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Erratum: Rethinking JAK2 inhibition: towards novel strategies of more specific and versatile Janus kinase inhibition
Correction to: Leukemia (2017) 31, 1023–1038; doi:10.1038/leu.2017.43; published online 17 February 2017 Following the publication of this article, the editors noted that Janus should be capitalized. The corre...
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An unusual, activating insertion/deletion MPL mutant in primary myelofibrosis
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Rethinking JAK2 inhibition: towards novel strategies of more specific and versatile janus kinase inhibition
Janus kinases (JAKs) are required for cytokine receptor signaling. Since the discovery of the highly prevalent JAK2 V617F mutation in myeloproliferative neoplasms (MPNs), JAK2 became a prime target for inhibit...
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Pathologic activation of thrombopoietin receptor and JAK2-STAT5 pathway by frameshift mutants of mouse calreticulin
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Open AccessThrombopoietin receptor is required for the oncogenic function of CALR mutants
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Oncogenic activation of MPL/thrombopoietin receptor by 17 mutations at W515: implications for myeloproliferative neoplasms
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Persistent STAT5 activation in myeloid neoplasms recruits p53 into gene regulation
STAT (Signal Transducer and Activator of Transcription) transcription factors are constitutively activated in most hematopoietic cancers. We previously identified a target gene, LPP/miR-28 (LIM domain containing ...
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Article
Differential association of calreticulin type 1 and type 2 mutations with myelofibrosis and essential thrombocytemia: relevance for disease evolution
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JAK/STAT signaling in hematological malignancies
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is central to signaling by cytokine receptors, a superfamily of more than 30 transmembrane proteins that recognize specifi...
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Article
Aberrant signal transduction pathways in myeloproliferative neoplasms
The BCR-ABL-negative myeloproliferative neoplasms (MPNs), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF), entered the spotlight in 2005 when the unique somatic acquired JAK...
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JAK kinases overexpression promotes in vitro cell transformation
Constitutive activation of the JAK-STAT pathway is frequent in cancer and contributes to oncogenesis. Here, we took advantage of the Ba/F3 cell line, a murine proB cell line dependent on IL-3 for growth, to an...
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Introduction to ‘A special spotlight review series on BCR–ABL-negative myeloproliferative neoplasms’