Source:http://linkedlifedata.com/resource/pubmed/id/16912223
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2006-11-20
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pubmed:abstractText |
The translocation t(12;22) involves MN1 and TEL and is rarely found in acute myeloid leukemia (AML). Recently, it has been shown in a mouse model that the fusion protein MN1-TEL can promote growth of primitive hematopoietic progenitor cells (HPCs) and, in cooperation with HOXA9, induce AML. We quantified MN1 expression by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) in 142 adult patients with AML with normal cytogenetics treated uniformly in trial AML-SHG 01/99. AML samples were dichotomized at the median MN1 expression. High MN1 expression was significantly correlated with unmutated NPM1 (P < .001), poor response to the first course of induction treatment (P = .02), a higher relapse rate (P = .03), and shorter relapse-free (P = .002) and overall survivals (P = .03). In multivariate analysis, MN1 expression was an independent prognostic marker (P = .02) in addition to age and Eastern Cooperative Oncology Group (ECOG) performance status. Excluding patients with NPM1(mutated)/FLT3ITD(negative), high MN1 expression was associated with shorter relapse-free survival (P = .057). MN1 was highly expressed in some patients with acute lymphoblastic but not chronic lymphocytic or myeloid leukemia. MN1 was highly expressed in HPCs compared with differentiated cells and was down-regulated during in vitro differentiation of CD34(+) cells, suggesting a functional role in HPCs. In conclusion, our data suggest MN1 overexpression as a new prognostic marker in AML with normal cytogenetics.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/MN1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/MN1-TEL fusion protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins, Fusion,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Markers, Biological,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/homeobox protein HOXA9
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
108
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3898-905
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:16912223-Adolescent,
pubmed-meshheading:16912223-Adult,
pubmed-meshheading:16912223-Animals,
pubmed-meshheading:16912223-Cytogenetic Analysis,
pubmed-meshheading:16912223-Disease-Free Survival,
pubmed-meshheading:16912223-Female,
pubmed-meshheading:16912223-Gene Expression Regulation, Leukemic,
pubmed-meshheading:16912223-Homeodomain Proteins,
pubmed-meshheading:16912223-Humans,
pubmed-meshheading:16912223-Leukemia, Lymphocytic, Chronic, B-Cell,
pubmed-meshheading:16912223-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:16912223-Leukemia, Myeloid, Acute,
pubmed-meshheading:16912223-Male,
pubmed-meshheading:16912223-Mice,
pubmed-meshheading:16912223-Middle Aged,
pubmed-meshheading:16912223-Oncogene Proteins, Fusion,
pubmed-meshheading:16912223-Predictive Value of Tests,
pubmed-meshheading:16912223-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16912223-Survival Rate,
pubmed-meshheading:16912223-Transcription Factors,
pubmed-meshheading:16912223-Tumor Markers, Biological,
pubmed-meshheading:16912223-Tumor Suppressor Proteins
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pubmed:year |
2006
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pubmed:articleTitle |
High meningioma 1 (MN1) expression as a predictor for poor outcome in acute myeloid leukemia with normal cytogenetics.
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pubmed:affiliation |
British Columbia Cancer Research Centre, 675 West 10th Ave, Vancouver, BC, Canada. heuser.michael@mh-hannover.de
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Comparative Study,
Research Support, Non-U.S. Gov't
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