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Myc is the protein encoded by the MYC gene that activates the cell cycle. It promotes cell replication through genetic coding for p14, inhibiting MDM2 and preventing the degradation of the pro-apoptotic protein p53.
When mutated, the gene may be amplified, giving a genotype found in many tumours. Typically, MYC mutations are found in Burkitt Lymphoma (BL), but can becoming more widely recognised in other non-Hodgkin lymphomas.
Much work has been done on the factors that myc activates and inhibits, as they themselves with hold further clues about the uncontrolled cell proliferation that is so characteristic in cancers. Examples of these downstream molecules include RNA molecules (miR-15a and miR-16-1) expression http://www.bioportfolio.com/news/article/835744/Myc-represses-miR-15a-miR-16-1-expression-through-recruitment-of-HDAC3.html.
But a picture is also being build around how myc expression is regulated, and possible upstream molecules include histone deacetylase 7 (HDAC7) http://www.bioportfolio.com/resources/pmarticle/118144/The-Role-Of-Histone-Deacetylase-7-hdac7-In-Cancer-Cell-Proliferation-Regulation.html , SOX2 (http://www.bioportfolio.com/resources/pmarticle/245136/SOX2-has-a-crucial-role-in-the-lineage-determination-and-proliferation-of.html) ubiquitin ligase CHIP which controls the stability of the myc protein. http://www.bioportfolio.com/resources/pmarticle/314694/The-Ubiquitin-Ligase-Chip-Regulates-C-myc-Stability-And-Transcriptional-Activity.html
Because the role of myc is so central to many cancers, studying the pathway gives researchers a wealth of information and possible targets to develop anti-cancer therapeutics for the millions of people affected by these cancers.