MYC- is a mutated MYC
MYC participates in the regulation of gene transcription. It binds to DNA in a non-specific manner. MYC controls genetic information flow from DNA to the mrna and plays an important role in controlling cell division. “That role is so powerful that cells co-evolved an emergency death pathway to keep c-Myc expression in check. If c-Myc’s production spins out of control in an otherwise normal cell, the cell immediately commits suicide through a process called apoptosis. But in cancer cells in which c-Myc is overproduced, this suicide pathway is compromised, allowing the cell to survive and proliferate (Young).” It is a very strong Proto-oncogene that can mutate into an oncogene that can cause cancer and tumors. MYC- Defects in MYC are a cause of Burkitt lymphoma. A form of undifferentiated malignant lymphoma commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. Effect of MYC- alone is unknown but is related to tumor cells.
Chromosomal aberrations involvingmyc family loci have been implicated in the generation of a variety of human tumors and are often strongly correlated to a poor prognosis. Among these are the translocations involving c-mycand the immunoglobulin loci that occur in a high percentage of human Burkitt＇s lymphoma, AIDS-associated lymphomas, and certain acute lymphoblastic leukemias, resulting in deregulated expression of c-myc Effect of MYC- alone is unknown but is related to tumor cells. It turns out that high levels of c-Myc send a tumor cell’s gene expression program into overdrive. Transcription increases dramatically, allowing malignant cells to overwhelm factors that might normally hamper their growth and proliferation. This surprising finding, published in this week’s issue of the journal Cell, provides a simple, elegant explanation for how a single protein can have such profound effect in so many and varied types of cancer. “MYC is a key driver in most major cancers, but it has been...
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