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Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia
by
Mohanty, Sagarajit
, Heuser, Michael
in
Acute myeloid leukemia
/ Animal models
/ Cell signaling
/ Chromosome aberrations
/ Cohesin
/ Cooperation
/ Epigenetics
/ Genetic transformation
/ Kinases
/ Leukemogenicity
/ Mutation
/ Myeloid leukemia
/ Prognosis
/ Review
/ Rodents
/ Therapeutic targets
/ Transcription factors
/ Tumors
2021
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Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia
by
Mohanty, Sagarajit
, Heuser, Michael
in
Acute myeloid leukemia
/ Animal models
/ Cell signaling
/ Chromosome aberrations
/ Cohesin
/ Cooperation
/ Epigenetics
/ Genetic transformation
/ Kinases
/ Leukemogenicity
/ Mutation
/ Myeloid leukemia
/ Prognosis
/ Review
/ Rodents
/ Therapeutic targets
/ Transcription factors
/ Tumors
2021
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Do you wish to request the book?
Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia
by
Mohanty, Sagarajit
, Heuser, Michael
in
Acute myeloid leukemia
/ Animal models
/ Cell signaling
/ Chromosome aberrations
/ Cohesin
/ Cooperation
/ Epigenetics
/ Genetic transformation
/ Kinases
/ Leukemogenicity
/ Mutation
/ Myeloid leukemia
/ Prognosis
/ Review
/ Rodents
/ Therapeutic targets
/ Transcription factors
/ Tumors
2021
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Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia
Journal Article
Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia
2021
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Overview
Acute myeloid leukemia is a clinically and biologically heterogeneous blood cancer with variable prognosis and response to conventional therapies. Comprehensive sequencing enabled the discovery of recurrent mutations and chromosomal aberrations in AML. Mouse models are essential to study the biological function of these genes and to identify relevant drug targets. This comprehensive review describes the evidence currently available from mouse models for the leukemogenic function of mutations in seven functional gene groups: cell signaling genes, epigenetic modifier genes, nucleophosmin 1 (NPM1), transcription factors, tumor suppressors, spliceosome genes, and cohesin complex genes. Additionally, we provide a synergy map of frequently cooperating mutations in AML development and correlate prognosis of these mutations with leukemogenicity in mouse models to better understand the co-dependence of mutations in AML.
Publisher
MDPI AG,MDPI
Subject
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