Varaico: Literature-Extracted Genetic Variants

Gene:FLT3
Variant:p.F691I
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FLT3

NM_004119.3:p.F691I

Associated Papers

Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.

Lo Schiavo F et al.

Molecular Cancer, 2025

Landscape of FLT3 Variations Associated with Structural and Functional Impact on Acute Myeloid Leukemia: A Computational Study.

Mirza Z et al.

International Journal of Molecular Sciences, 2024

Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least Resistance.

Staudt D et al.

International Journal of Molecular Sciences, 2018

Gilteritinib, a FLT3/AXL inhibitor, shows antileukemic activity in mouse models of FLT3 mutated acute myeloid leukemia.

Mori M et al.

Investigational New Drugs, 2017

The Future of Targeting FLT3 Activation in AML.

Leick MB et al.

Current Hematologic Malignancy Reports, 2017

The Potent ALK Inhibitor Brigatinib (AP26113) Overcomes Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors in Preclinical Models.

Zhang S et al.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2016

27780853 (PubMed )
Supplement: 10780432ccr160569-sup-163226_2_supp_3574910_tdyq9n.pdf

Identification of a germline F692L drug resistance variant in cis with Flt3-internal tandem duplication in knock-in mice.

Dovey OM et al.

Haematologica, 2016

Perspectives for therapeutic targeting of gene mutations in acute myeloid leukaemia with normal cytogenetics.

Falini B et al.

British Journal of Haematology, 2015

AMG 925 is a dual FLT3/CDK4 inhibitor with the potential to overcome FLT3 inhibitor resistance in acute myeloid leukemia.

Li C et al.

Molecular Cancer Therapeutics, 2015

FLT3 INHIBITORS: RECENT ADVANCES AND PROBLEMS FOR CLINICAL APPLICATION.

Kiyoi H

Nagoya Journal of Medical Science, 2015

Medical management of metastatic medullary thyroid cancer.

Maxwell JE et al.

Cancer, 2014

Targeting oncoprotein stability overcomes drug resistance caused by FLT3 kinase domain mutations.

Yu C et al.

Plos One, 2014

Ponatinib (AP24534) is a novel potent inhibitor of oncogenic RET mutants associated with thyroid cancer.

De Falco V et al.

The Journal of Clinical Endocrinology and Metabolism, 2013

Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.

Smith CC et al.

Blood, 2013

Ponatinib may overcome resistance of FLT3-ITD harbouring additional point mutations, notably the previously refractory F691I mutation.

Zirm E et al.

British Journal of Haematology, 2012

Investigational drugs targeting FLT3 for leukemia.

Ustun C et al.

Expert Opinion on Investigational Drugs, 2009

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

von Bubnoff N et al.

Cancer Research, 2009

Sensitivity toward sorafenib and sunitinib varies between different activating and drug-resistant FLT3-ITD mutations.

Kancha RK et al.

Experimental Hematology, 2007

The ability of sorafenib to inhibit oncogenic PDGFRbeta and FLT3 mutants and overcome resistance to other small molecule inhibitors.

Lierman E et al.

Haematologica, 2007

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

Cools J et al.

Cancer Research, 2004

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