Blood: IL10RA regulates the sensitivity of NPM1-ALK plus interstituated large cell lymphoma to keratosini
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Last Update: 2020-07-12
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Source: Internet
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Author: User
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Interstituatorcelllymphoma(alCL), also known as ki-1 lymphoma, is a T-cell malignant tumor that is mainly driven by an overactive interstitliated lymphoma kinase (ALK) fusion proteinALK inhibitors, such as gramibini, can replace standard chemotherapy, which has lower toxicity and side effects than chemotherapyin clinical trials, the objective remission rate of ALK inhibition therapy was 54-90% in children with lymphoma driven by NPM1-ALK fusion proteinHowever, some patients progress within the first 3 months of treatmentso far, the mechanism for progression of ALK inhibitor resistance is unclearby performing genome-wide CRISPR activation and knockout screening of ALCL cell lines, combined with RNA-seq data on tumor cells in patients with relapsed tumors treated with ALK inhibitors, Prokoph et al., found that abnormal increases in IL10RA can drive ALCL resistance to cratrice suppressed ALKThe IL10RA expression increase rewires the STAT3 signal transduction path, bypassing other critical phosphorylationcaused by NPM1-ALKThe expression of IL10RA was not related to the response of children with ALCL to standard chemotherapy, suggesting that co-chemotherapy of cortinib couldprevent specific recurrence of resistanceALK inhibitors
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