A molecular approach to leukemogenesis: mouse lymphomas contain an activated c-ras oncogene.
By inducing mouse thymomas with carcinogens and gamma-radiation, we have studied the potential of tumor DNA to induce foci in rodent fibroblasts. A high percentage of the tumors used transformed the cultured cells, and the oncogenic phenotype segregated with extra copies of the c-ras gene family. There appears to be selectivity in the activated gene because so far all analyzed tumors induced by carcinogen have activated the N-ras gene, and those induced by radiation have activated the K-ras gene. The K-ras gene is the cellular counterpart of the viral ras oncogene in Kirsten murine sarcoma virus, but the N-ras has not yet been found in a retrovirus. The transformed cells have a marked increase in expression of the oncogene at the RNA and protein level. This model system might be a powerful tool in the study of leukemogenesis.
D000818:Animals; D002273:Carcinogens; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D004273:DNA, Neoplasm / Q000235:genetics / Q000302:isolation & purification; D007942:Leukemia, Experimental / Q000235:genetics*; D007953:Leukemia, Radiation-Induced / Q000235:genetics*; D051379:Mice; D009857:Oncogenes / Q000528:radiation effects*; D012334:RNA, Neoplasm / Q000302:isolation & purification; D013945:Thymoma / Q000235:genetics*; D013953:Thymus Neoplasms / Q000235:genetics*; D014158:Transcription, Genetic
D002273:Carcinogens; D004273:DNA, Neoplasm; D012334:RNA, Neoplasm