Mechanisms of Cancer the Cancer Term Paper

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This then leads to the activation of a number of genes whose products trigger cell-cycle arrest, apoptosis, or DNA repair" (Lakin 1999, p. 7644).

In research led by Hussain, he investigated the targets of free radicals, which are DNA, proteins, RNA, and lipids. He noted that, "mutations in cancer-related genes or post-translational modifications of proteins by nitration, nitrosation, phosphorylation, acetylation or polyADP-ribosylation-by free radiacals or lipid peroxidation byproducts…are some of the key events that can increase the cancer risk" (Hussain 2003, p. 276). Furthermore, changes in DNA occur when the person has been exposed to high levels of nitric oxide or NO. p53 plays a role in that it acts as a mediator to stress but NO "causes p53 accumulation and post-translational modifications that inhibit cellular growth" (Hussain 2003, p. 278). His research has revealed that when exposed to NO during chronic inflammation sans wild-type p53, there might be increased risk due to negative inducible NO synthase or iNOS regulation. In the same study, the cellular workings of breast cancer was stated by that the "polymorphism of the gene encoding the antioxidant enzyme manganese superoxide dismutase (MnSOD), which convert O2 to H2O2 alters protein trafficking" (Hussain 2003, p. 282) thus increasing such risk. Lung cancer risk is increased due to the "polymorphism at Pro198LEU in the glutathione peroxidase 1 gene -- which converts H2O2 to water" (Hussain 2003, p. 282).

The concern for cancer is ever growing and no one is immune to such a disease, which can take place anywhere in the body due to abnormal cell growth. However, certain environmental factors may be done to reduce risk, such as eating better and becoming more active while discarding a smoking habit. Unfortunately, genetics plays a role and family history of cancer potentially increases one's risk. Studies have shown and been aforementioned in regards to the mechanisms of cells in cancer, which range from inflammation to free radicals.

References

American Cancer Society (n.d.) Cancer Facts & Figures 2010, [online] Available at: http://www.cancer.org/research/cancerfactsfigures/cancerfactsfigures/cancer-facts-and-figures-2010 [Accessed: April 19, 2011].

American Cancer Society (n.d.) What Causes Cancer?, [online] Available at: http://www.cancer.org/Cancer/CancerCauses/index [Accessed: April 19, 2011].

Croce, C. (2008) Oncogenes and Cancer, N Engl J. Med, 358, p. 502-511.

Hasty, P. (2005) the impact of DNA damage, genetic mutation and cellular responses on cancer prevention, longevity and aging: observations in humans and mice, Mech Ageing Dev, 126(1), p.71-77.

Harris N., Brill E., Shohat, O., Prokocimer, M., Wolf, D., Arai, N., Rotter, V. (1986) Molecular Basis for Heterogeneity of the Human p53 Protein, Molecular and Cellular Biology, 6(12), p.4650-4656.

Hussain, S. And Hofseth, L. (2003) Radical Causes of Cancer, Nat Rev Cancer, 3(4), p.276-285.

Pikarsky, E., Porat, R., Stein, I., Abramovitch, R., Amit, S., Kasem, S., et al. (2004) NF-kappaB functions as a tumour promoter in inflammation-associated cancer., Nature, 431, p.461-466.

Preston-Martin, S., Pike, M., & Ross, R. (1990) Increased Cell Division as a Cause of Human Cancer, Cancer Res, 50(0), p.7415-7421.

Rose-John, S. And Scheller, J., Elson, G., & Jones, S. (2006) Interleukin-6 biology is coordinated by membrane-bound and soluble receptors: role in inflammation and cancer, Journal of leukocyte biology, 80, p.227-236.

Schetter, a.…

Sources Used in Documents:

References

American Cancer Society (n.d.) Cancer Facts & Figures 2010, [online] Available at: http://www.cancer.org/research/cancerfactsfigures/cancerfactsfigures/cancer-facts-and-figures-2010 [Accessed: April 19, 2011].

American Cancer Society (n.d.) What Causes Cancer?, [online] Available at: http://www.cancer.org/Cancer/CancerCauses/index [Accessed: April 19, 2011].

Croce, C. (2008) Oncogenes and Cancer, N Engl J. Med, 358, p. 502-511.

Hasty, P. (2005) the impact of DNA damage, genetic mutation and cellular responses on cancer prevention, longevity and aging: observations in humans and mice, Mech Ageing Dev, 126(1), p.71-77.

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