MLL GENE REARRANGEMENT, CYTOGENETIC 11Q23 ABNORMALITIES, AND EXPRESSION OF THE NG2 MOLECULE IN INFANT ACUTE MYELOID-LEUKEMIA

Citation
Jm. Hilden et al., MLL GENE REARRANGEMENT, CYTOGENETIC 11Q23 ABNORMALITIES, AND EXPRESSION OF THE NG2 MOLECULE IN INFANT ACUTE MYELOID-LEUKEMIA, Blood, 89(10), 1997, pp. 3801-3805
Citations number
29
Categorie Soggetti
Hematology
Journal title
BloodACNP
ISSN journal
00064971
Volume
89
Issue
10
Year of publication
1997
Pages
3801 - 3805
Database
ISI
SICI code
0006-4971(1997)89:10<3801:MGRC1A>2.0.ZU;2-O
Abstract
To study prognostic factors in infant acute myeloid leukemia (AML), we analyzed 44 children treated on Childrens Cancer Group protocols for MLL gene rearrangement by Southern blot, cytogenetic 11q23 abnormaliti es, and reactivity with monoclonal antibody 7.1. This antibody detects the human homologue of the rat NG2 chondroitin sulfate proteoglycan m olecule, which has previously been reported to be ex pressed on human melanoma. NG2 has been found to be expressed on human leukemic blasts but not on other hematopoietic cells. In childhood AML, NG2 cell surfa ce expression correlated with poor outcome and with some but not all 1 1q23 rearrangements. In childhood acute lymphoblastic leukemia, NG2 ex pression correlated with poor outcome and with balanced 11q23 transloc ations. In this study, 29 of 44 (66%) of infants with AML showed MLL r earrangement and, as expected, this group had a high incidence of Fren ch-American-British M4/M5 morphology (22/29). Of the cases tested, 35. 1% (13/37) were NG2 positive. All (13/13) NG2-positive cases were rear ranged at MLL, whereas only 46% (11/24) of NG2-negative cases had MLL rearrangement. NG2 expression did not correlate with poor outcome (P = .31); there was a trend towards a worse outcome with MLL rearrangemen t (P = .13). Thus monoclonal antibody 7.1 does not detect all cases of MLL rearrangement in infant AML. (C) 1997 by The American Society of Hematology.