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Idh1 mutations contribute to the development of T-cell malignancies in genetically engineered mice

Authors: Kimberly Straley; Rohini Narayanaswamy; Andrew Wakeham; François Lemonnier; Bryan E. Snow; Carmen Dominguez-Brauer; Jing Ye; +10 Authors

Idh1 mutations contribute to the development of T-cell malignancies in genetically engineered mice

Abstract

Significance Isocitrate dehydrogenase 1 ( IDH1 ) mutations are drivers of hematological malignancy. Although these mutations are most often associated with myeloid disease, they are also found in lymphoid malignancies, including T-cell acute lymphoblastic leukemia (T-ALL). Treatment strategies targeting these mutations are currently being devised, including small-molecule inhibitors of the mutant IDH1 enzyme. A better understanding of the role of these mutations in tumorigenesis and their effects on tumor cells will allow these treatment strategies to be effectively translated to the clinic. Here we show that Idh1 mutations can contribute to the development of T-cell malignancies, including T-ALL, using a conditional knock-in mouse model. These mouse models provide a platform for further evaluation of treatment strategies for T-cell malignancy.

Keywords

Mice, Mutation, Animals, Exome, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Genes, p53, Isocitrate Dehydrogenase

  • BIP!
    Impact byBIP!
    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    19
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Average
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
19
Top 10%
Average
Top 10%
bronze