pubmed-article:10683371 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C0796520 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C1513792 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C0041485 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C1302234 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:10683371 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:10683371 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10683371 | pubmed:dateCreated | 2000-3-9 | lld:pubmed |
pubmed-article:10683371 | pubmed:abstractText | The t(5;12)(q33;p13) translocation associated with chronic myelomonocytic leukemia (CMML) generates a TEL/PDGFbetaR fusion gene. Here, we used a murine bone marrow transplant (BMT) assay to test the transforming properties of TEL/PDGFbetaR in vivo. TEL/PDGFbetaR, introduced into whole bone marrow by retroviral transduction, caused a rapidly fatal myeloproliferative disease that closely recapitulated human CMML. TEL/PDGFbetaR transplanted mice developed leukocytosis with Gr-1(+) granulocytes, splenomegaly, evidence of extramedullary hematopoiesis, and bone marrow fibrosis, but no lymphoproliferative disease. We assayed mutant forms of the TEL/PDGFbetaR fusion protein - including 8 tyrosine to phenylalanine substitutions at phosphorylated PDGFbetaR sites to which various SH2 domain-containing signaling intermediates bind - for ability to transform hematopoietic cells. All of the phenylalanine (F-) mutants tested conferred IL-3-independence to a cultured murine hematopoietic cell line, but, in the BMT assay, different F-mutants displayed distinct transforming properties. In transplanted animals, tyrosines 579/581 proved critical for the development of myeloproliferative phenotype. F-mutants with these residues mutated showed no sign of myeloproliferation but instead developed T-cell lymphomas. In summary, TEL/PDGFbetaR is necessary and sufficient to induce a myeloproliferative disease in a murine BMT model, and PDGFbetaR residues Y579/581 are required for this phenotype. | lld:pubmed |
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pubmed-article:10683371 | pubmed:language | eng | lld:pubmed |
pubmed-article:10683371 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10683371 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10683371 | pubmed:month | Feb | lld:pubmed |
pubmed-article:10683371 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:CarrollMM | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:WilliamsI RIR | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:GillilandD... | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:AsterJ CJC | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:CajaRR | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:Van EttenR... | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:SternbergD... | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:IlariaR LRLJr | lld:pubmed |
pubmed-article:10683371 | pubmed:author | pubmed-author:TomassonM HMH | lld:pubmed |
pubmed-article:10683371 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10683371 | pubmed:volume | 105 | lld:pubmed |
pubmed-article:10683371 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10683371 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10683371 | pubmed:pagination | 423-32 | lld:pubmed |
pubmed-article:10683371 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:10683371 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10683371 | pubmed:articleTitle | Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581. | lld:pubmed |
pubmed-article:10683371 | pubmed:affiliation | Department of Medicine, Brigham and Women's Hospital, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA. | lld:pubmed |
pubmed-article:10683371 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10683371 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10683371 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |