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JAK V617F missense mutation is absent in pancreatic cancer
  1. H M Kocher1,
  2. L Mears1,
  3. N C Lea2,
  4. K Raj2,
  5. G J Mufti2
  1. 1Barts and the London HPB Centre, The Royal London Hospital, London, UK
  2. 2Department of Haematological Medicine, King’s College Hospital, London, UK
  1. Correspondence to:
    Dr Hemant M Kocher
    Centre for Tumour Biology, Institute of Cancer, Barts and the London School of Medicine and Dentistry, London EC1M 6BQ, UK; Hemant.kocher{at}cancer.org.uk

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Aberrant constitutive activation of STAT3 (signal transducer and activator of transcription) leads to cellular transformation and aids tumorigenesis in pancreatic cancer and its inhibition can lead to growth arrest.1–4 The exact mechanism of this constitutive activation has not been elucidated, although downstream mediators may include ERK and p21 signalling.1–4 Blocking JAK2 (Janus Kinase), a known upstream activator of STAT3, by AG490, a tryphostin inhibitor, reduced phosphorylation of STAT3 and produced comparable in vitro effects, suggesting a role for JAK2 in pancreatic carcinogenesis.3

JAK2 V617F missense mutation has recently been shown by several independent groups to play an important role in myeloproliferative disorders5 as well as prothrombotic states such as Budd-Chiari syndrome …

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