Selective FLT3 inhibition of FLT3-ITD+ acute myeloid leukaemia resulting in secondary D835Y mutation: a model for emerging clinical resistance patterns

Imatinib is highly effective in newly diagnosed, but not in relapsed, Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL). BCR-ABL tyrosine kinase domain (TKD) mutations are associated with acquired imatinib resistance, but their role in primary resistance is uncertain. Using highly sensitive ligation-PCR and denaturing high-performance liquid chromatography (DHPLC), we identified baseline TKD mutations in 21% and 42% of imatinib-naïve patients with newly diagnosed (n=26) or recurrent (n=65) Ph+ ALL, respectively (P=ns). Within 4 weeks of starting the imatinib treatment, absolute levels of mutant bcr-abl transcripts increased significantly in patients with advanced, but not with de novo, Ph+ ALL. The net expansion of pre-existing mutant clones during imatinib treatment resulted in the rapid appearance of initially undetectable TKD mutations, which after 4 weeks were detectable in 70% of patients with advanced disease. There was a high degree of concordance between the type of mutations detected at relapse and during initial imatinib treatment. The profoundly different outgrowth dynamics of leukemic clones with bcr-abl mutations in imatinib-treated patients who differ in their disease history, provides clinical–translational evidence for a contributory role of non-mutational resistance mechanisms, possibly induced by prior chemotherapy. Moreover, the prevalence of pre-existing, clinically relevant TKD may have been underestimated in tyrosine kinase inhibitor-naïve patients with Ph+ ALL.

• Publication year

  2012

• Venue

  Leukemia

• Publication date

  2012-01-26

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/leu.2012.5PMID 22230800PMCID 3523391
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Validation of FLT3-ITD As a Therapeutic Target in Human Acute Myeloid Leukemia

  2011cited by this paper
• Philadelphia-positive acute lymphoblastic leukemia patients already harbor BCR-ABL kinase domain mutations at low levels at the time of diagnosis

  2011cited by this paper
• Independent prognostic variables in acute myeloid leukaemia.

  2011cited by this paper
• Analysis of in Vitro Activity of the Clinically-Active ABL/FLT3 Inhibitor Ponatinib (AP24534) Against AC220-Resistant FLT3-ITD Mutants

  2011cited by this paper
• The clinical development of FLT3 inhibitors in acute myeloid leukemia

  2011cited by this paper
• Loss of the wild-type allele contributes to myeloid expansion and disease aggressiveness in FLT3/ITD knockin mice.

  2011cited by this paper
• Phase 1/2 study to assess the safety, efficacy, and pharmacokinetics of barasertib (AZD1152) in patients with advanced acute myeloid leukemia.

  2011cited by this paper
• Activity of Allosteric, Switch-Pocket, ABL/FLT3 Kinase Inhibitor DCC2036 Against Cultured and Primary AML Progenitors with FLT-ITD or FLT3 Kinase Domain Mutations

  2011cited by this paper
• Abstract 4737: Saturation mutagenesis of FLT3-ITD: AC220-resistance-conferring kinase domain mutations are restricted to a limited number of residues and are cross-resistant to sorafenib in vitro

  2011cited by this paper
• PLX3397 Is An Investigational Selective FLT3 Inhibitor That Retains Activity Against the Clinically-Relevant FLT3-ITD/F691L “Gatekeeper” Mutation in Vitro

  2011cited by this paper
• Imidazo[4,5-b]pyridine derivatives as inhibitors of Aurora kinases: lead optimization studies toward the identification of an orally bioavailable preclinical development candidate.

  2010cited by this paper
• Phase 2 Study of MLN8237, An Investigational Aurora A Kinase (AAK) Inhibitor In Patients with Acute Myelogenous Leukemia (AML) or Myelodysplastic Syndromes (MDS)

  2010cited by this paper
• Will newer tyrosine kinase inhibitors have an impact in AML?

  2010cited by this paper
• Guidelines for the welfare and use of animals in cancer research

  2010cited by this paper
• FLT3-mutant allelic burden and clinical status are predictive of response to FLT3 inhibitors in AML.

