Although the molecular differences between embryonal rhabdomyosarcoma (ERMS) and alveolar rhabdomyosarcoma (ARMS) have been extensively interrogated, effective therapies tailored to a particular rhabdomyosarcoma subtype have yet to emerge. Patients with ERMS have shown incremental improvement using current multimodal therapy, but survival rates for metastatic ARMS remain poor. In this issue of the JCI, Durbin and colleagues demonstrate that integrin-linked kinase (ILK) acts as a tumor suppressor in ERMS and as a proto-oncogene in ARMS, and that the opposing functions of this enzyme are dependent on the JNK1 signaling pathway (see the related article beginning on page 1558). Their findings suggest that targeting ILK may represent a focused therapeutic strategy for the treatment of ARMS.
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