| pubmed-article:14504097 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C0021270 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C0919528 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C1333568 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C0023452 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C0332285 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C1305143 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C1519724 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C1511695 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:14504097 | lifeskim:mentions | umls-concept:C0332183 | lld:lifeskim |
| pubmed-article:14504097 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:14504097 | pubmed:dateCreated | 2004-1-19 | lld:pubmed |
| pubmed-article:14504097 | pubmed:abstractText | Point mutations of D835/I836 of the FLT3 gene have been reported in adult acute myeloid leukemia (AML), but not in pediatric AML or acute lymphoblastic leukemia (ALL). FLT3-D835/I836 mutations were found in 6 (5.4%) of 112 children with ALL older than 1 year and in 8 (16.0%) of 50 infants with ALL. Missense mutations were found in 11 patients, 3-base pair deletions in 2 patients, and a deletion/insertion in 1 patient. Remarkably, FLT3-D835/I836 mutations were found in 8 (18.2%) of 44 infants with ALL with MLL rearrangements and in 4 (21.5%) of 19 patients with hyperdiploid ALL, but they were not found in any patients older than 1 year who had TEL-AML1 (n = 11), E2APBX1 (n = 4), or BCR-ABL (n = 6) fusion genes. Although infant ALL patients with mutations had poorer prognoses than did those without mutations, pediatric ALL patients with mutations who were older than 1 year had good prognoses. We also found FLT3-D835 mutations in 2 of 11 leukemic cell lines with MLL rearrangements. FLT3 was highly phosphorylated in these cell lines with FLT3-D835 mutations, leading to constitutive activation of downstream targets such as signal transducer and activator of transcription 5 (STAT5) without FLT3 ligand stimulation. These results suggested that FLT3-D835/I836 mutations are one of the second genetic events in infant ALL with MLL rearrangements or pediatric ALL with hyperdiploidy. | lld:pubmed |
| pubmed-article:14504097 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14504097 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14504097 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:14504097 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14504097 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:14504097 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:TaketaniTakes... | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:TakiTomohikoT | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:HayashiYasuhi... | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:HanadaRyojiR | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:IshiiEiichiE | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:TsuchidaMasah... | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:SugitaKanjiK | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:SugitaKenichi... | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:IdaKohmeiK | lld:pubmed |
| pubmed-article:14504097 | pubmed:author | pubmed-author:FuruichiYoshi... | lld:pubmed |
| pubmed-article:14504097 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14504097 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:14504097 | pubmed:volume | 103 | lld:pubmed |
| pubmed-article:14504097 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14504097 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14504097 | pubmed:pagination | 1085-8 | lld:pubmed |
| pubmed-article:14504097 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:14504097 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14504097 | pubmed:articleTitle | FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy. | lld:pubmed |
| pubmed-article:14504097 | pubmed:affiliation | Gunma Children's Medical Center, 779 Shimohadoka, Kitatachibana, Gunma 377-8577, Japan. hayashiy-tky@umin.ac.jp | lld:pubmed |
| pubmed-article:14504097 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14504097 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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