Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-9-7
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1249-56
pubmed:dateRevised
2007-11-15
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
pubmed:year
1994
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.
pubmed:affiliation
Division of Hematology, University of Lausanne, Switzerland.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't