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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1992-2-27
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pubmed:abstractText |
Transgenic mice that contain constructs of the L-myc gene under the transcriptional control of the immunoglobulin heavy chain enhancer (E mu) develop thymic hyperplasia and are predisposed to T cell lymphomas. Here we describe a second form of malignancy that occurs in aging E mu L-myc transgenic mice. The mean latency period for the development of this malignancy is longer compared with the E mu L-myc T cell lymphomas but the overall incidence is increased threefold. The histopathological morphology is that of a highly malignant mesenchymal neoplasm that closely resembles human fibrous histiocytoma. The tumor cells were classified as myelomonocytic on the basis of several lineage-specific markers and the lack of rearrangements of the immunoglobulin heavy chain and the T cell receptor beta loci. Cultured tumor cells produce macrophage colony-stimulating factor (M-CSF) protein and express the M-CSF receptor, suggesting the involvement of an autocrine loop in this malignancy. Similar to the E mu L-myc T cell lymphomas, these tumors show high-level transgene expression but no detectable levels of endogenous c-myc mRNA, directly implicating the deregulated expression of L-myc in the generation of this malignancy. E mu L-myc myelomonocytic tumors show consistent trisomy of chromosome 16, implicating this as a secondary event in the development of this tumor. In the light of recent findings that L-myc is expressed in human myeloid leukemias and in several human myeloid tumor cell lines, the results described here might implicate L-myc in the development of naturally occurring myeloid neoplasias.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1310099-115001,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1310099-1986238,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1310099-2091750,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
175
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
313-22
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pubmed:dateRevised |
2010-9-7
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pubmed:meshHeading |
pubmed-meshheading:1310099-Aging,
pubmed-meshheading:1310099-Animals,
pubmed-meshheading:1310099-Blotting, Northern,
pubmed-meshheading:1310099-Enhancer Elements, Genetic,
pubmed-meshheading:1310099-Gene Expression,
pubmed-meshheading:1310099-Genes, myc,
pubmed-meshheading:1310099-Histiocytoma, Benign Fibrous,
pubmed-meshheading:1310099-Immunoglobulin Heavy Chains,
pubmed-meshheading:1310099-Lymphoma, T-Cell,
pubmed-meshheading:1310099-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:1310099-Mesenchymoma,
pubmed-meshheading:1310099-Mice,
pubmed-meshheading:1310099-Mice, Inbred C57BL,
pubmed-meshheading:1310099-Mice, Transgenic,
pubmed-meshheading:1310099-Receptor, Macrophage Colony-Stimulating Factor,
pubmed-meshheading:1310099-Tumor Cells, Cultured
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pubmed:year |
1992
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pubmed:articleTitle |
High frequency of myelomonocytic tumors in aging E mu L-myc transgenic mice.
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