The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond. - sprookjes - yvandenbroek - TriplyDB

The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

http://www.wikidata.org/entity/Q38216649

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Precision medicine for cancer with next-generation functional diagnostics Volasertib for AML: clinical use and patient consideration Selective inhibition of FLT3 by gilteritinib in relapsed or refractory acute myeloid leukaemia: a multicentre, first-in-human, open-label, phase 1-2 study.Phase 1 dose-finding study of rebastinib (DCC-2036) in patients with relapsed chronic myeloid leukemia and acute myeloid leukemia.Discovery of a Diaminopyrimidine FLT3 Inhibitor Active against Acute Myeloid Leukemia.Molecular therapy for acute myeloid leukaemia.Acute myeloid leukemia: 2014 update on risk-stratification and management.Current Approaches in the Treatment of Relapsed and Refractory Acute Myeloid Leukemia.Downregulated Poly-C binding protein-1 is a novel predictor associated with poor prognosis in Acute Myeloid Leukemia.The contributions of the European Medicines Agency and its pediatric committee to the fight against childhood leukemia A novel approach for the identification of efficient combination therapies in primary human acute myeloid leukemia specimens.A Genome-Wide CRISPR Screen Identifies Genes Critical for Resistance to FLT3 Inhibitor AC220.FLT3 mutational status is an independent risk factor for adverse outcomes after allogeneic transplantation in AML Revealing very small FLT3 ITD mutated clones by ultra-deep sequencing analysis has important clinical implications in AML patients.CDC25A governs proliferation and differentiation of FLT3-ITD acute myeloid leukemia.Gemtuzumab Ozogamicin Reduces Relapse Risk in FLT3/ITD Acute Myeloid Leukemia: A Report from the Children's Oncology Group Palbociclib treatment of FLT3-ITD+ AML cells uncovers a kinase-dependent transcriptional regulation of FLT3 and PIM1 by CDK6.Dual inhibition of AKT/FLT3-ITD by A674563 overcomes FLT3 ligand-induced drug resistance in FLT3-ITD positive AML.Acute Myeloid Leukemia: Advancements in Diagnosis and Treatment.The implication of FLT3 amplification for FLT targeted therapeutics in solid tumors.T-LAK cell-originated protein kinase presents a novel therapeutic target in FLT3-ITD mutated acute myeloid leukemia.Oncogene addiction: pathways of therapeutic response, resistance, and road maps toward a cure.Aminoisoquinoline benzamides, FLT3 and Src-family kinase inhibitors, potently inhibit proliferation of acute myeloid leukemia cell lines.An anti-CD3/anti-CLL-1 bispecific antibody for the treatment of acute myeloid leukemia.The artful management of older patients with acute myeloid leukemia.Life after transplant: are we becoming high maintenance in AML?Development and Characterization of FLT3-Specific Curcumin-Loaded Polymeric Micelles as a Drug Delivery System for Treating FLT3-Overexpressing Leukemic Cells.Acute myeloid leukemia: 2016 Update on risk-stratification and management.Treatment of Acute Myeloid Leukemia with the FLT3 Gene Mutation.Flt3 ligand-eGFP-reporter expression characterizes functionally distinct subpopulations of CD150+ long-term repopulating murine hematopoietic stem cells.Activation of protein phosphatase 2A in FLT3+ acute myeloid leukemia cells enhances the cytotoxicity of FLT3 tyrosine kinase inhibitors.Discovery of a highly potent FLT3 kinase inhibitor for FLT3-ITD-positive AML.Emerging therapies for acute myeloid leukemia: translating biology into the clinic.Cytogenetic Abnormalities in Myelodysplastic Syndromes: An Overview.p27 in FLT3-driven acute myeloid leukemia: many roads lead to ruin.Midostaurin: a novel therapeutic agent for patients with FLT3-mutated acute myeloid leukemia and systemic mastocytosis.Phase 1 study of quizartinib in combination with induction and consolidation chemotherapy in patients with newly diagnosed acute myeloid leukemia.Genomic instability is a principle pathologic feature of FLT3 ITD kinase activity in acute myeloid leukemia leading to clonal evolution and disease progression.Results of a phase 1 study of quizartinib as maintenance therapy in subjects with acute myeloid leukemia in remission following allogeneic hematopoietic stem cell transplant.Precision Medicine in Children and Young Adults with Hematologic Malignancies and Blood Disorders: The Columbia University Experience.

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The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

http://www.wikidata.org/entity/Q38216649

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The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

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The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

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The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

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Therapeutic advances in hematology

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The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.

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Amir T Fathi

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Mark J Levis

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Seth A Wander

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P2860

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Next-generation mTOR inhibitors in clinical oncology: how pathway complexity informs therapeutic strategy

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Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia.

The impact of FLT3 internal tandem duplication mutant level, number, size, and interaction with NPM1 mutations in a large cohort of young adult patients with acute myeloid leukemia.

Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia.

FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro.

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.

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