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The KMT2A/MLL consensus gene structure: a comprehensive update for research and diagnostic implications

Leukemia, 2024-06, Vol.38 (6), p.1403-1406

2024

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Functional characterisation of different MLL fusion proteins by using inducible Sleeping Beauty vectors

Cancer letters, 2014-10, Vol.352 (2), p.196-202

2014

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Inhibition of PIM1 blocks the autophagic flux to sensitize glioblastoma cells to ABT-737-induced apoptosis

Biochimica et biophysica acta. Molecular cell research, 2019-02, Vol.1866 (2), p.175-189

2019

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Secondary mutations in t(4;11) leukemia patients

Leukemia, 2013-06, Vol.27 (6), p.1425-1427

2013

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Identification and characterization of the elusive mutation causing the historical von Willebrand Disease type IIC Miami

Journal of thrombosis and haemostasis, 2016-09, Vol.14 (9), p.1725-1735

2016

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The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures

Leukemia, 2011-01, Vol.25 (1), p.135-144

2011

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An alternative splice process renders the MLL protein either into a transcriptional activator or repressor

Pharmazie, 2013-07, Vol.68 (7), p.601-607

2013

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Prognostic significance of minimal residual disease in infants with acute lymphoblastic leukemia treated within the Interfant-99 protocol

Leukemia, 2009-06, Vol.23 (6), p.1073-1079

2009

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Ligand-independent FLT3 activation does not cooperate with MLL-AF4 to immortalize/transform cord blood CD34+ cells

Leukemia, 2014-03, Vol.28 (3), p.666-674

2014

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Immunobiological diversity in infant acute lymphoblastic leukemia is related to the occurrence and type of MLL gene rearrangement

Leukemia, 2007-04, Vol.21 (4), p.633-641

2007

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Activated KRAS enhances extramedullar engraftment and impairs clonogenic potential of MLLAF4-expressing cord blood CD34+ HSPCs but is not sufficient to initiate leukemia

Experimental hematology, 2015-09, Vol.43 (9), p.S89-S89

2015

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The heterodimerization domains of MLL-FYRN and FYRC-are potential target structures in t(4;11) leukemia

Leukemia, 2011-04, Vol.25 (4), p.663-670

2011

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TRANSCRIPTOME ANALYSES REVEAL NEW MARKERS FOR THE DIAGNOSIS AND TREATMENT OF KMT2A (MLL)-REARRANGED LEUKEMIA

Hematology, Transfusion and Cell Therapy, 2021-10, Vol.43, p.S181-S181

2021

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A Case of Acute Myeloid Leukemia with Novel Translocation t(6;11)(p22.2;q23) and Concurrent Insertion ins(11;9)(q23;p21.3p21.3)

Pulmonary Care and Clinical Medicine, 2017, Vol.1021, p.93-98

2017

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Genomic breakpoints and clinical features of MLL-TET1 rearrangement in acute leukemias

Haematologica (Roma), 2013-04, Vol.98 (4), p.e55-e57

2013

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Molecular characterization and clinical course of MLL-ACTN4 rearrangement in therapy-related hematologic malignancies

Haematologica (Roma), 2014-04, Vol.99 (4), p.e49-e51

2014

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An Alu‐mediated novel large deletion is the most frequent cause of type 3 von Willebrand disease in Hungary

Journal of thrombosis and haemostasis, 2008-10, Vol.6 (10), p.1729-1735

2008

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Complex Three-Way Translocation Involving MLL, ELL, RREB1, and CMAHP Genes in an Infant with Acute Myeloid Leukemia and t(6;19;11)(p22.2;p13.1;q23.3)

Cytogenetic and genome research, 2013-01, Vol.141 (1), p.7-15

2013

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Vaccine-induced COVID-19 mimicry syndrome

eLife, 2022-01, Vol.11

2022

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The MLL recombinome

Klinische Pädiatrie, 2014-05, Vol.226 (3)