  2010cited by this paper
• Aurora kinase inhibitors: novel small molecules with promising activity in acute myeloid and Philadelphia-positive leukemias

  2010cited by this paper
• Structural and Functional Alterations of FLT3 in Acute Myeloid Leukemia

  2009cited by this paper
• FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro.

  2009cited by this paper
• AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML).

  2009cited by this paper
• Aurora kinase inhibitors: identification and preclinical validation of their biomarkers

  2008cited by this paper
• Highly sensitive and quantitative detection of BCR-ABL kinase domain mutations by ligation PCR

  2008cited by this paper
• Kinase domain point mutations in Philadelphia chromosome‐positive acute lymphoblastic leukemia emerge after therapy with BCR‐ABL kinase inhibitors

  2008cited by this paper
• Segmental uniparental disomy is a commonly acquired genetic event in relapsed acute myeloid leukemia.

  2008cited by this paper
• FLT3 D835/I836 mutations are associated with poor disease-free survival and a distinct gene-expression signature among younger adults with de novo cytogenetically normal acute myeloid leukemia lacking FLT3 internal tandem duplications.

  2008cited by this paper
• Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL).

  2007cited by this paper
• Hit generation and exploration: imidazo[4,5-b]pyridine derivatives as inhibitors of Aurora kinases.

  2007cited by this paper
• Imatinib combined with induction or consolidation chemotherapy in patients with de novo Philadelphia chromosome-positive acute lymphoblastic leukemia: results of the GRAAPH-2003 study.

  2007cited by this paper
• A Novel FLT3 Inhibitor FI-700 Selectively Suppresses the Growth of Leukemia Cells with FLT3 Mutations

  2007cited by this paper
• FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia.

  2007cited by this paper
• Mechanism of action of the Aurora kinase inhibitor CCT129202 and in vivo quantification of biological activity

  2007cited by this paper
• Imatinib compared with chemotherapy as front‐line treatment of elderly patients with Philadelphia chromosome‐positive acute lymphoblastic leukemia (Ph+ALL)

  2007cited by this paper
• Imatinib and methylprednisolone alternated with chemotherapy improve the outcome of elderly patients with Philadelphia-positive acute lymphoblastic leukemia: results of the GRAALL AFR09 study

  2006cited by this paper
• Clinical implications of FLT3 mutations in pediatric AML.

  2006cited by this paper
• Contribution of ABL Kinase Domain Mutations to Imatinib Resistance in Different Subsets of Philadelphia-Positive Patients: By the GIMEMA Working Party on Chronic Myeloid Leukemia

  2006cited by this paper
• Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

  2006cited by this paper
• Validating Aurora B as an anti-cancer drug target

  2006cited by this paper
• High complete remission rate and promising outcome by combination of imatinib and chemotherapy for newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia: a phase II study by the Japan Adult Leukemia Study Group.

  2006cited by this paper
• Alternating versus concurrent schedules of imatinib and chemotherapy as front-line therapy for Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL).

  2006cited by this paper
• Kinase Domain Mutants of Bcr-Abl Exhibit Altered Transformation Potency, Kinase Activity, and Substrate Utilization, Irrespective of Sensitivity to Imatinib

  2006cited by this paper
• The chromosomal passenger complex: guiding Aurora-B through mitosis

  2006cited by this paper
• Acute myeloid leukaemia with FLT3 gene mutations of both internal tandem duplication and point mutation type

  2005cited by this paper
• Clinical effect of imatinib added to intensive combination chemotherapy for newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leukemia

  2005cited by this paper
• Guide to Leukemia-Lymphoma Cell Lines on CD.

  2005cited by this paper
• Treatment of Philadelphia chromosome-positive acute lymphocytic leukemia with hyper-CVAD and imatinib mesylate.

  2004cited by this paper
• Variable sensitivity of FLT3 activation loop mutations to the small molecule tyrosine kinase inhibitor MLN518.

  2004cited by this paper
• FLT3 mutations are associated with other molecular lesions in AML.

