a disease as the general population.

The genetic variants that are studied and which have been linked to an increased risk for colorectal cancer are two variants located on chromosome 8 (one in the EIF3H gene and the other close to POU5F1P1) and then one variant on each of chromosomes 10, 11, 14 (close to the BMP4 gene), 15 (in the CRAC1 gene), 18 (in the SMAD7 gene) and 20.

Lung Cancer

Lung cancer causes more deaths worldwide than any other cancer. The single most important factor influencing the risk of developing lung cancer is smoking, but not all smokers develop lung cancer and some non-smokers do. Genetic factors may influence who ends up getting the disease.

Studies have indicated there may be an association between the diagnosis of lung cancer and two specific variants in the genome. One variant is located on chromosome 15 within the nicotinic acetylcholine receptor gene cluster. In smokers, this same variant also increases the risk for Nicotine Dependence and Peripheral Arterial Disease. The second variant is located on chromosome 5 near the TERT gene.

Advances in Detection

The earlier lung cancer is detected the better the chances of healing the patient, but in the initial stages tumor related complaints resemble a chronic inflammatory condition.

Until now the patient has to undergo complex invasive testing but there will hopefully soon be a better way.

After the patient blows into a piece of equipment for about 20 minutes the exhaled breath condensate is evaporated. The residue is tested to see if it contains certain bio-markers which can be identified by the use of antibodies, as being indicative of cancer cells. Diagnosis will be possible at an early pre-symptomatic stage with less trauma to the patient.

Basal Cell Carcinoma (Skin Cancer)

Basal Cell Carcinoma is the most commonly occurring cancer in humans and occurs in three main forms: melanoma, basal cell carcinoma, and squamous cell carcinoma. Basal cell carcinomas are malignant tumours that originate in the basal cells lining the inner part of the epidermis, and account for 75% of all diagnosed cases. This type of skin cancer appears most frequently on areas of the skin exposed to the sun, and it is believed that exposure to UV-rays of the sun are the main risk factor. It is likely that an interaction of genes and environment cause basal cell carcinoma. A light complexion provides less protection from UV radiation than a dark complexion. Because skin, hair and eye colour are largely determined by genetics, basal cell carcinoma results from a mixture of genetic and environmental factors, but there are also genetic risk factors that appear to act independently of exposure to UV radiation.

Three genetic variants may confer a significant risk of developing basal cell carcinoma in people of European descent. Two variants are located on chromosome 1, one of them close to the PADI6 and RCC2 genes and the third variant is on chromosome 5 near the TERT gene. These variants are not known to affect the hair, eye and skin color traits that are associated with poor UV protection. Therefore they probably represent risk factors that are separate from and therefore additional to UV radiation exposure.

Thyroid Cancer

Thyroid cancer is the most common endocrine cancer, and although it is the result of both environmental and genetic factors, it has one of the strongest genetic components of all cancers. Our cancer scan identifies the genetic variants and provides an interpretation of the associated risk for the development of thyroid cancer for individuals of European descent.

Two genetic variants have been identified on chromosomes 9 and 14. The variants contribute to an increased risk of the two main types of thyroid cancer, papillary and follicular. Furthermore, the risk alleles are associated with younger age at diagnosis.

Prostate Cancer

Prostate cancer is the most common non-skin-cancer among men. Genetic variants are a significant contributor to the risk of developing prostate cancer, in fact, of all cancer types, prostate cancer is most closely linked to genetic risk factors. Prostate growths can be benign (not cancer) or malignant (cancer), and in most cases, is a relatively slow growing cancer which may take a number of years to become detectable.

There are thirteen genetic variants that are known to increase the risk of developing prostate cancer: three in the chromosome 8q24 region, two on chromosome 17q (one of which is located within the TCF2 gene) and one on each of the following chromosomes: 2, 3, 5, 6, 7, 10, 11, and X.

Men with a single relative with prostate cancer are twice as likely to develop prostate cancer, while those with two or more relatives are nearly four times as likely to be diagnosed with the disease. The risk is even higher if the affected family members were diagnosed before the age of 65.

Bladder cancer

Urinary bladder cancer is the sixth most common form of cancer and has been linked to exposure to various types of toxic substances such as cigarette smoke and industrial chemicals, but genetic factors play a significant role. The risk of bladder cancer is three times greater in men than in women, and increases with age.

