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Genetic and epigenetic inactivation of SESTRIN1 controls mTORC1 and response to EZH2 inhibition in follicular lymphoma

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Science Translational Medicine  28 Jun 2017:
Vol. 9, Issue 396, eaak9969
DOI: 10.1126/scitranslmed.aak9969

Lymphoma’s loss is a therapeutic gain

Follicular lymphoma is a relatively common and difficult-to-treat hematologic malignancy, for which no specific targeted therapy is available. Knowing that deletions of chromosome 6q are common in this tumor type, Oricchio et al. examined the genes on this chromosome and identified SESTRIN1 as a likely tumor suppressor. The authors examined the mechanism by which the loss of SESTRIN1 contributes to tumorigenesis and identified a mechanistic connection between SESTRIN1 and EZH2, an epigenetic modifier that plays a role in multiple cancer types. The authors demonstrated that the effectiveness of targeting EZH2 depends on SESTRIN1 genetic and epigenetic status and also reported that mutations in EZH2 itself can sensitize cancer cells to additional targeted therapies.

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