  2004cited by this paper
• Early prediction of response in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) treated with imatinib.

  2004cited by this paper
• Resistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back

  2003cited by this paper
• The cellular geography of Aurora kinases

  2003cited by this paper
• Detection of FLT3 internal tandem duplication and D835 mutations by a multiplex polymerase chain reaction and capillary electrophoresis assay.

  2003cited by this paper
• Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.

  2003cited by this paper
• FLT3 mutations in acute myeloid leukemia cell lines

  2003cited by this paper
• A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias.

  2002cited by this paper
• High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance.

  2002cited by this paper
• Internal tandem duplication of FLT3 in relapsed acute myeloid leukemia: a comparative analysis of bone marrow samples from 108 adult patients at diagnosis and relapse.

  2002cited by this paper
• BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study.

  2002cited by this paper
• Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation.

  2002cited by this paper
• Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis.

  2002cited by this paper
• Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome.

  2001cited by this paper
• Absence of the wild-type allele predicts poor prognosis in adult de novo acute myeloid leukemia with normal cytogenetics and the internal tandem duplication of FLT3: a cancer and leukemia group B study.

  2001cited by this paper
• Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathways.

  2000cited by this paper
• Close physical linkage of the FLT1 and FLT3 genes on chromosome 13 in man and chromosome 5 in mouse.

  1993cited by this paper

• Targeting HDAC8 sensitizes tyrosine kinase inhibitors in the elimination of B-cell acute lymphoblastic leukemia cells through degradation of HIF-1α

  2025cites this paper
• IHCH9033, a novel class I HDAC inhibitor, synergizes with FLT3 inhibitor and rescues quizartinib resistance in FLT3-ITD AML via enhancing DNA damage response

  2025cites this paper
• Rational design of next-generation FLT3 inhibitors in acute myeloid leukemia: From laboratory to clinics.

  2025cites this paper
• FLT3: A 35-Year Voyage from Discovery to the Next Generation of Targeted Therapy in AML

  2025cites this paper
• Discovery of Anticancer Indole-Based 4,5-Dihydroisoxazole Derivative with Selectivity toward Leukemia Cells.

  2025cites this paper
• Discovery of Potent Dual PROTAC Degraders Targeting BET-Kinase To Overcome FLT3 Inhibitor Resistance.

  2025cites this paper
• The Emergence of a Novel Insertional Mutation in the BCR::ABL/p210 Oncogene in B-Cell Acute Lymphoblastic Leukemia (B-ALL) Correlates with the Development of Resistance to Several Tyrosine Kinase Inhibitors

  2025cites this paper
• Preferential Genetic Pathways Lead to Relapses in Adult B-Cell Acute Lymphoblastic Leukemia

  2024cites this paper
• Targeting hematological malignancies with isoxazole derivatives.

  2024cites this paper
• New ABL1 Kinase Domain Mutations in BCR::ABL1‐Positive Acute Lymphoblastic Leukemia

  2024cites this paper
• Tyrosine kinase inhibitor resistance in de novo BCR::ABL1–positive BCP-ALL beyond kinase domain mutations

  2024cites this paper
• Discovery of a potent Gilteritinib-based FLT3-PROTAC degrader for the treatment of Acute myeloid leukemia.

  2024cites this paper
• Discovery of a Novel Orally Bioavailable FLT3-PROTAC Degrader for Efficient Treatment of Acute Myeloid Leukemia and Overcoming Resistance of FLT3 Inhibitors.

  2024cites this paper
• The Therapeutic Potential of a Strategy to Prevent Acute Myeloid Leukemia Stem Cell Reprogramming in Older Patients

  2023cites this paper
• Blockade of de novo pyrimidine biosynthesis triggers autophagic degradation of oncoprotein FLT3-ITD in acute myeloid leukemia

  2023cites this paper
• Diagnosis and Molecular Pathology of Lymphoblastic Leukemias and Lymphomas in the Era of Genomics and Precision Medicine: Historical Evolution and Current Concepts—Part 2: B-/T-Cell Acute Lymphoblastic Leukemias

  2023cites this paper
• Droplet digital polymerase chain reaction improves the detection of BCR‐ABL1 kinase domain mutation in Philadelphia chromosome‐positive acute lymphoblastic leukemia

  2023cites this paper
• FLT3 inhibitors and novel therapeutic strategies to reverse AML resistance: an updated comprehensive review.

