MOZ is fused top300 in an acute monocytic leukemia with t(8;22)

Chaffanet, Max; Gressin, Lætitia; Preudhomme, Claude; Soenen, Valérie; Birnbaum, Daniel; Pébusque, Marie‐Josèphe

doi:10.1002/(sici)1098-2264(200006)28:2<138::aid-gcc2>3.0.co;2-2

Cited by 166 publications

(104 citation statements)

References 36 publications

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“…MOZ-CBP lacks the SM domain of MOZ, but gains almost all of CBP (Figure 3a). Mirroring the homology between p300 and CBP, the MOZ gene is fused to that of p300 in translocation t(8;22)(p11;q13) (Chaffanet et al, 2000;Kitabayashi et al, 2001b). Moreover, in t(10;16)(q22;p13) associated with childhood AML or therapeutic myelodysplastic syndromes, the MORF gene on 10q22 (Champagne et al, 1999) is fused to that of CBP (Panagopoulos et al, 2001;Kojima et al, 2003).…”

Section: Moz and Morf In Leukemia Leiomyomata And Other Malignanciesmentioning

confidence: 99%

MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells

2007

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Genes of the human monocytic leukemia zinc-finger protein MOZ (HUGO symbol, MYST3) and its paralog MORF (MYST4) are rearranged in chromosome translocations associated with acute myeloid leukemia and/or benign uterine leiomyomata. Both proteins have intrinsic histone acetyltransferase activity and are components of quartet complexes with noncatalytic subunits containing the bromodomain, plant homeodomain-linked (PHD) finger and proline-tryptophan-tryptophan-proline (PWWP)-containing domain, three types of structural modules characteristic of chromatin regulators. Although leukemia-derived fusion proteins such as MOZ-TIF2 promote self-renewal of leukemic stem cells, recent studies indicate that murine MOZ and MORF are important for proper development of hematopoietic and neurogenic progenitors, respectively, thereby highlighting the importance of epigenetic integrity in safeguarding stem cell identity.

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Section: Moz and Morf In Leukemia Leiomyomata And Other Malignanciesmentioning

confidence: 99%

MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells

2007

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“…Recent biochemical purifications revealed that both the Drosophila and mammalian MOF proteins reside in multi-protein complexes and that most of these interacting proteins are conserved between Drosophila and mammals (Table 2; Dou et al, 2005;Smith et al, 2005;Mendjan et al, 2006). Co-purification of four human MSL proteins (hMSL1, hMSL2, hMSL3 and hMOF) showed that the MSL (Borrow et al, 1996;Carapeti et al, 1998;Champagne et al, 1999Champagne et al, , 2001Chaffanet et al, 2000;Kitabayashi et al, 2001;Pelletier et al, 2002;Bristow and Shore, 2003;Deguchi et al, 2003;Kindle et al, 2005;Katsumoto et al, 2006;Thomas et al, 2006;Ohta et al, 2007 Abbreviation: HAT, histone acetyltransferases.…”

Section: The Histone Acetyltransferase Mofmentioning

confidence: 99%

Males absent on the first (MOF): from flies to humans

2007

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Histone modifications such as acetylation, methylation and phosphorylation have been implicated in fundamental cellular processes such as epigenetic regulation of gene expression, organization of chromatin structure, chromosome segregation, DNA replication and DNA repair. Males absent on the first (MOF) is responsible for acetylating histone H4 at lysine 16 (H4K16) and is a key component of the MSL complex required for dosage compensation in Drosophila. The human ortholog of MOF (hMOF) has the same substrate specificity and recent purification of the human and Drosophila MOF complexes showed that these complexes were also highly conserved through evolution. Several studies have shown that loss of hMOF in mammalian cells leads to a number of different phenotypes; a G 2 /M cell cycle arrest, nuclear morphological defects, spontaneous chromosomal aberrations, reduced transcription of certain genes and an impaired DNA repair response upon ionizing irradiation. Moreover, hMOF is involved in ATM activation in response to DNA damage and acetylation of p53 by hMOF influences the cell's decision to undergo apoptosis instead of a cell cycle arrest. These data, highlighting hMOF as an important component of many cellular processes, as well as links between hMOF and cancer will be discussed.

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“…Some cases have been previously reported in detail, namely M45-1, M45-3, M45-4, M45-5, M45-7, M45-11, M45-13, M45-16, M45-19, M45-20, M45-21, M45-23, M45-26, 7 M45-052, 13 M45-031, 14 M45-032 6 M45-062 and M45-063. 4 Three BM samples were used as normal controls (normal bone marrow (NBM)). They were collected from breast cancer patients without micrometastases.…”

Section: Patientsmentioning

confidence: 99%

“…It fuses two genes encoding histone acetyltransferases (HAT), MYST3 (also called MOZ) located at 8p11 to CREBBP (also called CBP) located at 16p13. [1][2][3] Variant translocations involve other HAT-encoding genes, such as EP300 at 22q13, 4 MYST4 at 10q22, NCOA2 at 8q13 5 or NCOA3 at 20q12. 6 MYST3-linked acute myeloid leukemias (AMLs) share specific features, such as frequent extramedullary involvement, disseminated intravascular coagulation, erythrophagocytosis and a poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases

Murati¹,

Gervais²,

Carbuccia³

et al. 2008

Leukemia

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The t(8;16)(p11;p13) is a rare translocation involved in de novo and therapy-related myelomonocytic and monocytic acute leukemia. It fuses two genes encoding histone acetyltransferases (HATs), MYST3 located at 8p11 to CREBBP located at 16p13. Variant translocations involve other HAT-encoding genes such as EP300, MYST4, NCOA2 or NCOA3. MYST3-linked acute myeloid leukemias (AMLs) share specific clinical and biological features and a poor prognosis. Because of its rarity, the molecular biology of MYST3-linked AMLs remains poorly understood. We have established the genome and gene expression profiles of a multicentric series of 61 M4/M5 AMLs including 18 MYST3-linked AMLs by using array comparative genome hybridization (aCGH) (n ¼ 52) and DNA microarrays (n ¼ 44), respectively. We show that M4/5 AMLs have a variety of rare genomic alterations. One alteration, a gain of the MYB locus, was found recurrently and only in the MYST3-linked AMLs (7/18 vs 0/34). MYST3-AMLs have also a specific a gene expression profile, which includes overexpression of MYB, CD4 and HOXA genes. These features, reminiscent of T-cell acute lymphoid leukemia (ALL), suggest the targeting of a common T-myeloid progenitor.

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MOZ is fused top300 in an acute monocytic leukemia with t(8;22)

Cited by 166 publications

References 36 publications

MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells

MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells

Males absent on the first (MOF): from flies to humans

Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases

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