ArticleLeukemia2006
JAK2 V617F is a rare finding in de novo acute myeloid leukemia, but STAT3 activation is common and remains unexplained.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 137 citations in OpenAlex.
- A phase II study of the EGFR inhibitor gefitinib in patients with acute myeloid leukemia.Leukemia research · 2014Trial
- The prognostic impact of germline 46/1 haplotype of Janus kinase 2 in cytogenetically normal acute myeloid leukemia.Haematologica · 2011Trial
- Trial
- Vitamin D Deficiency in Leukemia: Implications for Pathophysiology, Treatment, and Supportive Care.Nutrients · 2026Review
- A novel function of STAT3β in suppressing interferon response improves outcome in acute myeloid leukemia.Cell death & disease · 2024Article
- Expression of JAK/STAT Signaling Proteins at Diagnosis and Remission in Patients with Acute Myeloid Leukemia.Oman medical journal · 2024Article
- JAK/STAT in leukemia: a clinical update.Molecular cancer · 2024Review
- Clonal haematopoiesis - a novel entity that modifies pathological processes in elderly.Cell death discovery · 2023Review
- Ceramide nanoliposomes augment the efficacy of venetoclax and cytarabine in models of acute myeloid leukemia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Inflammation-driven activation of JAK/STAT signaling reversibly accelerates acute myeloid leukemia in vitro.Blood advances · 2020Article
- The novel Isatin analog KS99 targets stemness markers in acute myeloid leukemia.Haematologica · 2020Article
- Identification and Validation ofOncoTargets and therapy · 2020Article
- STAT3β is a tumor suppressor in acute myeloid leukemia.Blood advances · 2019Article
- De Novo JAK2 V617 F Positive AML: The Picture is Getting Clearer.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2019Article
- The promise of Janus kinase inhibitors in the treatment of hematological malignancies.Cytokine · 2017Review
- Prevalence of the Janus kinase 2 V617F mutation in Philadelphia-negative myeloproliferative neoplasms in a Portuguese population.Biomedical reports · 2017Article
- ALOX5 exhibits anti-tumor and drug-sensitizing effects in MLL-rearranged leukemia.Scientific reports · 2017Article
- Vitamin D in hematological disorders and malignancies.European journal of haematology · 2017Review
- New insights into the Shwachman-Diamond Syndrome-related haematological disorder: hyper-activation of mTOR and STAT3 in leukocytes.Scientific reports · 2016Article
- 'Acute myeloid leukemia: a comprehensive review and 2016 update'.Blood cancer journal · 2016Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Signal transducer and activator of transcription (STAT) proteins are phosphorylated and activated by Janus kinases (JAKs). Recently, several groups identified a recurrent somatic point mutation constitutively activating the hematopoietic growth factor receptor-associated JAK2 tyrosine kinase in diverse chronic myeloid disorders - most commonly classic myeloproliferative disorders (MPD), especially polycythemia vera. We hypothesized that the JAK2 V617F mutation might also be present in samples from patients with acute myeloid leukemia (AML), especially erythroleukemia (AML-M6) or megakaryoblastic leukemia (AML-M7), where it might mimic erythropoietin or thrombopoietin signaling. First, we documented STAT3 activation by immunoblotting in AML-M6 and other AML subtypes. Immunoperoxidase staining confirmed phosphorylated STAT3 in malignant myeloblasts (21% of cases, including all AML-M3 samples tested). We then analyzed genomic DNA from 162 AML, 30 B-cell lymphoma, and 10 chronic lymphocytic leukemia (CLL) samples for JAK2 mutations, and assayed a subset for SOCS1 and FLT3 mutations. Janus kinase2 V617F was present in 13/162 AML samples (8%): 10/13 transformed MPD, and three apparent de novo AML (one of 12 AML-M6, one of 24 AML-M7, and one AML-M2 - all mixed clonality). FLT3 mutations were present in 5/32 (16%), while SOCS1 mutations were totally absent. Lymphoproliferative disorder samples were both JAK2 and SOCS1 wild type. Thus, while JAK2 V617F is uncommon in de novo AML and probably does not occur in lymphoid malignancy, unexplained STAT3 activation is common in AML. Janus kinase2 extrinsic regulators and other proteins in the JAK-STAT pathway should be interrogated to explain frequent STAT activation in AML.
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