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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1994-10-18
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pubmed:abstractText |
The pH chromosome, resulting from the t(9;22) translocation, is the most frequently observed cytogenetic aberration in acute lymphoblastic leukemia (ALL). Two genes, bcr and abl, are involved in this translocation. As a consequence, parts of the bcr and abl genes are fused, resulting in chimeric bcr-abl genes encoding chimeric BCR-ABL proteins. Three bcr-abl genes and proteins have been identified: e1-a2 P190bcr-abl, b2-a2 P210bcr-abl, and b3-a2 P210bcr-abl. Since these chimeric proteins only occur in Ph-chromosome-positive leukemic cells, they are by definition tumor-specific markers. Ph-chromosome-positive ALL is correlated with a bad prognosis, therefore the detection of chimeric BCR-ABL proteins is of prime importance in ALL diagnosis. In the present study, we report on the generation of a monoclonal antibody termed ER-FP1, raised against the tumor-specific e1-a2 BCR-ABL junction in P190bcr-abl. We show that ER-FP1 reacts highly specifically with e1-a2 P190bcr-abl in different assays. The reactivity of ER-FP1 with e1-a2 P190bcr-abl in soluble form was analyzed in an immunoprecipitation assay; specificity was confirmed by peptide inhibition studies. Binding of ER-FP1 to e1-a2 P190bcr-abl at the single cell level was detected by using immunofluorescence techniques. Immunological double-staining experiments using ER-FP1 and a monoclonal antibody recognizing all BCR-ABL proteins confirmed the specificity of ER-FP1 for the e1-a2 fusion point.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0887-6924
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1503-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:8090030-Adult,
pubmed-meshheading:8090030-Antibodies, Monoclonal,
pubmed-meshheading:8090030-Antibody Specificity,
pubmed-meshheading:8090030-Chromosomes, Human, Pair 22,
pubmed-meshheading:8090030-Chromosomes, Human, Pair 9,
pubmed-meshheading:8090030-Fluorescent Antibody Technique,
pubmed-meshheading:8090030-Fusion Proteins, bcr-abl,
pubmed-meshheading:8090030-Genes, abl,
pubmed-meshheading:8090030-Humans,
pubmed-meshheading:8090030-Male,
pubmed-meshheading:8090030-Middle Aged,
pubmed-meshheading:8090030-Philadelphia Chromosome,
pubmed-meshheading:8090030-Precipitin Tests,
pubmed-meshheading:8090030-Precursor Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:8090030-Protein-Tyrosine Kinases,
pubmed-meshheading:8090030-Translocation, Genetic
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pubmed:year |
1994
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pubmed:articleTitle |
Recognition of the ALL-specific BCR-ABL junction in P190bcr-abl by monoclonal antibody ER-FP1.
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pubmed:affiliation |
Department of Immunology, Erasmus University, Rotterdam, The Netherlands.
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pubmed:publicationType |
Journal Article,
Case Reports,
Research Support, Non-U.S. Gov't
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