The first MYC gene was identified in the late 1970s in the avian acute leukemia virus MC29. This virus was known to cause a range of malignancies and the sequence in the viral genome responsible for the transforming capacity was named v-myc (short for viral myelocytomatosis, a leukemia caused by the virus). In 1979, a cellular homologue was identified in several species and was subsequently called c-MYC, where “c” denotes cellular. In contrast to other oncogenes known at the time, MYCdid not seem to be activated by point mutations in the coding sequence. Instead studies in the early 1980s led to the identification of three novel mechanisms of oncogene activation: insertional mutagenesis (virus integration into the host genome at or near proto-oncogenes resulting in high levels of expression driven by the viral promoter), chromosomal translocation, and gene amplification (see also “MYC in Cancer”...
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