Environmental Carcinogenesis

Background A normal gene cell transforms into a cancer cell once genes that regulate cell growth and differentiation are altered. These genetic changes may include the gain or loss of entire chromosomes, or the mutation of a DNA nucleotide. It takes, however, a series of mutations on only a certain number of genes for a normal cell to become cancerous. During the development of a malignant tumor, DNA damage occurs as an accumulation of mutations in as many as six or more genes.

Background (cont.) Two types of genes are affected by these genetic changes: oncogenes and tumor suppressing genes (these genes also play important roles in tumor development).

(Proto-)oncogenes In normal cells: In cancer cells: A proto-oncogene codes for proteins that stimulate cell division. In cancer cells: When a mutation occurs in a proto-oncogene, it can become a carcinogenic oncogene that causes these proteins to be overactive, resulting in the formation of large numbers of cells.

More on (proto-)oncogenes Proto-oncogenes: They promote cell growth and mitosis in a variety of ways; many can produce hormones between cells that encourage mitosis. Oncogenes: They are analogous to an accelerator on a car in that they cause the rate of cell division to increase. Oncogenes may be altered genes (mutations of proto-oncogenes) or normal genes expressed at inappropriately high levels. When oncogenes are present, the phenotype of cancer cell development will be expressed.

Proliferation: Rapid reproduction of a cell

Tumor suppressor genes In normal cells: Tumor suppressor genes code for proteins that inhibit cell division. In cancer cells: When a mutation occurs in a tumor suppressor gene, the inhibitory proteins may not function properly, and inappropriate growth of cells (which can be caused by the oncogene, for example) remains unchecked.

More on tumor suppressor genes Tumor suppressor genes can prevent cells with damaged DNA from multiplying until the damaged DNA is repaired. If the damage cannot be repaired, the gene would allow for apoptosis (cell suicide) to remove the threat it poses in the organism. These genes are often disabled by cancer-promoting genetic changes, which would then lead to the growth of cancer cells.

Tumor suppressor genes  oncogenes

Angiogenic genes Angiogenic genes control the creation of blood vessels. Although they are vital towards growth, development, and wound healing, they actually help tumors to transition from a dormant state to a malignant one. This lead to the use of angiogenesis inhibitors (some are a normal part of the body's control, some are administered as drugs). The tumors increase in size because angiogenic genes provide a constant supply of blood to the tumor, meaning less water, oxygen and vitamins will be reaching the healthy tissues. This higher nutrient supplies means that cancer cells are less likely to die, thus maintaining the tumor’s size.

Metastasis genes Since metastasis is the spread of a disease from one organ or part to another non-adjacent organ or part, metastasis genes control where such cells go. These genes are the ones that would allow cancer cells to spread to other parts of the body.

Works Cited http://envirocancer.cornell.edu/Factsheet/Genetics/fs6.TSgenes.cfm http://www.enotes.com/carcinogenesis-reference/carcinogenesis-172934 http://www.cancer.org/Cancer/CancerCauses/OtherCarcinogens/GeneralInformationaboutCarcinogens/known-and-probable-human-carcinogens