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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1994-9-7
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pubmed:abstractText |
L-selectin is expressed by most leukocytes and mediates the initial step of adhesion to vascular endothelium. A feature of this adhesion receptor is to be shed from the cell surface. We report here the presence of high levels of the shed form of L-selectin (sL-selectin) in plasma from patients with acute leukemia. We also show that sL-selectin purified from acute leukemia plasma exhibits functional activity. The mean (+/- 1 SD) plasma level of sL-selectin among 100 healthy individuals was 2.1 +/- 0.7 micrograms/mL. This value was increased (> 2 SD above the mean) in 63% of 58 patients with acute lymphoblastic leukemia (ALL) and 59% of 93 patients with acute myelogenous leukemia ([AML] P < .001). Repeated measurements in 24 patients showed normal-range levels in 16 of 16 patients in complete remission and high levels in eight of eight patients with therapy-resistant acute leukemia or leukemia relapse. Furthermore, elevated sL-selectin levels were detected in cerebrospinal fluid of three patients with ALL suffering from a relapse limited to the central nervous system. Epitope mapping with monoclonal antibodies demonstrated that L-selectin shedding from leukemic blasts was accompanied by conformational changes of its epidermal growth factor-like domain. A functional role for sL-selectin purified from leukemic plasma was supported by its ability to completely inhibit L-selectin-dependent adhesion of blast cells to tumor necrosis factor-alpha (TNF-alpha)-activated endothelium in vitro. These results suggest that sL-selectin may have an important role in the regulation of leukemic cell adhesion to endothelium. In addition, monitoring of the sL-selectin level may be useful for evaluating leukemia activity, in particular for the detection of leukemia relapse.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1249-56
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7519478-Antigens, CD,
pubmed-meshheading:7519478-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:7519478-Blast Crisis,
pubmed-meshheading:7519478-Blotting, Western,
pubmed-meshheading:7519478-Cell Adhesion,
pubmed-meshheading:7519478-Cell Adhesion Molecules,
pubmed-meshheading:7519478-Cells, Cultured,
pubmed-meshheading:7519478-Endothelium, Vascular,
pubmed-meshheading:7519478-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:7519478-Humans,
pubmed-meshheading:7519478-Immunophenotyping,
pubmed-meshheading:7519478-L-Selectin,
pubmed-meshheading:7519478-Leukemia, Myeloid, Acute,
pubmed-meshheading:7519478-Lymphocytes,
pubmed-meshheading:7519478-Precursor Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:7519478-Predictive Value of Tests,
pubmed-meshheading:7519478-Prognosis,
pubmed-meshheading:7519478-Reference Values,
pubmed-meshheading:7519478-Tumor Markers, Biological,
pubmed-meshheading:7519478-Umbilical Veins
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pubmed:year |
1994
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pubmed:articleTitle |
High levels of the shed form of L-selectin are present in patients with acute leukemia and inhibit blast cell adhesion to activated endothelium.
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pubmed:affiliation |
Division of Hematology, University of Lausanne, Switzerland.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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