scholarly journals MLL Gene Rearrangement, Cytogenetic 11q23 Abnormalities, and Expression of the NG2 Molecule in Infant Acute Myeloid Leukemia

Blood ◽  
1997 ◽  
Vol 89 (10) ◽  
pp. 3801-3805 ◽  
Author(s):  
Joanne M. Hilden ◽  
Franklin O. Smith ◽  
Joy L. Frestedt ◽  
Ronald McGlennen ◽  
William B. Howells ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Gene Rearrangement ◽  
Cell Surface Expression ◽  
Poor Outcome ◽  
Mll Gene ◽  
11Q23 Abnormalities ◽  
Mll Gene Rearrangement ◽  
Acute Myeloid

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 abnormalities, and reactivity with monoclonal antibody 7.1. This antibody detects the human homologue of the rat NG2 chondroitin sulfate proteoglycan molecule, which has previously been reported to be expressed 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 surface expression correlated with poor outcome and with some but not all 11q23 rearrangements. In childhood acute lymphoblastic leukemia, NG2 expression correlated with poor outcome and with balanced 11q23 translocations. In this study, 29 of 44 (66%) of infants with AML showed MLL rearrangement and, as expected, this group had a high incidence of French-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 rearranged 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 rearrangement (P = .13). Thus monoclonal antibody 7.1 does not detect all cases of MLL rearrangement in infant AML.

scholarly journals MLL Gene Rearrangement, Cytogenetic 11q23 Abnormalities, and Expression of the NG2 Molecule in Infant Acute Myeloid Leukemia

Blood ◽  
1997 ◽  
Vol 89 (10) ◽  
pp. 3801-3805 ◽  
Author(s):  
Joanne M. Hilden ◽  
Franklin O. Smith ◽  
Joy L. Frestedt ◽  
Ronald McGlennen ◽  
William B. Howells ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Gene Rearrangement ◽  
Cell Surface Expression ◽  
Poor Outcome ◽  
Mll Gene ◽  
11Q23 Abnormalities ◽  
Mll Gene Rearrangement ◽  
Acute Myeloid

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 abnormalities, and reactivity with monoclonal antibody 7.1. This antibody detects the human homologue of the rat NG2 chondroitin sulfate proteoglycan molecule, which has previously been reported to be expressed 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 surface expression correlated with poor outcome and with some but not all 11q23 rearrangements. In childhood acute lymphoblastic leukemia, NG2 expression correlated with poor outcome and with balanced 11q23 translocations. In this study, 29 of 44 (66%) of infants with AML showed MLL rearrangement and, as expected, this group had a high incidence of French-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 rearranged 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 rearrangement (P = .13). Thus monoclonal antibody 7.1 does not detect all cases of MLL rearrangement in infant AML.

Translocation (10;11)(p13;p15) in an Infant Acute Myeloid Leukemia with MLL Gene Rearrangement

1999 ◽  
Vol 114 (1) ◽  
pp. 68-70
Author(s):  
Fernando Marco ◽  
Encarnación Bureo ◽  
M.Dolores Delgado ◽  
Carlos Richard ◽  
M.Angeles Cuadrado ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Gene Rearrangement ◽  
Mll Gene ◽  
Mll Gene Rearrangement ◽  
Acute Myeloid

Therapy-Related Acute Myeloid Leukemia 6 Years after Clonal Detection of inv(11)(q21q23) and MLL Gene Rearrangement

2006 ◽  
Vol 83 (3) ◽  
pp. 247-251 ◽  
Author(s):  
Naoko Takei ◽  
Kazumi Suzukawa ◽  
Harumi Mukai ◽  
Takayoshi Itoh ◽  
Yasushi Okoshi ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Gene Rearrangement ◽  
Mll Gene ◽  
Mll Gene Rearrangement ◽  
Acute Myeloid

scholarly journals The t(11;16)(q23;p13) Translocation in Myelodysplastic Syndrome Fuses the MLL Gene to the CBP Gene

Blood ◽  
1997 ◽  
Vol 89 (11) ◽  
pp. 3945-3950 ◽  
Author(s):  
Tomohiko Taki ◽  
Masahiro Sako ◽  
Masahiro Tsuchida ◽  
Yasuhide Hayashi
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myelodysplastic Syndrome ◽  
Myeloid Leukemia ◽  
Dna Methyltransferase ◽  
Creb Binding Protein ◽  
Mll Gene ◽  
Recurrent Translocation ◽  
Coactivator Protein ◽  
11Q23 Abnormalities ◽  
Acute Myeloid

Abstract The recurrent translocation t(11; 16)(q23; p13) has been reported to be associated with therapy-related acute leukemia. The MLL gene involved in other 11q23 abnormalities was also rearranged by this translocation. We analyzed two patients with myelodysplastic syndrome with t(11; 16) and showed that the MLL gene on 11q23 was fused with CREB-binding protein (CBP) gene on 16p13 in these patients. The CBP gene encodes a transcriptional adaptor/coactivator protein and it is mutated in patients with Rubinstein-Taybi syndrome. The CBP gene is also involved in acute myeloid leukemia (AML) with t(8; 16)(p11; p13). In-frame MLL-CBP fusion transcripts combine the MLL AT-hook motifs and DNA methyltransferase homology region with a largely intact CBP. Our results combined with the finding of the MOZ-CBP fusion in t(8; 16)-AML suggest that the CBP gene may be associated with leukemogenesis through translocations.

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