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Have you ever wondered how cancer forms? Well, cancer starts when a cell's DNA becomes altered. When the DNA is altered, the cells reproduce without restriction and do not die like a normal cell. These extra cells form a mass of tissue that is a tumor. Cancer forms in the genes of our cells, and is able to be carried in the offspring of the person with cancer.
[Research Support, U.S. Gov't, P.H.S.]. Am J Pathol, 145(4), 837-845. Tan, W. W. H., J.E. ;Schulman, P. (2012, 29 Feb 2012). Malignant Melanoma Retrieved 15 March, 2012, from http://emedicine.medscape.com/article/280245-overview Toh, B., Wang, X. J., Keeble, J., Sim, W. J., Khoo, K., Wong, W. C., .
Implications of Cancer Stem Cell Theory for Cancer Chemoprevention by Natural Dietary Compounds. Retrieved December 12, 2013, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248810/ Nikitina, E. G., Urazova, L. N., & Stegny, V. N. (2012). MicroRNAs and Human Cancer.Experimental Oncology, 34(1), 2-8. Retrieved from http://archive.nbuv.gov.ua/portal/chem_biol/eol/2012_1/002.pdf Wang, K., Wu, X., & Huang, J. (2013, February 28).
Cancer cells within the tumor will then use the newly formed blood vessels as a port to metastasize to other localities. Including the drugs for colon cancer, a growing number of anticancer agents have been shown to inhibit hypoxia inducible factor (HIF) gene activity. For many of these, the mechanism of action has been established and involves a reduction in HIF-1 mRNA or protein levels by suppressing the HIF gene expression (Semenza, 2007). Hypoxia is the principal trigger to stimulate VEGF gene transcription and subsequently to angiogenesis. VEGF is responsible triggering the various steps in the angiogenesis cascade such as proliferation, migration and cell survival.
Intrinsic apoptotic pathway is widely implicated as a barrier to cancer pathogenesis than extrinsic apoptosis pathway (Hanahan and Weinberg 2011). In order to understand anti-apop... ... middle of paper ... ...F. Burrows (2006). “Dimericansamycins—A new class of antitumor Hsp90 modulatorswith prolonged inhibitory activity.”Int. J. Cancer120: 918–926. 32.
(2010, June 06). Retrieved from http://www.cancer.gov/cancertopics/factsheet/Therapy/radiation Stem cell transplant. (2012, August 22). Retrieved from http://www.mayoclinic.org/tests-procedures/stem-cell-transplant/basics/definition/prc-20013565 Thompson, G., & Leber, B. (2012, December 14).
This uncontrollable division of cells is cancer. Another gene that could be mutated is a Proto-Oncogene. An oncogene is a proto-oncogene that has been mutated to accelerate proliferation, which in response causes cancer. Another tumor suppressor gene is called the p53 gene. This is a tumor suppressor gene that acts as a check point in cellular proliferation.
One of the recent developments in the research behind oncogenesis and its relationship to cancer is the theory of “oncogenic addiction”. This theory explains the phenomena of “a tumor cell seemingly exhibiting dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival” (Sharma & Settleman 2007). These findings suggest that there may be a way to “switch off the crucial pathway of dependence”, which in theory should negatively affect or inhibit the cancer, “while sparing normal cells that are not similarly addicted” (Sharma & Settleman 2007). This has been established with the ability to inactivate “counterparts of oncogenic proteins in normal tissues” and see that there is toleration without “obvious consequences” (Sharma & Settleman 2007). This is the concept of “addiction” in cancer, and the dependence on particular genes to activate prolifer... ... middle of paper ... ...need to be developed to begin this study, we can infer from past research the steps in which determination of these relationships could be done.