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==C-myc's Role in Cancer==
[[Image:800px-Signal transduction v1.png|Apoptosis signal pathway|400 px|thumb]]
C-myc's proliferation is induced by enhancers that help to increase immunoglobin genes functions. It has been seen that the greater amount of C-myc present the higher the chances that cancer is also present. Cancer is often able to grow best in people with weakened immune systems. Since the immune system is weak the T-cells pass over the cancer without noticing that anything is wrong. This combined with the fact that these enhancers cause C-myc to rapidly produce cells is causing cancer in a body that cannot fight it off. The newly formed cells continue to grow on each other. This causes a tumor that is cancerous that is unnoticed. The most common form of cancer that c-myc plays a role in is Burkitt's Lymphoma.


C-myc can not be induced by enhancers unless it has translocated from its normal spot on chromosome 8 to another chromosome.  When C-myc is translocated to a spot next to a gene that is an immunoglobin enhancer gene it can eventually become a tumor.  The reason for this is that when these genes code for the body to make more B-cells, they inadvertantly turn on the gene adjacent to them as well.  Since C-myc is now the new gene next to the enhancer gene it starts to create a lot of C-myc RNA and it then becomes C-myc transcription factor.  The factor then induces cells to divide very rapidly.  The cells then keep dividing until they have formed a cancerous tumor.  This process shows that one cell is all that is needed to create a tumor.  It has been estimated that 100,000 of the cancer related deaths per year in the United Sates are associated with changes in the C-myc gene or its expression.


== References ==
== References ==

Revision as of 08:17, 3 November 2009

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IntroductionIntroduction


c-Myc is a protein that binds to DNA and regulates transcription, a transcription factor. Bishop and collegues discovered viruses that induced chicken sarcomas. They studied the virus and identified an oncogene that would cause uncontrolled cellular proliferation. The viral oncogene that caused the sarcomas was identified as v-myc. Later on the homologous gene in chickens was discovered, and called c-myc. These findings provided evidence that activated c-Myc proteins were significant in cellular growth regulation.

Role in CancerRole in Cancer

Apoptosis signal pathway

c-Myc is further along in the signal transduction pathway of the epithelial growth factor receptor (EGF receptor) which deals with the proliferation of cells. Mutations of c-Myc have a strong correlation to cancer. Normally c-myc is tightly regulated and c-Myc is short lived, but cancer cells express c-myc uncontrollably and are unable to degrade the c-Myc protein. This over expression and inability to rid the protein causes it to be active much longer, thus causing it to promote the over expression of genes needed for cell proliferation causing cancer. Over expression of c-Myc is prevalent in 80% of brest cancers, 70% colorectal cancers, 90% of gynecological cancers, 50% of hepatocellular carcinomas and is particularly prevalent Burkitt’s Lymphoma.

General Functions of C-mycGeneral Functions of C-myc

C-myc is used in cell cycle entry, proliferation, and differentiation. C-myc also helps to bind DNA which activates transcription. The c-myc lives a very short life. It is controlled by the level and temporal pattern of expression of their corresponding gene. Without C-myc an organism is unable to survive since there is nothing allowing cells to differentiate or proliferate. The organisms cannot survive after the pre-T-cell receptor proliferation is unable to be completed.

C-myc is also involved in the body's system of remembering past diseases. T-cells help the body to remember diseases it has previously had. C-myc controls the regulation of T-cells. Without C-myc the T-cells would not be triggered to multiply when a disease that the body has seen before infiltrates the body again.



ReferencesReferences


Dang, C.V.(1999) c-Myc Target Genes Involved in Cell Growth, Apoptosis, and Metabolism. Molecular and Cellular Biology, 19: 1-11.

Kandil, A.N. (1991) Determination of the c-MYC DNA-binding site. Proc. natl. Acad. Sci. USA Vol. 88, pp6162-6166, July 1991 Genetics

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Jason Kwon, Ann Taylor