Literature DB >> 2915575

Oncogene expression in Rauscher murine leukemia virus induced erythroid, myeloid and lymphoid cell lines.

N J de Both1, M J van der Feltz, A Mooren, D Vermaas, P Klaassen, E H Rhijnsburger, M E Kranendonk-Odijk.   

Abstract

A comparative study on the expression of nuclear and cytoplasmic oncogenes was carried out using the Northern blotting technique, in Rauscher virus induced primary leukemias and the more malignant transformed cell lines derived from them. The latter grow permanently in vitro. Hyperplastic spleens obtained from mice recovering from anemia were analysed as controls. In addition to the detection of mRNAs, Southern blotting was carried out to observe whether rearrangement or amplification of oncogenes had occurred. The results show that the nuclear oncogenes c-myc, c-myb and p53 are strongly expressed in leukemic tissue, whereas c-fos transcripts show a much weaker hybridization. The expression of two of these oncogenes, c-myc and c-myb was followed during differentiation in myeloid leukemic cells and showed a gradual decrease when compared with the actin gene, which is constitutively transcribed. A large number of cytoplasmic oncogenes is expressed in the leukemic cells lines, i.e. c-abl, c-fms, c-fes, c-src, c-ros, c-H-ras, c-K-ras and N-ras. Of these, transcripts coding for c-abl and c-src were absent in blast cells of acute erythroid leukemias. Transcripts coding for c-erb, c-mos and c-sis could also not be detected. A number of putative oncogenes which are reported to play a role in Moloney and Friend virus induced leukemias for instance pim-1, fis-1, fim-1 and fim-2 were also used for screening. Only expression of pim-1 in Rauscher virus induced myeloid leukemic cells and in primary acute erythroid leukemias could be observed. At the DNA level no rearrangement or amplification of any of the oncogenes investigated could be detected. The results show that a number of oncogenes are expressed simultaneously in the same leukemic tissue or cell lines. It therefore seems likely that the presence of transcripts of different oncogenes is associated with the progression of leukemia, but is not the primary cause of leukemogenesis or of the transformation of these cells into established cell lines.

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Year:  1989        PMID: 2915575     DOI: 10.1016/0145-2126(89)90031-3

Source DB:  PubMed          Journal:  Leuk Res        ISSN: 0145-2126            Impact factor:   3.156


  2 in total

1.  A genetic linkage map of mouse chromosome 10: localization of eighteen molecular markers using a single interspecific backcross.

Authors:  M J Justice; L D Siracusa; D J Gilbert; N Heisterkamp; J Groffen; K Chada; C M Silan; N G Copeland; N A Jenkins
Journal:  Genetics       Date:  1990-08       Impact factor: 4.562

2.  Molecular cloning of the Rauscher murine leukemia virus. Disease spectrum and integration pattern.

Authors:  M J van der Feltz; M E Kranendonk-Odijk; E H Rhijnsburger; J Stark; K Stoker; N J de Both
Journal:  Arch Virol       Date:  1989       Impact factor: 2.574

  2 in total

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