The genetic factors that play a significant role include three genetic variants on chromosomes 3, 5, and 8 that increase the risk of developing bladder cancer.

The Risk Levels of Variant Genes In Our Cancer Screen

Cancer is a complex disease and environmental and lifestyle factors play significant roles often impacting genetic vulnerability. Age, Ethnicity and sex obviously have an impact on the level of vulnerability to certain of the potential cancers.

The following chart indicates increased risk levels for genetic variants and other influencing factors. Not having a genetic variant does not exclude the possibility of a particular disease an environmental, lifestyle and genetic factors not included in our screen may play a role.

The following chart indicates increased risk levels for genetic variants and other influencing factors.

Genetic variants screened	Approximate Increased risk screened level if variant found			Relative Vulnerability
				Age	Sex		Ethnicity
	5-10%	10-20%	20%		Male	Female	Caucasian	African	Asian
Thyroid Cancer
Basel Cell(Skin) Cancer
Lung Cancer
Colorectal Cancer
Prostate Cancer
Bladder Cancer
Breast Cancer

Cancer Scan Results

The results of your DNAffirm Genetic Cancer Scan will be explained in terms you and your physician will understand, and decisions can be made as to whether additional prevention or detection strategies may be beneficial.

The genetic tests for carcinoma provide a numerical value to the risk, which is always less than 100%, and most often substantially less than that. Carrying a genetic risk variant for a disease does not mean you will develop a disease, and not having a certain risk variant does not eliminate the possibility of developing a disease. Variants impact the likelihood that one may develop the disease, and understanding the genetic risk is empowering information.

It is possible to take preventative action through lifestyle modification and certain medications. The situation should be discussed with your physician.

The genetic tests performed in the cancer scan are risk tests, more analogous to biomarker risk tests such as LDL-Cholesterol and PSA, rather than a definitive Mendelian genetic test, like for Huntington’s disease, which is essentially definitive.

A result that indicates a variant should direct you to discuss the implications with health care professionals and take the necessary steps to minimize contributory risk factors.

An Important Causative Factor in Carcinoma

A great deal of publicity is always generated by walks and runs etc. which heroically attempt to raise funds in the treatment and possible cures of cancer.

Cancer is a complex environmental/genetic disease with innumerable causative factors. Despite the complexity of the disease incremental progress is made when we focus on individual biological missteps that play a definitive role.

The DNAffirm Genetic Cancer Scan looks at some critical genetic factors that influence an individual's level of risk. The underlying broader question is what influences the gene mutations that we screen for, because they indicate elevated risk.

Here again we are confronted with multiple factors but one that holds much promise is understanding the role of CLIP-170 (Cytoplasmic Linked Protein) which plays a determinant role in cell duplication and DNA distribution. Credit for a great deal of research in this area must be given to Xiaoqui Liu, a Purdue University researcher. When CLIP-170 is removed from cells cell duplication produces imperfect copies of the original DNA and those cells can become cancerous. Normal cells have a highly regulated process to avoid aneuploidy, the unequal distribution of chromosomes, a syndrome linked to cancer.

As a cell divides it creates a second copy of its own DNA and generates two centrosomes, poles that act as magnets to draw the DNA to them. When this occurs the cell divides in a process called mitosis producing two normal identical cells.

When CLIP-170 is removed more than two centrosomes are formed, pulling copies of the DNA in multiple directions. The cell can be described as becoming confused and potentially cancerous.

A cyclin dependent kinase called Cdc2 is considered the master regulator of cell growth and activates CLIP-170 triggering it to function properly. Understanding these complex genetic factors is a significant step in attempting to mitigate the onset of cancer.

The DNAffirm Genetic Cancer Scan identifies important genetic risk factors even before symptoms are evident. The DNA extraction and genetic analysis are done on the inner cheek swabs containing buccal cells which are collected by the individual.

An easy to use no cost collection kit will be sent on request by Viaguard. The laboratory fee of $989 is remitted with the samples when they submitted for analysis. The analysis and report are available about 21 days after receipt of the samples.

 

Cancer and Genetics

 

Recent advances in technology and gene sequencing enable us to generate accurate, detailed results much more efficiently and economically than even a few years ago. Viaguard’s genetic cancer screen, once several thousand dollars now costs a few hundred.

 

Genetically linked diseases fall into two broad categories.