  2023cites this paper
• Resistance of Lung Cancer to EGFR-Specific Kinase Inhibitors: Activation of Bypass Pathways and Endogenous Mutators

  2023cites this paper
• Treatment of Adult Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia

  2022cites this paper
• NF-κB: A Druggable Target in Acute Myeloid Leukemia

  2022cites this paper
• JAK2 Alterations in Acute Lymphoblastic Leukemia: Molecular Insights for Superior Precision Medicine Strategies

  2022influential citation
• Translatome proteomics identifies autophagy as a resistance mechanism to on-target FLT3 inhibitors in acute myeloid leukemia

  2022cites this paper
• Combining Mass Spectrometry-Based Phosphoproteomics with a Network-Based Approach to Reveal FLT3-Dependent Mechanisms of Chemoresistance

  2021cites this paper
• Dual Kinase Targeting in Leukemia

  2021cites this paper
• Discovery of novel 4-azaaryl-N-phenylpyrimidin-2-amine derivatives as potent and selective FLT3 inhibitors for acute myeloid leukaemia with FLT3 mutations.

  2021cites this paper
• FLT3 Tyrosine Kinase Inhibitors for the Treatment of Fit and Unfit Patients with FLT3-Mutated AML: A Systematic Review

  2021cites this paper
• Next‐generation sequencing improves BCR‐ABL1 mutation detection in Philadelphia chromosome‐positive acute lymphoblastic leukaemia

  2021cites this paper
• Sensitivity and reliability of DNA-based mutation analysis by allele-specific digital PCR to follow resistant BCR-ABL1-positive cells

  2021cites this paper
• Autophagy activation mediates resistance to FLT3 inhibitors in acute myeloid leukemia with FLT3-ITD mutation

  2021cites this paper
• Identification of a highly efficient dual type I/II FMS-like tyrosine kinase inhibitor that disrupts the growth of leukemic cells.

  2021cites this paper
• Emerging tyrosine kinase inhibitors for the treatment of adult acute lymphoblastic leukemia

  2021cites this paper
• Therapeutic approach and outcome of children with Philadelphia chromosome‐positive acute lymphoblastic leukemia at first relapse in the era of tyrosine kinase inhibitors: An SFCE retrospective study

  2021cites this paper
• CCT245718, a dual FLT3/Aurora A inhibitor overcomes D835Y-mediated resistance to FLT3 inhibitors in acute myeloid leukaemia cells

  2021cites this paper
• Inhibition of translation initiation factor eIF4a inactivates heat shock factor 1 (HSF1) and exerts anti-leukemia activity in AML

  2021cites this paper
• Next‐generation sequencing for BCR‐ABL1 kinase domain mutations in adult patients with Philadelphia chromosome‐positive acute lymphoblastic leukemia: A position paper

  2020cites this paper
• Overcoming Resistance to FLT3 Inhibitors in the Treatment of FLT3-Mutated AML

  2020cites this paper
• Phase I Oncology Drug Development

  2020cites this paper
• Population-based utilization and costs associated with tyrosine kinase inhibitors for first-line treatment of chronic myelogenous leukemia among elderly patients

  2020cites this paper
• New approaches to the treatment of older adults with acute lymphoblastic leukemia.

  2020cites this paper
• A variant e13a3 BCR-ABL1 fusion transcript in refractory adult B-cell acute lymphoblastic leukemia achieving complete remission with CAR-Tcell therapy.

  2020cites this paper
• Molecular Diagnosis of FLT3 Mutations in Acute Myeloid Leukemia Patients

  2020cites this paper
• Preclinical Studies to Enable First in Human Clinical Trials

  2020cites this paper
• Recent researches for dual Aurora target inhibitors in antitumor field.

