Cellular expression of antiapoptotic BCL-2 oncoprotein in newly diagnosed childhood acute lymphoblastic leukemia: A Children's Cancer Group Study Journal Article


Authors: Uckun, F. M.; Yang, Z. W.; Sather, H.; Steinherz, P.; Nachman, J.; Bostrom, B.; Crotty, L.; Sarquis, M.; Ek, O.; Zeren, T.; Tubergen, D.; Reaman, G.; Gaynon, P.
Article Title: Cellular expression of antiapoptotic BCL-2 oncoprotein in newly diagnosed childhood acute lymphoblastic leukemia: A Children's Cancer Group Study
Abstract: We found a marked variation in BCL-2 oncoprotein expression levels of primary leukemic cells from 338 children with newly diagnosed acute lymphoblastic leukemia (ALL). None of the high-risk features predictive of poor treatment outcome in childhood ALL, such as older age, high white blood cell (WBC) count, organomegaly, T-lineage immunophenotype, ability of leukemic cells to cause overt leukemia in severe combined immunodeficient (SCID) mice, presence of MLL-AF4, and BCR-ABL fusion transcripts were associated with high levels of BCL-2 expression, overall, high BCL-2 levels were not associated with slow early response, failure to achieve complete remission, or poor event-free survival. High BCL-2 levels in primary leukemic cells predicted slow early response only in T-lineage ALL patients, which comprised approximately 15% of the total patient population. Even for this small subset of patients, the level of BCL-2 expression did not have a significant impact an the shortterm event-free survival. (C) 1997 by The American Society of Hematology.
Keywords: survival; antigen expression; apoptosis; severe combined immunodeficiency; gene-expression; intensive therapy; induced; disease-free; unfavorable presenting features; lymphoma-cells; intrinsic radiation-resistance; primary clonogenic blasts
Journal Title: Blood
Volume: 89
Issue: 10
ISSN: 0006-4971
Publisher: American Society of Hematology  
Date Published: 1997-05-15
Start Page: 3769
End Page: 3777
Language: English
ACCESSION: WOS:A1997XD97600031
PROVIDER: wos
PUBMED: 9160683
DOI: 10.1182/blood.V89.10.3769
Notes: Article -- Source: Wos
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  1. Peter G Steinherz
    221 Steinherz