2021
DOI: 10.3390/cancers13246192
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Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia

Abstract: 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 functiona… Show more

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Cited by 4 publications
(2 citation statements)
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References 286 publications
(368 reference statements)
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“…NUP98 fusions often show mutations in signaling genes like FLT3, NRAS, and KIT, indicating the requirement of Class-I mutations for NUP98 fusion mediated AML development [113,116]. Different murine model studies have also shown that NUP98 fusions alone induce long-latency myeloid disease, but when they collaborate with different proliferative events like FLT3 or NRAS mutations, they induce a lethal short-latency AML phenotype [126][127][128][129][130]. Retroviral insertional mutagenesis is an excellent tool to identify cooperative events for carcinogenesis [131].…”
Section: Cooperating Abnormalities In Nup98 Rearranged Amlmentioning
confidence: 99%
“…NUP98 fusions often show mutations in signaling genes like FLT3, NRAS, and KIT, indicating the requirement of Class-I mutations for NUP98 fusion mediated AML development [113,116]. Different murine model studies have also shown that NUP98 fusions alone induce long-latency myeloid disease, but when they collaborate with different proliferative events like FLT3 or NRAS mutations, they induce a lethal short-latency AML phenotype [126][127][128][129][130]. Retroviral insertional mutagenesis is an excellent tool to identify cooperative events for carcinogenesis [131].…”
Section: Cooperating Abnormalities In Nup98 Rearranged Amlmentioning
confidence: 99%
“…FLT3 , NRAS , KRAS and PTPN11 variants have been detected in a small fraction of MPN and MDS/MPN cases and are considered late events in MPN disease progression towards sAML [ 54 ]. In mice, knock-in of FLT3-ITD or FLT3-TKD, as well as NRAS p.G12D and KRAS p.G12D, induced a myeloproliferative neoplasm, and an AML phenotype was obtained by combination with other variants [ 55 ].…”
Section: Molecular Pathogenesis Of Mpn-bpmentioning
confidence: 99%