  2020cites this paper
• Ultra-accurate Duplex Sequencing for the assessment of pretreatment ABL1 kinase domain mutations in Ph+ ALL

  2020cites this paper
• Theoretical Studies Aimed at Finding FLT3 Inhibitors and a Promising Compound and Molecular Pattern with Dual Aurora B/FLT3 Activity

  2020cites this paper
• Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells

  2020cites this paper
• A series of novel aryl-methanone derivatives as inhibitors of FMS-like tyrosine kinase 3 (FLT3) in FLT3-ITD-positive acute myeloid leukemia.

  2020cites this paper
• Quizartinib-resistant FLT3-ITD acute myeloid leukemia cells are sensitive to the FLT3-Aurora kinase inhibitor CCT241736.

  2020influential citation
• A new pre-emptive TKIs strategy for preventing relapse based on BCR/ABL monitoring for Ph+ALL undergoing allo-HCT: a prospective clinical cohort study

  2020cites this paper
• Extracellular Vesicles and Chemotherapy Resistance in the AML Microenvironment

  2020cites this paper
• Natural and Semisynthetic Chalcones as Dual FLT3 and Microtubule Polymerization Inhibitors.

  2020cites this paper
• Discovery and rational design of 2-aminopyrimidine-based derivatives targeting Janus kinase 2 (JAK2) and FMS-like tyrosine kinase 3 (FLT3).

  2020cites this paper
• Mutated clones driving leukemic transformation are already detectable at the single-cell level in CD34-positive cells in the chronic phase of primary myelofibrosis

  2020cites this paper
• FLT3 inhibitor quizartinib (AC220)

  2019cites this paper
• Dual FLT3 inhibitors: Against the drug resistance of acute myeloid leukemia in recent decade.

  2019cites this paper
• Identification and evaluation of novel drug combinations of Aurora kinase inhibitor CCT137690 for enhanced efficacy in oral cancer cells

  2019cites this paper
• Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms

  2019cites this paper
• Overview and Current News in Acute Lymphoblastic Leukemia

  2019cites this paper
• Genetic and Epigenetic Profiling in Personalized Medicine: Advances in Treatment of Acute Myeloid Leukemia

  2019cites this paper
• Successful treatment with gilteritinib for initially FMS‐like tyrosine kinase 3 gene internal tandem duplications‐positive elderly refractory acute myeloid leukemia that changed into FMS‐like tyrosine kinase 3 gene tyrosine kinase domain‐positive after cord blood transplantation

  2019cites this paper
• Novel Therapies in Acute Myeloid Leukemia.

  2019cites this paper
• Arsenic Trioxide and Sorafenib Induce Synthetic Lethality of FLT3-ITD Acute Myeloid Leukemia Cells

  2018cites this paper
• Selective Inhibition of the Myeloid Src-Family Kinase Fgr Potently Suppresses AML Cell Growth in Vitro and in Vivo.

  2018cites this paper
• SOHO State of the Art Update and Next Questions: Philadelphia Chromosome‐Positive Acute Lymphoblastic Leukemia

  2018cites this paper
• Current paradigms in the management of Philadelphia chromosome positive acute lymphoblastic leukemia in adults

  2018cites this paper
• High-throughput Identification of FLT3 Wild-type and Mutant Kinase Substrate Preferences and Application to Design of Sensitive In Vitro Kinase Assay Substrates*

  2018cites this paper
• Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least Resistance

  2018cites this paper
• Planning Your Next Move in Philadelphia Chromosome Positive Leukaemias

  2018cites this paper
• Correction to: MYC-dependent downregulation of telomerase by FLT3 inhibitors is required for their therapeutic efficacy on acute myeloid leukemia

  2018cites this paper
• Inhibition of FLT3 and PIM Kinases by EC-70124 Exerts Potent Activity in Preclinical Models of Acute Myeloid Leukemia

  2018cites this paper
• Direct and rapid identification of T315I-Mutated BCR-ABL expressing leukemic cells using infrared microspectroscopy.

