D. Gary Gilliland

FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model.

Comprehensive genotypic analysis of leukemia: clinical and therapeutic implications.

Evaluation of the risk of therapy-related MDS/AML after autologous stem cell transplantation.

A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9.

The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex (9;12) translocations in human leukemia, induces distinct myeloproliferative disease in mice.

Role of FLT3 in leukemia.

PML/RARalpha and FLT3-ITD induce an APL-like disease in a mouse model.

Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemia.

Core-binding factors in haematopoiesis and leukaemia.

Focus on acute leukemias.

CT53518, a novel selective FLT3 antagonist for the treatment of acute myelogenous leukemia (AML).

Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412.

The roles of FLT3 in hematopoiesis and leukemia.

Genetics of myeloid leukemias.

The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.

Molecular genetics of human leukemias: new insights into therapy.

A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657.

A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.

MOZ-TIF2-induced acute myeloid leukemia requires the MOZ nucleosome binding motif and TIF2-mediated recruitment of CBP.

Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness.

PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease.

CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy.

FLT3-activating mutations in acute promyelocytic leukaemia: a rationale for risk-adapted therapy with FLT3 inhibitors.

The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia.

Proteolytic processing in development and leukemogenesis.

The FIP1L1-PDGFRalpha kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia.

The role of signal transducer and activator of transcription factors in leukemogenesis.

NPM-ALK fusion kinase of anaplastic large-cell lymphoma regulates survival and proliferative signaling through modulation of FOXO3a.

Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease.

Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs.

Oncogenic K-ras in mouse models of myeloproliferative disease and acute myeloid leukemia.

Positive and negative regulatory roles of the WW-like domain in TEL-PDGFbetaR transformation.

The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management.

Platelet-derived growth factor receptor inhibition to treat idiopathic hypereosinophilic syndrome.

Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AML.

Stable expression of small interfering RNA sensitizes TEL-PDGFbetaR to inhibition with imatinib or rapamycin.

Variable sensitivity of FLT3 activation loop mutations to the small molecule tyrosine kinase inhibitor MLN518.

Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation.

Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412.

Prediction of resistance to small molecule FLT3 inhibitors: implications for molecularly targeted therapy of acute leukemia.

Blasts from the past: new lessons in stem cell biology from chronic myelogenous leukemia.

PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder.

KIAA1509 is a novel PDGFRB fusion partner in imatinib-responsive myeloproliferative disease associated with a t(5;14)(q33;q32).

The molecular basis of leukemia.

Global effects of BCR/ABL and TEL/PDGFRbeta expression on the proteome and phosphoproteome: identification of the Rho pathway as a target of BCR/ABL.

MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors.

Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl.

Prognostic, therapeutic, and mechanistic implications of a mouse model of leukemia evoked by Shp2 (PTPN11) mutations.

EGFR inhibition in non-small cell lung cancer: resistance, once again, rears its ugly head.

Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype.

Constitutively activated FGFR3 mutants signal through PLCgamma-dependent and -independent pathways for hematopoietic transformation.

Activation mutations of human c-KIT resistant to imatinib mesylate are sensitive to the tyrosine kinase inhibitor PKC412.

Leukaemia stem cells and the evolution of cancer-stem-cell research.

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.

The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both "atypical" myeloproliferative disorders and myelodysplastic syndromes.

Drug therapy for acute myeloid leukemia.

JAK2 in myeloproliferative disorders is not just another kinase.

Activity of the tyrosine kinase inhibitor PKC412 in a patient with mast cell leukemia with the D816V KIT mutation.

Cancer biology: summing up cancer stem cells.

The JAK2V617F tyrosine kinase mutation in myeloproliferative disorders: status report and immediate implications for disease classification and diagnosis.

The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRbeta and FIP1L1-PDGFRalpha in vitro and in vivo.

The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.

Mutation studies in CD3+, CD19+ and CD34+ cell fractions in myeloproliferative disorders with homozygous JAK2(V617F) in granulocytes.

Genetics of myeloid malignancies: pathogenetic and clinical implications.

JAK2 mutation in essential thrombocythaemia: clinical associations and long-term prognostic relevance.

Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation.

The clinical phenotype of wild-type, heterozygous, and homozygous JAK2V617F in polycythemia vera.

Your health in the 21st century. Do stem cells cause cancer?

X-inactivation-based clonality analysis and quantitative JAK2V617F assessment reveal a strong association between clonality and JAK2V617F in PV but not ET/MMM, and identifies a subset of JAK2V617F-negative ET and MMM patients with clonal hematopoiesis.

Rare occurrence of the JAK2 V617F mutation in AML subtypes M5, M6, and M7.

Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.

Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model.

Prospective analysis of TEL/AML1-positive patients treated on Dana-Farber Cancer Institute Consortium Protocol 95-01.

Detection of the FIP1L1-PDGFRA fusion in idiopathic hypereosinophilic syndrome and chronic eosinophilic leukemia.

Absence of the transcription factor CCAAT enhancer binding protein alpha results in loss of myeloid identity in bcr/abl-induced malignancy.

Roles of tyrosine 589 and 591 in STAT5 activation and transformation mediated by FLT3-ITD.

Oncogenic K-ras cooperates with PML-RAR alpha to induce an acute promyelocytic leukemia-like disease.

International Working Group (IWG) consensus criteria for treatment response in myelofibrosis with myeloid metaplasia, for the IWG for Myelofibrosis Research and Treatment (IWG-MRT).

Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent.

Eosinophilic disorders: molecular pathogenesis, new classification, and modern therapy.

JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model.

MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.

Cell-autonomous and -nonautonomous contributions of STAT1 in murine models of tumorigenesis.

Activating alleles of JAK3 in acute megakaryoblastic leukemia.

Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9.

MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients.

Cdx4 dysregulates Hox gene expression and generates acute myeloid leukemia alone and in cooperation with Meis1a in a murine model.

Concurrent MPL515 and JAK2V617F mutations in myelofibrosis: chronology of clonal emergence and changes in mutant allele burden over time.

JAK-2 mutations and their relevance to myeloproliferative disease.

Jak2: normal function and role in hematopoietic disorders.

FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis.

FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress.

JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis.

The retinoblastoma binding protein RBP2 is an H3K4 demethylase.

The homeobox gene CDX2 is aberrantly expressed in most cases of acute myeloid leukemia and promotes leukemogenesis.

Oncogenes in myeloproliferative disorders.

A novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemia.

Ott1(Rbm15) has pleiotropic roles in hematopoietic development.

Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel.

Highly sensitive method for genomewide detection of allelic composition in nonpaired, primary tumor specimens by use of affymetrix single-nucleotide-polymorphism genotyping microarrays.

Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders.

FGFR3 activates RSK2 to mediate hematopoietic transformation through tyrosine phosphorylation of RSK2 and activation of the MEK/ERK pathway.

Uniform sensitivity of FLT3 activation loop mutants to the tyrosine kinase inhibitor midostaurin.

A role for JAK2 mutations in myeloproliferative diseases.

FLT3 mutations confer enhanced proliferation and survival properties to multipotent progenitors in a murine model of chronic myelomonocytic leukemia.

PU.1 is a major downstream target of AML1 (RUNX1) in adult mouse hematopoiesis.

Host genetic variation contributes to phenotypic diversity in myeloproliferative disorders.

SOS1 mutations are rare in human malignancies: implications for Noonan Syndrome patients.

Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles.

The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes.

High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia.

Structural and numerical variation of FLT3/ITD in pediatric AML.

FoxO transcription factors and stem cell homeostasis: insights from the hematopoietic system.

Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera.

Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells.

Kinase activation and transformation by NUP214-ABL1 is dependent on the context of the nuclear pore.

K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to gamma-secretase inhibitors.

Deregulation of signaling pathways in acute myeloid leukemia.

Genetic profiling of myeloproliferative disorders by single-nucleotide polymorphism oligonucleotide microarray.

Myeloproliferative disorders.

Notch signaling specifies megakaryocyte development from hematopoietic stem cells.

Going with the flow: JAK-STAT signaling in JMML.

Activating mutations in ALK provide a therapeutic target in neuroblastoma.

Ott1 (Rbm15) is essential for placental vascular branching morphogenesis and embryonic development of the heart and spleen.

High-throughput sequencing screen reveals novel, transforming RAS mutations in myeloid leukemia patients.

Constitutive JAK3 activation induces lymphoproliferative syndromes in murine bone marrow transplantation models.

Skewing of X-inactivation ratios in blood cells of aging women is confirmed by independent methodologies.

A radical bailout strategy for cancer stem cells.

The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model.

A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasms.

The leukemic stem cell niche: current concepts and therapeutic opportunities.

Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies.

Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells.

Hedgehog signaling is dispensable for adult murine hematopoietic stem cell function and hematopoiesis.

[The OTT-MAL fusion oncogene: another Notch in megakaryoblastic leukemia].

A progenitor cell origin of myeloid malignancies.

Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1.

Direct inhibition of the NOTCH transcription factor complex.

Tyrosine phosphorylation inhibits PKM2 to promote the Warburg effect and tumor growth.

Constitutively active AKT depletes hematopoietic stem cells and induces leukemia in mice.

Leukemia stem cells.

Prevalence and prognostic impact of allelic imbalances associated with leukemic transformation of Philadelphia chromosome-negative myeloproliferative neoplasms.

The Apc(min) mouse has altered hematopoietic stem cell function and provides a model for MPD/MDS.

The JAK2(V617F) tyrosine kinase mutation in myeloproliferative disorders: Summary of published literature and a perspective.

Cdx4 is dispensable for murine adult hematopoietic stem cells but promotes MLL-AF9-mediated leukemogenesis.

Hematopoietic stem cell defects in mice with deficiency of Fancd2 or Usp1.

Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells.

Transcriptional profiling of polycythemia vera identifies gene expression patterns both dependent and independent from the action of JAK2V617F.

Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia.

Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3.

mTOR activation induces tumor suppressors that inhibit leukemogenesis and deplete hematopoietic stem cells after Pten deletion.

Safety and efficacy of TG101348, a selective JAK2 inhibitor, in myelofibrosis.

Common and overlapping oncogenic pathways contribute to the evolution of acute myeloid leukemias.

Crosstalk between NOTCH and AKT signaling during murine megakaryocyte lineage specification.

Differential niche and Wnt requirements during acute myeloid leukemia progression.

Coordinate loss of a microRNA and protein-coding gene cooperate in the pathogenesis of 5q- syndrome.

AKT/FOXO signaling enforces reversible differentiation blockade in myeloid leukemias.

KIT with D816 mutations cooperates with CBFB-MYH11 for leukemogenesis in mice.

A Functional Role For The Histone Demethylase Utx In Normal And Malignant Hematopoietic Cells.