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TY - JOUR AU - Cooper, Geoffrey M. AU - Neiman, Paul E. PY - 1981 DA - 1981/08/01 TI - Two distinct candidate transforming genes of lymphoid leukosis virus-induced neoplasms JO - Nature SP - 857 EP - 858 VL - 292 IS - 5826 AB - Avian lymphoid leukosis viruses (LLVs) are oncogenic retro-viruses which induce tumours with relatively long latent periods and which seem to lack viral transforming genes1. We previously reported that high molecular weight DNAs of seven LLV-induced tumours efficiently transformed NIH 3T3 mouse cells on transfection and that the transformed NIH cells did not contain viral DNA sequences detectable by hybridization with probes homologous either to the entire LLV genome or to the long terminal redundancy (LTR) of LLV DNA2. These results suggested that oncogenesis by LLVs involved indirect activation of cellular transforming gene(s) which were not linked to LLV DNA. Hayward et al.3 recently found that 80–90% of LLV-induced metastatic bursal lymphomas contained exogenous LTR sequences near the cellular gene (c-myc) homologous to the presumptive transforming gene of myelocytomatosis virus strain MC29, a highly oncogenic avian acute leukaemia virus. Integration of LTR sequences containing the viral transcriptional promoter apparently increases transcription of c-myc in these lymphomas3. We now report that the LLV-induced tumours used as donors of DNA in our previous transfection experiments also contain LTR sequences near c-myc. However, further analysis of the NIH cells transformed by DNAs of LLV-induced bursal neoplasms indicates that transformation was not mediated by transfer of the tumour c-myc gene. These observations suggest that at least two different cellular genes with potential oncogenic activity are activated by different mechanisms in LLV-induced neoplasms. SN - 1476-4687 UR - https://doi.org/10.1038/292857a0 DO - 10.1038/292857a0 ID - Cooper1981 ER -