NUP98::Nsd1 and FLT3-ITD collaborate to generate acute myeloid leukemia

Matsukawa, Toshihiro; Yin, Mianmian; Nigam, Nupur; Negi, Vijay; Li, Li; Small, Donald; Zhu, Yuelin J.; Walker, Robert L.; Meltzer, Paul S.; Aplan, Peter D.

doi:10.1038/s41375-023-01913-0

Cited by 1 publication

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References 15 publications

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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 Rearrangements in AML: Molecular Mechanisms and Clinical Implications

Mohanty

2023

Onco

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NUP98 fusions constitute a small subgroup of AML patients and remain a high-risk AML subtype. There are approximately 30 types of NUP98 fusions identified in AML patients. These patients show resistance to currently available therapies and poor clinical outcomes. NUP98 fusions with different fusion partners have oncogenic transformation potential. This review describes how the NUP98 gene acquires oncogenic properties after rearrangement with multiple partners. In the mechanistic part, the formation of nuclear bodies and dysregulation of the HoxA/Meis1 pathway are highlighted. This review also discusses mutational signatures among NUP98 fusions and their significance in leukemogenesis. It also discusses the clinical implications of NUP98 fusions and their associated mutations in AML patients. Furthermore, it highlights therapeutic vulnerabilities in these leukemias that can be exploited as therapeutic strategies. Lastly, this review discusses the gaps in our knowledge regarding NUP98 fusions in AML, as well as future research opportunities.

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Section: Cooperating Abnormalities In Nup98 Rearranged Amlmentioning

confidence: 99%

NUP98 Rearrangements in AML: Molecular Mechanisms and Clinical Implications

Mohanty

2023

Onco

View full text Add to dashboard Cite

show abstract

NUP98::Nsd1 and FLT3-ITD collaborate to generate acute myeloid leukemia

Cited by 1 publication

References 15 publications

NUP98 Rearrangements in AML: Molecular Mechanisms and Clinical Implications

NUP98 Rearrangements in AML: Molecular Mechanisms and Clinical Implications

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