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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
1991-12-18
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pubmed:abstractText |
Transgenic mice that contain the L-myc gene under the control of the immunoglobulin heavy-chain enhancer (E mu) express the transgene preferentially in T cells, develop thymic hyperplasia and are predisposed to T-cell lymphomas. An analogous E mu N-myc transgene is expressed preferentially in pre-B and B cells and provokes the development of B-cell neoplasias. Animals with an E mu pim-1 construct express the transgene in both B and T cells, but succumb to T-cell lymphomas. Complementation of the E mu N- and L-myc transgenic mice by breeding with E mu pim-1 animals leads to much more rapid development and a dramatically higher incidence of lymphoid malignancies, but the lineage specificity prescribed by the E mu N- and L-myc transgenes is maintained. The different oncogenic potential of myc genes is illustrated by the average latency period of tumor manifestation in double transgenics. Whereas c-myc/pim-1 animals develop pre-B-cell leukemia prenatally, the mean latency period for N-myc/pim-1 and L-myc/pim-1 mice is 36 and 94 days respectively. The N- and L-myc transgenes are expressed at high levels in tumors from double transgenic mice, but expression of the endogenous c- and N-myc genes is undetectable, directly implicating the myc transgenes in the tumor formation process.
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pubmed:grant |
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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 |
Nov
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:geneSymbol |
L-myc,
N-myc,
pim-1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1941-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:1658705-Animals,
pubmed-meshheading:1658705-Blotting, Northern,
pubmed-meshheading:1658705-Blotting, Southern,
pubmed-meshheading:1658705-Down-Regulation,
pubmed-meshheading:1658705-Enhancer Elements, Genetic,
pubmed-meshheading:1658705-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:1658705-Gene Rearrangement, B-Lymphocyte, Heavy Chain,
pubmed-meshheading:1658705-Gene Rearrangement, B-Lymphocyte, Light Chain,
pubmed-meshheading:1658705-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor,
pubmed-meshheading:1658705-Genes, myc,
pubmed-meshheading:1658705-Immunoglobulin kappa-Chains,
pubmed-meshheading:1658705-Lymphocyte Activation,
pubmed-meshheading:1658705-Lymphoma,
pubmed-meshheading:1658705-Mice,
pubmed-meshheading:1658705-Mice, Transgenic,
pubmed-meshheading:1658705-Protein-Serine-Threonine Kinases,
pubmed-meshheading:1658705-Proto-Oncogene Proteins,
pubmed-meshheading:1658705-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:1658705-Proto-Oncogene Proteins c-pim-1,
pubmed-meshheading:1658705-Transcription, Genetic
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pubmed:year |
1991
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pubmed:articleTitle |
E mu N- and E mu L-myc cooperate with E mu pim-1 to generate lymphoid tumors at high frequency in double-transgenic mice.
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pubmed:affiliation |
Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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