Mll Af9 Mouse

Interchromosomal recombination of Mll and Af9 genes mediated by cre

MLLENL and MLL AF9 cells cultured in myeloidpromoting conditions

The MllAF9 knockin mouse model Homologous recombination was used in

Iron metabolism in the MLLAF9 AML mouse model A MLLAF9 AML

Iron metabolism in the MLLAF9 AML mouse model A MLLAF9 1 AML cells

Iron metabolism in the MLLAF9 AML mouse model A MLLAF9 AML

A pooled in vivo shRNA screen in an MLLAF9 mouse AML m Openi

The MllAF9 knockin mouse model Homologous recombination was used in

Establishment of the LARP4B knockdown MLLAF9 AML mouse model A

Hif-1α Deletion May Lead to Adverse Treatment Effect in a Mouse Model ...

Hif1 Deletion May Lead to Adverse Treatment Effect in a Mouse Model

MLLAF9 leukemia is delayed in Mbnl1 knockout mice a Scheme of mouse

Protocol To Establish A Stable MLLAF9 AML Mouse Model PDF

Hif1 Deletion May Lead to Adverse Treatment Effect in a Mouse Model

Utilizing AML mouse models to compare proteome vs transcriptome A

Whole exome sequencing WES of mouse MLLAF9AML a b Upper panels

Protocol to establish a stable MLLAF9AML mouse model PMC

The Notch signaling pathway is silenced in a mouse AML model induced by

miR99 KD depletes LSCs in the MLLAF9 mouse model of AML by inducing

Iron metabolism in the MLLAF9 AML mouse model A MLLAF9 1 AML cells

PDF An Immunocompetent Mouse Model for MLLAF9 Leukemia Reveals the

LAIR1 enhances development of MLLAF9 mouse AML during serial

Whole exome sequencing WES of mouse MLLAF9AML a b Upper panels

Protocol to establish a stable MLLAF9AML mouse model PMC

Establishment of the LARP4B knockdown MLLAF9 AML mouse model A

Effects of MCSF isoforms on the progression of MLLAF9induced mouse

Effects of Socs2 knockdown in an MLLAF9 driven mouse model of AML

miR99 KD depletes LSCs in the MLLAF9 mouse model of AML by inducing

An Immunocompetent Mouse Model for MLLAF9 Leukemia Reveals the

Establishment of the LARP4B knockdown MLLAF9 AML mouse model A

Protocol to establish a stable MLLAF9AML mouse model PMC

The MllAF9 knockin mouse model Homologous recombination was used in

Hif1 Deletion May Lead to Adverse Treatment Effect in a Mouse Model

Whole exome sequencing WES of mouse MLLAF9AML a b Upper panels

The MllAF9 knockin mouse model Homologous recombination was used in

(PDF) Hif-1α Deletion May Lead to Adverse Treatment Effect in a Mouse ...

