pubmed-article:11133737 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
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pubmed-article:11133737 | lifeskim:mentions | umls-concept:C0598766 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1514562 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1883221 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C0439677 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1883204 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1334043 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1518071 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C1880389 | lld:lifeskim |
pubmed-article:11133737 | lifeskim:mentions | umls-concept:C2697616 | lld:lifeskim |
pubmed-article:11133737 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11133737 | pubmed:dateCreated | 2001-1-22 | lld:pubmed |
pubmed-article:11133737 | pubmed:abstractText | The effect of mutations in the Src homology 2 (SH2) domain of the BCR/ABL oncogene on leukemogenesis was tested in a quantitative murine bone marrow transduction/transplantation assay that accurately models human Philadelphia-positive B-lymphoid leukemia and chronic myeloid leukemia (CML). The SH2 domain was not required for induction of B-lymphoid leukemia in mice by BCR/ABL. Under conditions where the p190 and p210 forms of BCR/ABL induce fatal CML-like myeloproliferative disease within 4 weeks, p210 SH2 mutants induced CML-like disease in some mice only after a significant delay, with other recipients succumbing to B-lymphoid leukemia instead. In contrast, p190 BCR/ABL SH2 point and deletion mutants rapidly induced CML-like disease. These results provide the first direct evidence of significant differences in cell signaling by the Bcr/Abl tyrosine kinase between these distinct leukemias. Contrary to previous observations, high levels of phosphatidylinositol 3-kinase (PI 3-kinase) activity in primary malignant lymphoblasts and myeloid cells from recipients of marrow transduced with the BCR/ABL SH2 mutants were found. Hence, the decreased induction of CML-like disease by the p210 BCR/ABL SH2 mutants is not due to impaired activation of PI 3-kinase. | lld:pubmed |
pubmed-article:11133737 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11133737 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11133737 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11133737 | pubmed:language | eng | lld:pubmed |
pubmed-article:11133737 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11133737 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:11133737 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11133737 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11133737 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11133737 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11133737 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11133737 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:11133737 | pubmed:author | pubmed-author:VarticovskiLL | lld:pubmed |
pubmed-article:11133737 | pubmed:author | pubmed-author:Van EttenR... | lld:pubmed |
pubmed-article:11133737 | pubmed:author | pubmed-author:IlariaR LRL | lld:pubmed |
pubmed-article:11133737 | pubmed:author | pubmed-author:RoumiantsevSS | lld:pubmed |
pubmed-article:11133737 | pubmed:author | pubmed-author:de AosI EIE | lld:pubmed |
pubmed-article:11133737 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11133737 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11133737 | pubmed:volume | 97 | lld:pubmed |
pubmed-article:11133737 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11133737 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11133737 | pubmed:pagination | 4-13 | lld:pubmed |
pubmed-article:11133737 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:11133737 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11133737 | pubmed:articleTitle | The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase. | lld:pubmed |
pubmed-article:11133737 | pubmed:affiliation | Center for Blood Research, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. | lld:pubmed |
pubmed-article:11133737 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11133737 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11133737 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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