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Peering into the aftermath: JAKi rips STAT3 in cancer

Nature Medicine volume 16, pages 1085–1087 (2010)Cite this article

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Persistent activation of the transcription factor signal transducer and activator of transcription-3 (STAT3) occurs in a large number of solid malignancies, and a plethora of genetic studies suggest that inhibition of this oncogenic transcriptional regulator, which supports the proliferation and survival of malignant cells, could be an effective treatment modality. A recent study by Hedvat et al.1 described the development of a specific inhibitor of the tyrosine kinase Janus kinase-2 (JAK2), which has a central role in STAT3 activation in various human cancer cells1. This study suggests that small-molecule inhibitors of JAK2 that are currently being developed for treatment of myeloproliferative diseases may also be valuable therapeutic tools for a large variety of solid tumors.

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Figure 1: STAT3 can be activated by a variety of upstream signals.

Katie Vicari

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Authors and Affiliations

  1. Florian R. Greten is in the Second Department of Medicine, Klinikum Rechts der Isar, Technische Universität München, München, Germany.,

    Florian R Greten

  2. Michael Karin is in the Department of Pharmacology, University of California, San Diego, La Jolla, California, USA.,

    Michael Karin

Authors
  1. Florian R Greten
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  2. Michael Karin
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Correspondence to Florian R Greten or Michael Karin.

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The authors declare no competing financial interests.

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Greten, F., Karin, M. Peering into the aftermath: JAKi rips STAT3 in cancer. Nat Med 16, 1085–1087 (2010). https://doi.org/10.1038/nm1010-1085

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