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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2005-11-29
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pubmed:abstractText |
Evidence suggests that cyclooxygenase-2 (COX-2) increases tumorigenic potential by promoting resistance to apoptosis. Because B chronic lymphoid leukemia (B-CLL) cells exhibit a defective apoptotic response, we analyzed CD19(+) B lymphocytes purified from the peripheral blood of B-CLL patients. Microarray analysis showed a variable (up to 38-fold) increase in the steady-state mRNA levels of COX-2 in B-CLL lymphocytes compared with normal CD19(+) B lymphocytes. The up-regulation of COX-2 in B-CLL cells was confirmed by reverse transcriptase-polymerase chain reaction and Western blot analyses. Moreover, immunohistochemical analysis of B-CLL bone marrow infiltrates confirmed clear expression of COX-2 in leukemic cells. Ex vivo treatment with the COX-2 inhibitor NS-398 significantly decreased the survival of leukemic cells by increasing the rate of spontaneous apoptosis in 13 of 16 B-CLL samples examined, but it did not affect the survival of normal lymphocytes. Pretreatment with NS-398 significantly potentiated the cytotoxicity induced by chlorambucil in 8 of 16 B-CLL samples examined. Moreover, although recombinant tumor necrosis factor-related apoptosis inducing ligand (TRAIL)/Apo2L showed little cytotoxic effect in most B-CLL samples examined, pretreatment with NS-398 sensitized 8 of 16 B-CLL samples to TRAIL-induced apoptosis. Taken together, our data indicate that COX-2 overexpression likely represents an additional mechanism of resistance to apoptosis in B-CLL and that pharmacological suppression of COX-2 might enhance chemotherapy-mediated apoptosis.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16314473-10753955,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16314473-10766802,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0002-9440
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1599-607
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16314473-Aged,
pubmed-meshheading:16314473-Aged, 80 and over,
pubmed-meshheading:16314473-B-Lymphocytes,
pubmed-meshheading:16314473-Cell Division,
pubmed-meshheading:16314473-Cyclooxygenase 2,
pubmed-meshheading:16314473-Female,
pubmed-meshheading:16314473-Flow Cytometry,
pubmed-meshheading:16314473-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:16314473-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16314473-Humans,
pubmed-meshheading:16314473-Leukemia, Lymphocytic, Chronic, B-Cell,
pubmed-meshheading:16314473-Lymphocytes,
pubmed-meshheading:16314473-Male,
pubmed-meshheading:16314473-Membrane Proteins,
pubmed-meshheading:16314473-Middle Aged,
pubmed-meshheading:16314473-Neoplasm Staging
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pubmed:year |
2005
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pubmed:articleTitle |
Potential pathogenetic implications of cyclooxygenase-2 overexpression in B chronic lymphoid leukemia cells.
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pubmed:affiliation |
Department of Morphology and Embryology, Human Anatomy Section, University of Ferrara, Italy. secchier@mail.umbi.umd.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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