  2018cites this paper
• Therapeutic Vulnerabilities in FLT3-Mutant AML Unmasked by Palbociclib

  2018influential citation
• Aurora Kinase Inhibitors in Head and Neck Cancer.

  2018cites this paper
• Cabozantinib is well tolerated in acute myeloid leukemia and effectively inhibits the resistance‐conferring FLT3/tyrosine kinase domain/F691 mutation

  2018cites this paper
• A novel BCR-ABL1 mutation in a patient with Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia

  2018cites this paper
• A novel, dual pan-PIM/FLT3 inhibitor SEL24 exhibits broad therapeutic potential in acute myeloid leukemia

  2018cites this paper
• Upfront treatment with the first and second-generation tyrosine kinase inhibitors in Ph-positive acute lymphoblastic leukemia

  2017cites this paper
• CCT137690, Inhibitor of Aurora Kinase, Can Stimulate Apoptosis in Chronic Myeloid Leukemia Cells

  2017cites this paper
• Molekulare Mechanismen der Resistenz gegenüber Tyrosinkinaseinhibitoren bei Leukämien

  2017cites this paper
• MYC-dependent downregulation of telomerase by FLT3 inhibitors is required for their therapeutic efficacy on acute myeloid leukemia

  2017cites this paper
• Screening ABL1 kinase domain mutations in patients with de novo Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL)

  2017cites this paper
• Characteristics and mutation analysis of Ph-positive leukemia patients with T315I mutation receiving tyrosine kinase inhibitors

  2017cites this paper
• Which tyrosine kinase inhibitor should we use to treat Philadelphia chromosome-positive acute lymphoblastic leukemia?

  2017cites this paper
• Novel Therapies for Acute Myeloid Leukemia: Are We Finally Breaking the Deadlock?

  2017cites this paper
• Haematological Malignancies Targeting the FLT 3 Mutation in Acute Myeloid Leukaemia

  2017cites this paper
• Clinical Applications and Pitfalls of MRD in ALL: 006‐MTPII‐01

  2017cites this paper
• Therapeutic targeting of leukemic stem cells in acute myeloid leukemia – the biological background for possible strategies

  2017cites this paper
• Targeted therapies in Acute Myeloid Leukemia: a focus on FLT-3 inhibitors and ABT199

  2017cites this paper
• T‐cell‐rich HLA‐haploidentical hematopoietic stem cell transplantation for relapsed/refractory pediatric Philadelphia chromosome‐positive acute lymphoblastic leukemia without posttransplant tyrosine kinase inhibitor therapy

  2017cites this paper
• Gene Mutations as Emerging Biomarkers and Therapeutic Targets for Relapsed Acute Myeloid Leukemia

  2017cites this paper
• Growth of tyrosine kinase inhibitor-resistant Philadelphia-positive acute lymphoblastic leukemia: Role of bone marrow stromal cells

  2017cites this paper
• The role of FLT3 inhibitors in the treatment of FLT3‐mutated acute myeloid leukemia

  2017cites this paper
• The Aurora kinase inhibitors in cancer research and therapy

  2016cites this paper
• Clinical impact of ABL1 kinase domain mutations and IKZF1 deletion in adults under age 60 with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL): molecular analysis of CALGB (Alliance) 10001 and 9665

  2016cites this paper
• Identifying high-risk adult AML patients: epigenetic and genetic risk factors and their implications for therapy

  2016cites this paper
• Clinical significance of quantitative monitoring and mutational analysis of BCR-ABL1 transcript in Philadelphia chromosome positive B lymphoblastic leukemia

  2016cites this paper
• The development of targeted new agents to improve the outcome for children with leukemia

  2016cites this paper
• Genetic Mutations in Acute Myeloid Leukemia

  2016influential citation
• Discovery and Rational Design of Pteridin-7(8H)-one-Based Inhibitors Targeting FMS-like Tyrosine Kinase 3 (FLT3) and Its Mutants.

  2016cites this paper