 

Monogenetic diseases result from a mutation in a single gene, i.e. huntingtons disease,and the mutation on chromosone 4. These diseases are minimally impacted by environmental factors.

 

Most genetically linked diseases are caused by a multiplex of genetic and environmental factors. The seven cancers screened in the Viaguard test fall into this category.

 

Various genetic factors influence these cancers but certain genetic linkages indicate a strong predisposition. Test results indicate the level of that predisposition compared to others of a similar ethno-geographic origin.

 

Those in a higher probability category may be well advised to make life style changes and improve their avoidance prospects.

 

Viaguard Cancer Screen and the Origins of Cancer

 

Human genes linked to cancer have been traced back 600 million years to an Oncogene-myc found in fresh water polyps which are about 2 mm in size.

 

This gene has been conserved through 600 million years of evolution and functions by enabling the production of a protein which regulates the behaviour of up to 15% of all human genes.

 

Deactivation of the myc gene leads to uncontrolled cell proliferation and cancer evident in about 30% of all human cancers.

 

Ongoing studies are attempting to identify which genes are regulated by myc and which genes lead to cancer. Viaguard’s Cancer Screening test is based on those genes found that have demonstrated significant links to a predisposition to cancer.

 

Cancer and the role of the PTEN gene

 

The PTEN gene located on chromosome 10, position 23.3 plays a significant role in a number of cancers. Normally this gene is a cancer suppressor because it facilitates the cellular production of an enzyme called phosphatise which regulates cell division. This enzyme prompts cells to stop dividing and in effect terminate themselves by fragmentation iin a process called apoptosis. If the PTEN gene becomes mutated genetically or by environmental factors the phosphatise enzyme doesn’t function properly leading to rampant cell division with resultant tumours. Persons with a genetic mutant gene often display symptoms of a large head size and autism. The cancers resulting from this particular mutation are linked to breast, thyroid, ovarian, and prostate carcinoma. When the mutation has occurred as a result of environmental factors during a person’s lifetime it is known as a somatic mutation.

 

The Inhibition of Metastases (Malignancy)

 

Pectins, which are found in a variety of fruits, are long chain polysaccharides whose molecular structure resembles the sugar galactose. In a situation with similarities to competitive inhibition, galactose binds with galectins, a class of carbohydrate binding proteins which normally lie on the surface of cells. Galectins allow cells to communicate, and adhere to each other. This is a normal cellular function where the number of Galectins on the cell surface is small.

Cancerous cells have an increased number of Galectin-3 on their surface, which facilitates cells attaching to each other and forming groups that survive locally and systemically in a malignant process known as metastasis.

The competitive inhibiting effect of pectin is that it links with galectins on the cell surface, restricting the ability of galactin-3 molecules to link with each other in a metastatic process.

This is the theory, but the problem has been that the molecular size of pectin molecules does not allow for normal absorption from the gastrointestinal tract into the blood stream. As a result of extensive research, a methodology has been developed which accomplishes two important modifications. The molecular size of citrus pectin, which is 50,000 to 150,000 Daltons, can be reduced by modification to about 10,000 to 20,000 Daltons, which allows for absorption from the gastrointestinal tract. At the same time, the process ensures minimal esterification by methyl groups, which by attaching to the pectin molecules, diminish its inhibitory effect. While ordinary citrus pectins can have up to 75% esterified molecules, modified citrus pectins (MCP) can reduce that number to as little as 10%. While studies are ongoing, there is a body of evidence pointing towards the anti-carcinogenic effect of MCPs in a range of cancers including prostate, breast, and skin cancer.

This would lead us to believe that persons showing a predisposition to these types of cancers after a Viaguard Genetic Cancer Screening test should include modified citrus pectin, which is available commercially at modest prices as a dietary supplement.

 

The Epigenetic Cancer-Linked Effects of Smoking

 

The role of smoking as a causative factor in cancer goes well beyond the obvious risk of lung cancer. Studies have shown that cigarette smoke causes epigenetics changes with as methylation which alters genetic expression.

In the case of gene p16 a so called tumour suppressant gene, methylation interferes with the normal protective functions of the gene resulting in the development of cancer in many parts of the body.

Studies have concentrated on the development of cervical neoplasia, and the results indicate that the women who were smokers, or who took up smoking were three times as likely as non-smokers to acquire p16 methylation.