Molecular basis of 11q23 rearrangements in hematopoietic malignant proliferations.
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MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25)The cloning, mapping and expression of a novel gene, BRL, related to the AF10 leukaemia geneThe human GRAF gene is fused to MLL in a unique t(5;11)(q31;q23) and both alleles are disrupted in three cases of myelodysplastic syndrome/acute myeloid leukemia with a deletion 5qThe elongation domain of ELL is dispensable but its ELL-associated factor 1 interaction domain is essential for MLL-ELL-induced leukemogenesisLeukemic HRX fusion proteins inhibit GADD34-induced apoptosis and associate with the GADD34 and hSNF5/INI1 proteinsEEN encodes for a member of a new family of proteins containing an Src homology 3 domain and is the third gene located on chromosome 19p13 that fuses to MLL in human leukemiaIdentification and characterization of the ARP1 gene, a target for the human acute leukemia ALL1 genemiR-34: from bench to bedsideStructure of the MLT gene and molecular characterization of the genomic breakpoint junctions in the t(11;18)(q21;q21) of marginal zone B-cell lymphomas of MALT typeMolecular analysis of an unstable genomic region at chromosome band 11q23 reveals a disruption of the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) in human lymphomaHuman LPP gene is fused to MLL in a secondary acute leukemia with a t(3;11) (q28;q23)HRX leukemic fusion proteins form a heterocomplex with the leukemia-associated protein SET and protein phosphatase 2AENL, the MLL fusion partner in t(11;19), binds to the c-Abl interactor protein 1 (ABI1) that is fused to MLL in t(10;11)+.Functional specificity of CpG DNA-binding CXXC domains in mixed lineage leukemia.Fish analysis at diagnosis in acute lymphoblastic leukemia.Diagnostic tool for the identification of MLL rearrangements including unknown partner genesBacktracking leukemia to birth: identification of clonotypic gene fusion sequences in neonatal blood spots.Cytogenetics and molecular genetics of childhood leukemia.The management of patients with leukaemia: the role of cytogenetics in this molecular era.The leukemia-associated-protein (LAP) domain, a cysteine-rich motif, is present in a wide range of proteins, including MLL, AF10, and MLLT6 proteins.Tumorigenesis in mice with a fusion of the leukaemia oncogene Mll and the bacterial lacZ gene.The oncogenic capacity of HRX-ENL requires the transcriptional transactivation activity of ENL and the DNA binding motifs of HRX.The structure of the human ALL-1/MLL/HRX gene.The partial tandem duplication of ALL1 (MLL) is consistently generated by Alu-mediated homologous recombination in acute myeloid leukemia.Chromatin-related properties of CBP fused to MLL generate a myelodysplastic-like syndrome that evolves into myeloid leukemiaDiscovery of MLL1 binding units, their localization to CpG Islands, and their potential function in mitotic chromatin.The amino terminus of the mixed lineage leukemia protein (MLL) promotes cell cycle arrest and monocytic differentiationC/EBPbeta suppression by interruption of CUGBP1 resulting from a complex rearrangement of MLL.The partial tandem duplication of ALL1 in acute myeloid leukemia with normal cytogenetics or trisomy 11 is restricted to one chromosome.MLL is fused to CBP, a histone acetyltransferase, in therapy-related acute myeloid leukemia with a t(11;16)(q23;p13.3).Nuclear punctate distribution of ALL-1 is conferred by distinct elements at the N terminus of the proteinEtoposide-initiated MLL rearrangements detected at high frequency in human primitive hematopoietic stem cells with in vitro and in vivo long-term repopulating potential.A diagnostic biochip for the comprehensive analysis of MLL translocations in acute leukemia.Neonatal leukaemia cutis.Granulocytic differentiation of leukemic cells with t(9;11)(p22;q23) induced by all-trans-retinoic acid.Variant and masked translocations in acute promyelocytic leukemia.Genomic instability in 1p and human malignancies.Analysis of the t(6;11)(q27;q23) in leukemia shows a consistent breakpoint in AF6 in three patients and in the ML-2 cell line.Acute myeloid leukemia in a 38-year-old hemodialyzed patient with von Hippel-Lindau disease.An ins(X;11)(q24;q23) fuses the MLL and the Septin 6/KIAA0128 gene in an infant with AML-M2.
P2860
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P2860
Molecular basis of 11q23 rearrangements in hematopoietic malignant proliferations.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
1995年论文
@zh
1995年论文
@zh-cn
name
Molecular basis of 11q23 rearrangements in hematopoietic malignant proliferations.
@en
type
label
Molecular basis of 11q23 rearrangements in hematopoietic malignant proliferations.
@en
prefLabel
Molecular basis of 11q23 rearrangements in hematopoietic malignant proliferations.
@en
P356
P1476
Molecular basis of 11q23 rearrangements in hematopoietic malignant proliferations
@en
P2093
P2860
P356
10.1002/GCC.2870130202
P577
1995-06-01T00:00:00Z