ReviewClinical cancer research : an official journal of the American Association for Cancer Research2010
Therapeutic potential of Janus-activated kinase-2 inhibitors for the management of myelofibrosis.
Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
- Article
- miR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2.JCI insight · 2020Article
- The Network of Inflammatory Mechanisms in Lupus Nephritis.Frontiers in medicine · 2020Review
- A Case of Chronic Myelogenous Leukemia Occurring in a Patient Treated for Essential Thrombocythemia.The American journal of case reports · 2019Article
- Review
- Usefulness of spleen volume measured by computed tomography for predicting clinical outcome in primary myelofibrosis.International journal of hematology · 2016Article
- Practical management of patients with myelofibrosis receiving ruxolitinib.Expert review of hematology · 2013Review
- Splenomegaly in myelofibrosis--new options for therapy and the therapeutic potential of Janus kinase 2 inhibitors.Journal of hematology & oncology · 2012Review
- Mechanisms of fibrosis: therapeutic translation for fibrotic disease.Nature medicine · 2012Review
- Article
- Heat shock protein 90 inhibitor is synergistic with JAK2 inhibitor and overcomes resistance to JAK2-TKI in human myeloproliferative neoplasm cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Normal and malignant megakaryopoiesis.Expert reviews in molecular medicine · 2011Review
- Article
- JAK2 Allele Burden in the Myeloproliferative Neoplasms: Effects on Phenotype, Prognosis and Change with Treatment.Therapeutic advances in hematology · 2011Article
- Bim and Mcl-1 exert key roles in regulating JAK2V617F cell survival.BMC cancer · 2011Article
- Screening for hotspot mutations in PI3K, JAK2, FLT3 and NPM1 in patients with myelodysplastic syndromes.Clinics (Sao Paulo, Brazil) · 2011Article
- Article
- Jak/STAT pathways in cytokine signaling and myeloproliferative disorders: approaches for targeted therapies.Genes & cancer · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Myelofibrosis (either primary or postpolycythemia vera/essential thrombocythemia) is a chronic and debilitating myeloproliferative neoplasm for which there is no well-accepted standard of care. Clinical manifestations of this disease (e.g., cytopenias, splenomegaly, bone marrow fibrosis) and constitutional symptoms (e.g., hypercatabolic state, fatigue, night sweats, fever) create significant treatment challenges. For example, progressive splenomegaly increases the risk for more serious clinical sequelae (e.g., portal hypertension, splenic infarction). Myelofibrosis arises from hematopoietic stem cells or early progenitor cells. However, the molecular mechanisms underlying its pathogenesis and clinical presentation are poorly understood, delaying the development of effective and targeted treatments. Recent studies have implicated mutations that directly or indirectly lead to the deregulated activation of Janus-activated kinase 2 (JAK2). Appreciation for the activation of JAK2 and the importance of increased levels of circulating proinflammatory cytokines in the pathogenesis and clinical manifestations of myelofibrosis has led to novel therapeutic agents targeting JAKs. This review will briefly discuss the origins of the JAK2 hypothesis, the clinical relevance of JAK2 mutations in myelofibrosis, and recent clinical progress in targeting JAKs as a therapeutic intervention for patients with this chronic and debilitating disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.