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During the 7th Society of Hematologic Oncology (SOHO) annual meeting, in Houston, TX, US, a session on acute myeloid leukemia (AML) was held. Yuichiro Semba, Kyushu University Graduate School of Medical Sciences, Fukuoka, JP, presented a talk entitled “CRISPR-Cas9 Screen Identifies XPO7 as a Novel Therapeutic Target for TP53-Mutated AML”.1
AML is a heterogeneous disease characterized by various genetic aberrations, some of which can be prognostic. It has already been established that patients with complex karyotype have poor outcomes.2 Mutations in TP53 are commonly associated with a complex karyotype, with an incidence of 69-78%, are a strong AML risk-factor.1,2 In this pre-clinical genomic study, the investigators sought to identify specific gene targets and pathways that are critical for the survival of TP53-mutated AML cells with the hope of findings novel drug targets. For this, they performed a genome-wide CRISPR-Cas9 screen in AML cell lines in vitro.
The investigators identified a synthetic lethal association between expression of XPO7 and TP53 with XPO7 loss leading to the suppression of TP53-mutated AML cell proliferation. Based on these results and the fact that XPO7 mRNA is significantly upregulated in AML patients (The Cancer Genome Atlas database)3 it is likely that the nuclear transport protein XPO7 may serve as a novel therapeutic target for TP53-mutated AML.
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