1982
DOI: 10.1128/jvi.42.3.773-779.1982
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Isolation and characterization of c-myc, a cellular homolog of the oncogene (v-myc) of avian myelocytomatosis virus strain 29

Abstract: The chicken genome contains nucleotide sequences homologous to the transforming genes (oncogenes) of a number of avian retroviruses. We have isolated chicken DNA (c-myc) that is homologous to the oncogene (v-myc) of the avian myelocytomatosis virus MC29 and have compared the structures of the cellular and viral genes. Results from restriction endonuclease mapping of c-myc and from analysis of heteroduplexes between the DNAs of the cellular and viral genes show that c-myc is homologous to 1,500 nucleotides in v… Show more

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Cited by 257 publications
(87 citation statements)
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“…A turning point came from the study of oncogenic viruses, especially from the Retroviridae family which led to a "shocking" discovery. These viruses induced cancer through the expression of oncogenes, which had their corresponding cellular variants [39][40][41][42][43][44][45][46][47]. These oncogenes included v-raf, c-my, c-rel, and k-ras among others.…”
Section: Tumour Antigenicitymentioning
confidence: 99%
“…A turning point came from the study of oncogenic viruses, especially from the Retroviridae family which led to a "shocking" discovery. These viruses induced cancer through the expression of oncogenes, which had their corresponding cellular variants [39][40][41][42][43][44][45][46][47]. These oncogenes included v-raf, c-my, c-rel, and k-ras among others.…”
Section: Tumour Antigenicitymentioning
confidence: 99%
“…THE C-MYC PROTO-ONCOGENE was first described in 1982 (1) as the cellular homologue to the transforming sequences of the avian myelocytomatosis retrovirus. It was soon recognized that activated, oncogenic c-Myc is a key transforming agent in the etiology of human Burkitt's lymphoma (BL).…”
mentioning
confidence: 99%
“…The c-Myc gene principally activated through amplification and chromosomal translocation is closely involved in 20% of established human malignant tumors such as breast cancer, colon cancer, cervical cancer, melanoma, osteosarcoma, malignant glioma, and lung cancer according to the survey. 7,8,28,29 In esophageal cancer, accumulating evidence have convincingly defined that c-Myc gene, adversely inducing apoptosis and driving proliferation and invasion of ESCC, was discovered as its capability to motivate differentiation of normal embryonic stem cells as well as play a pivotal role in self-renewal, pluripotency maintenance, and carcinogenic potential. 30,31 With performing RT-qPCR and Western blot analysis, the expression level of c-Myc was assessed as signally higher in ESCC tissues and cell lines compared with bordering nonneoplastic tissues and normal cells.…”
Section: Discussionmentioning
confidence: 99%