2014

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Combined effects of the two reciprocal t(4;11) fusion proteins MLL AF4 and AF4 MLL confer resistance to apoptosis, cell cycling capacity and growth transformation

Oncogene, 2007-05, Vol.26 (23), p.3352-3363

2007

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Inhibition of class I HDACs abrogates the dominant effect of MLL-AF4 by activation of wild-type MLL

Oncogenesis (New York, NY), 2014-11, Vol.3 (11), p.e127-e127

2014

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A common 253‐kb deletion involving VWF and TMEM16B in German and Italian patients with severe von Willebrand disease type 3

Journal of thrombosis and haemostasis, 2007-04, Vol.5 (4), p.722-728

2007

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Transcription linked to recombination : a gene-internal promoter coincides with the recombination hot spot II of the human MLL gene

Oncogene, 2007-03, Vol.26 (10), p.1361-1371

2007

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Monitoring minimal residual disease by quantification of genomic chromosomal breakpoint sequences in acute leukemias with MLL aberrations

Leukemia, 2006-03, Vol.20 (3), p.451-457

2006

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The KMT2A/MLL consensus gene structure: a comprehensive update for research and diagnostic implications

Functional characterisation of different MLL fusion proteins by using inducible Sleeping Beauty vectors

Inhibition of PIM1 blocks the autophagic flux to sensitize glioblastoma cells to ABT-737-induced apoptosis

Secondary mutations in t(4;11) leukemia patients

Identification and characterization of the elusive mutation causing the historical von Willebrand Disease type IIC Miami

The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures

An alternative splice process renders the MLL protein either into a transcriptional activator or repressor

Prognostic significance of minimal residual disease in infants with acute lymphoblastic leukemia treated within the Interfant-99 protocol

Ligand-independent FLT3 activation does not cooperate with MLL-AF4 to immortalize/transform cord blood CD34+ cells

Immunobiological diversity in infant acute lymphoblastic leukemia is related to the occurrence and type of MLL gene rearrangement

Activated KRAS enhances extramedullar engraftment and impairs clonogenic potential of MLLAF4-expressing cord blood CD34+ HSPCs but is not sufficient to initiate leukemia

The heterodimerization domains of MLL-FYRN and FYRC-are potential target structures in t(4;11) leukemia

TRANSCRIPTOME ANALYSES REVEAL NEW MARKERS FOR THE DIAGNOSIS AND TREATMENT OF KMT2A (MLL)-REARRANGED LEUKEMIA

A Case of Acute Myeloid Leukemia with Novel Translocation t(6;11)(p22.2;q23) and Concurrent Insertion ins(11;9)(q23;p21.3p21.3)

Genomic breakpoints and clinical features of MLL-TET1 rearrangement in acute leukemias

Molecular characterization and clinical course of MLL-ACTN4 rearrangement in therapy-related hematologic malignancies

An Alu‐mediated novel large deletion is the most frequent cause of type 3 von Willebrand disease in Hungary

Complex Three-Way Translocation Involving MLL, ELL, RREB1, and CMAHP Genes in an Infant with Acute Myeloid Leukemia and t(6;19;11)(p22.2;p13.1;q23.3)

Vaccine-induced COVID-19 mimicry syndrome

The MLL recombinome

Combined effects of the two reciprocal t(4;11) fusion proteins MLL AF4 and AF4 MLL confer resistance to apoptosis, cell cycling capacity and growth transformation

Inhibition of class I HDACs abrogates the dominant effect of MLL-AF4 by activation of wild-type MLL

A common 253‐kb deletion involving VWF and TMEM16B in German and Italian patients with severe von Willebrand disease type 3

Transcription linked to recombination : a gene-internal promoter coincides with the recombination hot spot II of the human MLL gene

Monitoring minimal residual disease by quantification of genomic chromosomal breakpoint sequences in acute leukemias with MLL aberrations

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