Cases of death caused by cancer are increasing, and according to researchers, cancer is caused by different factors including gene-environmental interactions. Gene-environmental interaction is a condition where genetic and environmental exposure interact causing a disease; therefore, absent of either genetic or environmental exposure does not cause the disease. This paper will discuss gene-environmental interactions as a cause of cancer.
Current research on the mechanism of cancer highlights that almost all cancers are caused both environmental and genetic factor; this means that environmental exposures and genetic changes come together to form the disease (Clapp et al, 2005). This process is described in six alterations, which may overwhelm the natural defense found in the body cells and tissues leading to the development of a tumor.
According to the intestinal biopsy samples analysis carried at different stages of growth of malignant, copies of APC, a tumor suppressor gene found on chromosome 5, mutated when in dysplastic lesions as well as in early adenomas (Brennan, 2002). Also, there was a case of mutation in RAS oncogene; this was spotted in advanced adenomas. More cases of mutations were detected in DCC tumor gene suppressor found in advanced polyps, with most mutations being observed in p53 genes tumor suppressor; these mutations happened at the termination of the process of carcinogenesis. Such kind of mutations have been associated to genetic and environmental exposures (Brennan, 2002). A disease such as ulcerative colitis is autoimmune and leads to colon mucosa inflammation, as well as increase risk of developing colorectal cancer. The alterations in the genes can be prevented through the prevention of carcinogenic exposures emanating from the environment.
Other researchers have revealed other gene-environment interactions; according to Clapp et al (2005), people with certain genetic predispositions have more risk of being affected by environmental exposures when compared to others. For instance, people who have BRCa1 or BRCA2 gene are more vulnerable to environmental exposure effects; p53 gene alterations make these people unable to suppress the multiplication of cancer cells or mutation of the NAT gene modifying its ability to transform environmental chemicals to produce cancer readily (Clapp et al, 2005). However, more research has shown that, in a given population, only a small percentage of people have genetic predispositions. This means that many cases of cancer emanating from exposure to carcinogens is only as a result of exposure itself, and not as a result of excess risk in subgroups characterized by rare or particular genetic predisposition. However, according to Clapp et al (2005), this argument does not keep in mind that there are some sub-groups in the population, which are affected more by cancer than others, and if this is the case, then, there must have something that make them more vulnerable to cancer than others.
According to the formation of cancer from gene-environment interactions, the combination of exposures is a requirement to produce tumor; therefore, prevention measures should be directed at preventing the components from interacting, this is to say that individual components cannot cause cancer (Lohmueller, 2003). However, prevention should not be aimed at preventing one cause against the other; prevention efforts should be at reducing exposures from avoidable sources such as occupational and environmental sources.
In conclusion, gene-environment interactions are the main causes of all cancers, and are because of exposure to carcinogens. To prevent the development of cancer, it is only wise to prevent gene-environment interactions from any source that is avoidable. However, more research need to be done to ascertain what make some sub-groups in a population to register more cancer cases than others.
Brennan, P. (2002). Gene-environment interaction and the etiology of cancer: what does it mean and how can we measure it? Carcinogenesis, 23(3), pp. 381-387.
Clapp, R. et al. (2005). Environmental and Occupational Causes of Cancer. A Review of Recent Scientific Literature, 6(3), pp.1-29.
Lohmueller, K. et al. (2003). Meta-analysis of genetic association studies supports a contribution of common variants to susceptibility to common disease. Nature Genetics, 33(5), pp. 177-182.