Varaico: Literature-Extracted Genetic Variants

Gene:FLT3
Variant:p.Y842H
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FLT3

NM_004119.3:p.Y842H

Associated Papers

Whole Exome Sequencing of Intermediate-Risk Acute Myeloid Leukemia without Recurrent Genetic Abnormalities Offers Deeper Insights into New Diagnostic Classifications.

Guijarro F et al.

International Journal of Molecular Sciences, 2024

39201354 (PubMed )
Supplement: ijms-25-08669-s001.zip › ijms-3087068-supplementary › Supplementary_Tables_S1-S5.xlsx › Table_S1

Alkynyl nicotinamides show antileukemic activity in drug-resistant acute myeloid leukemia.

Ramdas B et al.

The Journal of Clinical Investigation, 2024

Multi-target measurable residual disease assessed by error-corrected sequencing in patients with acute myeloid leukemia: An ALFA study.

Hirsch P et al.

Blood Cancer Journal, 2024

38871702 (PubMed )
Supplement: 41408_2024_1078_MOESM1_ESM.pdf

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

Characterisation of FLT3 alterations in childhood acute lymphoblastic leukaemia.

Gutierrez-Camino A et al.

British Journal of Cancer, 2024

38049555 (PubMed )
Supplement: 41416_2023_2511_MOESM1_ESM.pdf

Understanding the Role of Activation Loop Mutants in Drug Efficacy for FLT3-ITD.

Kazi JU et al.

Cancers, 2023

Mutation spectrum of FLT3 and significance of non-canonical FLT3 mutations in haematological malignancy.

Ge SS et al.

British Journal of Haematology, 2023

Indole-based FLT3 inhibitors and related scaffolds as potential therapeutic agents for acute myeloid leukemia.

Ezelarab HAA et al.

Bmc Chemistry, 2023

Targeting FLT3 Mutation in Acute Myeloid Leukemia: Current Strategies and Future Directions.

Fedorov K et al.

Cancers, 2023

Multi-omics analysis defines highly refractory RAS burdened immature subgroup of infant acute lymphoblastic leukemia.

Isobe T et al.

Nature Communications, 2022

36042201 (PubMed )
Supplement: 41467_2022_32266_MOESM12_ESM.xlsx › Data9

SmMIP-tools: a computational toolset for processing and analysis of single-molecule molecular inversion probes-derived data.

Medeiros JJF et al.

Bioinformatics (oxford, England), 2022

35150236 (PubMed )
Supplement: btac081_supplementary_data.zip › Table_S6.xlsx › High_Confidence_SNVs

Distinct genomic landscape of Chinese pediatric acute myeloid leukemia impacts clinical risk classification.

Liu T et al.

Nature Communications, 2022

35347147 (PubMed )
Supplement: 41467_2022_29336_MOESM8_ESM.xlsx › Sheet1

Momelotinib is a highly potent inhibitor of FLT3-mutant AML.

Azhar M et al.

Blood Advances, 2022

Selectively targeting FLT3-ITD mutants over FLT3-wt by a novel inhibitor for acute myeloid leukemia.

Wang A et al.

Haematologica, 2021

32299905 (PubMed )
Supplement: 2019_244186_WANG_SUPPL.pdf

Mechanisms Underlying Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia.

Eguchi M et al.

Biomedicines, 2020

The functional landscape of the human phosphoproteome.

Ochoa D et al.

Nature Biotechnology, 2020

31819260 (PubMed )
Supplement: EMS84831-supplement-Table_S5.xlsx › clinvar_data

Gilteritinib is a clinically active FLT3 inhibitor with broad activity against FLT3 kinase domain mutations.

Tarver TC et al.

Blood Advances, 2020

FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor development.

Kiyoi H et al.

Cancer Science, 2020

Resistance to FLT3 inhibitors in acute myeloid leukemia: Molecular mechanisms and resensitizing strategies.

Zhou J et al.

World Journal of Clinical Oncology, 2018

A novel irreversible FLT3 inhibitor, FF-10101, shows excellent efficacy against AML cells with FLT3 mutations.

Yamaura T et al.

Blood, 2018

The molecular mechanism behind resistance of the kinase FLT3 to the inhibitor quizartinib.

Friedman R

Proteins, 2017

Tyrosine 842 in the activation loop is required for full transformation by the oncogenic mutant FLT3-ITD.

Kazi JU et al.

Cellular and Molecular Life Sciences : Cmls, 2017

Characterizing and Overriding the Structural Mechanism of the Quizartinib-Resistant FLT3 "Gatekeeper" F691L Mutation with PLX3397.

Smith CC et al.

Cancer Discovery, 2015

Computer-guided design, synthesis, and biological evaluation of quinoxalinebisarylureas as FLT3 inhibitors.

Göring S et al.

Chemmedchem, 2015

FLT3 INHIBITORS: RECENT ADVANCES AND PROBLEMS FOR CLINICAL APPLICATION.

Kiyoi H

Nagoya Journal of Medical Science, 2015

Next-generation sequencing-based multigene mutational screening for acute myeloid leukemia using MiSeq: applicability for diagnostics and disease monitoring.

Luthra R et al.

Haematologica, 2014

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

Smith CC et al.

Blood, 2013

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

Moore AS et al.

Leukemia, 2012

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.

Smith CC et al.

Nature, 2012

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

Emerging Flt3 kinase inhibitors in the treatment of leukaemia.

Tickenbrock L et al.

Expert Opinion on Emerging Drugs, 2006

Development of a human acute myeloid leukaemia screening panel and consequent identification of novel gene mutation in FLT3 and CCND3.

Smith ML et al.

British Journal of Haematology, 2005

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD-transformed hematopoietic cells.

Bagrintseva K et al.

Blood, 2004

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."