Recurrent translocation t(10;17)(p15;q21) in minimally differentiated acute myeloid leukemia results inZMYND11/MBTD1fusion

2015 ◽  
Vol 55 (3) ◽  
pp. 237-241 ◽  
Author(s):  
Jasmijn D.E. de Rooij ◽  
Marry M. van den Heuvel-Eibrink ◽  
Wouter J.W. Kollen ◽  
Edwin Sonneveld ◽  
Gertjan J.L. Kaspers ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Recurrent Translocation ◽  
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.

scholarly journals Reciprocal T(7;11)(P15;P15): A Rare but Recurrent Translocation in Acute Myeloid Leukemia. Report of 3 Cases

2013 ◽  
Vol 24 ◽  
pp. ix52
Author(s):  
M. Manabe ◽  
J. Okita ◽  
N. Harada ◽  
T. Takakuwa ◽  
Y. Aoyama ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Recurrent Translocation ◽  
Acute Myeloid

scholarly journals Erratum: Characterization of a recurrent translocation t(2;3)(p15–22;q26) occurring in acute myeloid leukemia

Leukemia ◽  
2006 ◽  
Vol 20 (6) ◽  
pp. 1195-1195
Author(s):  
M Trubia ◽  
F Albano ◽  
F Cavazzini ◽  
G R Cambrin ◽  
G Quarta ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Recurrent Translocation ◽  
Acute Myeloid

scholarly journals MYC Amplification in the Form of Ring Chromosomes 8 in Acute Myeloid Leukemia with t(11;16)(q13;p11.2)

2017 ◽  
Vol 153 (3) ◽  
pp. 131-137 ◽  
Author(s):  
Katsuya Yamamoto ◽  
Shinichiro Kawamoto ◽  
Keiji Kurata ◽  
Akihito Kitao ◽  
Yu Mizutani ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Ring Chromosome ◽  
Chromosome 8 ◽  
Small Ring ◽  
Ring Chromosomes ◽  
Multiple Copies ◽  
Recurrent Translocation ◽  
Acute Myeloid

Oncogene amplification is uncommon in acute myeloid leukemia (AML). Cytogenetically, it is primarily found as double minute chromosomes (dmin) or homogeneously staining regions (hsr). A 62-year-old woman was admitted to our hospital because of anemia and thrombocytopenia. Her bone marrow was hypercellular with 78.6% myeloperoxidase- positive blasts. Some had micronuclei. The patient was diagnosed with AML M2 and remains in complete remission (CR) after induction therapy. G-banding at diagnosis showed 51,XX,t(11;16)(q13;p11.2),+r1,+mar1×4. Spectral karyotyping confirmed t(11;16) and revealed that the ring and the marker chromosomes were derived from multiple copies of ring chromosome 8. Fluorescence in situ hybridization (FISH) with a MYC probe at 8q24 detected amplified MYC signals on 1 large and 4 small ring chromosomes 8. One MYC signal was deleted from one of the 2 chromosomes 8. FISH with a FUS probe at 16p11.2 showed monoallelic deletion of FUS. Immunohistochemistry demonstrated MYC protein overexpression at diagnosis and almost negative expression in CR. These results indicate that MYC amplification could occur in ring chromosomes without dmin. A cryptic MYC deletion suggests that an episome model could be applicable to MYC amplification in ring chromosomes as observed for dmin and hsr. Furthermore, considering 2 further reported cases, t(11;16)(q13;p11) may be a very rare but recurrent translocation in AML.

scholarly journals A recurrent translocation, t(3;11)(q21;q13), found in two distinct cases of acute myeloid leukemia

1995 ◽  
Vol 83 (2) ◽  
pp. 119-120 ◽  
Author(s):  
Juan C. Cigudosa ◽  
M.José Calasanz ◽  
M.Dolores Odero ◽  
Julián Marin ◽  
Enrique Bengoechea ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Recurrent Translocation ◽  
Acute Myeloid

A novel recurrent translocation t(7;17)(q22;p13) and a late-appearing t(2;3)(p13;q26.2) with dysmegakaryopoiesis in acute myeloid leukemia

2012 ◽  
Vol 36 (4) ◽  
pp. e84-e86 ◽  
Author(s):  
Katsuya Yamamoto ◽  
Atsuo Okamura ◽  
Yumiko Inui ◽  
Kimikazu Yakushijin ◽  
Hiroshi Matsuoka ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Recurrent Translocation ◽  
Acute Myeloid

Identification of a fusion gene composed of a Hippo pathway gene MST2 and a common translocation partner ETV6 in a recurrent translocation t(8;12)(q22;p13) in acute myeloid leukemia

2015 ◽  
Vol 94 (8) ◽  
pp. 1431-1433 ◽  
Author(s):  
Shinichi Ogawa ◽  
Yasuhisa Yokoyama ◽  
Kazumi Suzukawa ◽  
Toru Nanmoku ◽  
Naoki Kurita ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Fusion Gene ◽  
Hippo Pathway ◽  
Pathway Gene ◽  
Recurrent Translocation ◽  
Acute Myeloid
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