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Significance Recurrence of cancer in patients treated with radiation therapy infers that tumor cells have the capacity to escape the lethal effects of irradiation. Surviving tumor cells rely on signaling pathways triggered by hematopoietic interleukins in a mechanism that is poorly understood. We find that the adaptor protein Lnk is key in this process, acting as a negative regulator of interleukin 11 survival signaling. In Lnk knockout derived mice, hematopoietic stem cells have a marked level of irradiation resistance, causing B-cell malignancies. Such observations are consistent with the physiology seen in a subset of human leukemia patients that have Lnk gene mutations. Inhibition of interleukin 11 signaling in the mouse model circumvented this irradiation-resistance phenomenon and is suggestive of a potential for therapeutic intervention.

Lnk adaptor suppresses radiation resistance and radiation-induced B-cell malignancies by inhibiting IL-11 signaling