PDF Hif1 Deletion May Lead to Adverse Treatment Effect in a Mouse

The Polycomb complex PRC2 supports aberrant selfrenewal in a mouse

Serial transplantation of mouse MLLAF9acute myeloid leukemia AML

The Polycomb complex PRC2 supports aberrant selfrenewal in a mouse

Incidence of leukaemias in Mll translocator mice A Diagram of Mll

Complementary activities of DOT1L and Menin inhibitors in MLL

MLLAF9 leukemia is delayed in Mbnl1 knockout mice a Scheme of mouse

Schwaller Lab Department of Biomedicine

Integrated transcriptomic and epigenetic data analysis

Establishment of the Six1knockdown acute myeloid leukemia AML murine

P2X7 promotes the progression of MLLAF9 induced acute myeloid leukemia

Defective erythropoiesis in AML mice a The strategy used to

IL1b promoted MLLAF9 AML progression partly via niche cells A The

Development of AML in mice transplanted with ATG5WT and Atg5FL

Loss of Vcam1 inhibits the establishment and progression of

Heritable genetic background alters survival and phenotype of MllAF9

Inducible MLLAF9 Expression Drives an AML Program during Human

Distribution and phenotypic evolution of LAMs in BM and SP in MLLAF9

MLLAF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive

A high level of residual AML cell infiltration in skin tissue of

DOT1L is required for MLLAF9induced acute leukemia progression in

LSC frequency was increased in Tgif1 mice with AML compared to

MLLAF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive

Integrated transcriptomic and epigenetic data analysis

Flow analysis showing cell lineages of BM cells of MLLAF9AML mice and

HSF1 is required for the initiation and maintenance of MLLAF9induced

Heritable genetic background alters survival and phenotype of MllAF9

Inducible MLLAF9 Expression Drives an AML Program during Human

Full article Aggressive leukemia driven by MLLAF9

MLLAF9 cells generated from Trp53 BM cells were sensitive to

Isolation of LPMs large peritoneal macrophages in the MLLAF9induced

Incidence of leukemia in mice expressing MLLAF9 or MLLAF9 with

Microenvironment Determines Lineage Fate in a Human Model of MLLAF9

Meningioma 1 is indispensable for mixed lineage leukemiarearranged

Hematopoietic Stem Cell HSCIndependent Progenitors Are Susceptible

PRDM16 represses MLLAF9 leukemia in vivo See also Figure S2 A

Surface phenotype of AMLs in MllAF9 mice MllAF9 mice with signs of

Arhgap4 significantly supports AML progression A The schematic of

Loss of CAMKIV decreases MLLAF9 AML development a Mice transplanted

expression of MbS4 in MLLAF9 cells inhibits leukemia progression

AML cells are not dependent on SETBP1 for their survival A Schema of

Expression of BCL2 protein family members in primary MLLAF9 AMLs

ATF4 deletion delays leukemogenesis in MLLAF9induced AML model A

Homoharringtonine exhibits potent antitumor effect and modulates DNA

$Bone marrow mesenchymal stromal cells support translation in refractory ...$

Bone marrow mesenchymal stromal cells support translation in refractory

Histology of leukaemias arising in MllAF9 mice Histology was carried

Role of the bone marrow vascular niche in chemotherapy for MLLAF9

SUV39H1 regulates the progression of MLLAF9induced acute myeloid

Frontiers Histone H3K36me2Specific Methyltransferase ASH1L Promotes

Modeling BCRABL and MLLAF9 leukemia in a human bone marrowlike

Glucose uptake after antileukaemia drugs A Schematic workflow of bone

CRISPRCas9 engineering of the MllAf9 fusion gene in hematopoietic

LAIR1 signalling is essential for human leukaemia development

Fig S5 Representative of flow cytometric analysis of BM SP and PB

Decoupling of TumorInitiating Activity from Stable Immunophenotype in

PDF miR101 suppresses the development of MLLrearranged acute

MLLAF9 EphA2 knockout mice have similar leukemogenic potential A

Myeloid leukemia in MllAf9 and Mll Enl translocator mice have

ASH1L promotes the MLLAF9induced leukemia development in vivo A

MLLAF9induced AML in Tgif1 mice was more aggressive with a shorter

Establishment of MLLAF9 leukemia cells expressing a model tumor

BENC is required for maintenance of MLLAF9 leukaemia in mice and

In Vivo Screening Unveils Pervasive RNABinding Protein Dependencies in

Figure S4 Mice transformed with MLLAF9NRAS develop acute leukemia

An MllAF9 Fusion Gene Made by Homologous Recombination Causes Acute

Genetic deletion of Rictor accelerates the initiation of MLLdriven

An MllAF9 Fusion Gene Made by Homologous Recombination Causes Acute

MLLAF9 regulates transcriptional initiation in mixed lineage leukemic

Metabolic phenotype of MLLAF9 AML cells Schematic outline of results

Molecular insights into chemotherapy resistance mediated by MLLAF9

Blocking antiLILRB3 antibody prevents monocytic AML development a

Selective Antileukemic Activity of Prototype CKI Inhibitors A

Antitumor effect of Alox5 in MLLAF9AML a Inhibitory effect of

Secondary transplants indicate the absence of residual AML cells and

Loss of Arid1b promotes MLLAF9 leukemogenesis A In vivo leukemogenesis

Selective regulation of transcription by MLLAF9 a Schematic of

Young MllAF9 mice exhibit increased myeloproliferation MllAF9

Twist family BHLH transcription factor 1 is required for the

Arid2 has dual roles in MLLAF9 leukemogenesis AC In vivo

Antiselfrenewal and leukemogenesis abilities by bort in Download

PIRB suppresses differentiation and enhances development of MLLAF9

Identification and characterization of leukemia stem cells in murine

Xenograft Mouse Model

MLL-AF9 Cell Culture

MLL AF9 Protein

Rflsi ⅲ Mouse

Tet On MLL AF9 Mouse Model

MLL-AF9 Spleen Cell Culture

Mllt3 AF9

MLL Fusion Proteins

APV Cannula of Mouse

AF9 Immunofluorescence

THP-1 Leukemia Mouse Model

MLL AF9 Spleen Liver. He Staining

Mof Vector

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