ReviewHematology. American Society of Hematology. Education Program2009
Therapeutic potential of JAK2 inhibitors.
Review in Hematology. American Society of Hematology. Education Program, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- Philadelphia-negative classical myeloproliferative neoplasms: critical concepts and management recommendations from European LeukemiaNet.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011Guideline
- A Phase Ib/II Study of the JAK1 Inhibitor, Itacitinib, plusThe oncologist · 2019Trial
- The clinical benefit of ruxolitinib across patient subgroups: analysis of a placebo-controlled, Phase III study in patients with myelofibrosis.British journal of haematology · 2013Trial
- Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis.The New England journal of medicine · 2010Trial
- Scutellarein attenuates cancer cachexia-induced muscle atrophy via targeted inhibition of the JAK/STAT pathway.Journal of advanced research · 2026Article
- Insights into IL-6/JAK/STAT3 signaling in the tumor microenvironment: Implications for cancer therapy.Cytokine & growth factor reviews · 2025Review
- [The role of AKT inhibitors combined with Ruxolitinib in ameliorating myeloproliferative disorders in mice with CALR gene mutations].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Article
- Efficacy of JAK1/2 inhibition in murine myeloproliferative neoplasms is not mediated by targeting oncogenic signaling.Nature communications · 2025Article
- Integrated bioinformatic analyses investigate macrophage-M1-related biomarkers and tuberculosis therapeutic drugs.Frontiers in genetics · 2023Article
- Screening for Inhibitors of YAP Nuclear Localization Identifies Aurora Kinase A as a Modulator of Lung Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- A computationally affordable approach for accurate prediction of the binding affinity of JAK2 inhibitors.Journal of molecular modeling · 2022Article
- The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension.International journal of molecular sciences · 2021Review
- Loss of ZIP facilitates JAK2-STAT3 activation in tamoxifen-resistant breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Therapeutic targeting of JAKs: from hematology to rheumatology and from the first to the second generation of JAK inhibitors.Mediterranean journal of rheumatology · 2020Review
- Epigenetics in SLE.Current rheumatology reports · 2017Review
- How Does the L884P Mutation Confer Resistance to Type-II Inhibitors of JAK2 Kinase: A Comprehensive Molecular Modeling Study.Scientific reports · 2017Article
- DNA methylation in systemic lupus erythematosus.Epigenomics · 2017Review
- Targeting epigenetic regulations in cancer.Acta biochimica et biophysica Sinica · 2016Review
- Phase I Study of OPB-31121, an Oral STAT3 Inhibitor, in Patients with Advanced Solid Tumors.Cancer research and treatment · 2015Article
- Molecular classification of gastric cancer: Towards a pathway-driven targeted therapy.Oncotarget · 2015Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The discovery of an activating tyrosine kinase mutation JAK2V617F in myeloproliferative neoplasms (MPNs), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) has resulted in the development of JAK2 inhibitors, of which several are being evaluated in phase I/II clinical studies. It is important to recognize that because the V617F mutation is localized in a region outside the adenosine triphosphate (ATP)-binding pocket of JAK2 enzyme, ATP-competitive inhibitors of JAK2 kinase (like the current JAK2 inhibitors in the clinic) are not likely to discriminate between wild-type and mutant JAK2 enzymes. Therefore, JAK2 inhibitors, by virtue of their near equipotent activity against wild-type JAK2 that is important for normal hematopoiesis, may have adverse myelosuppression as an expected side effect, if administered at doses that aim to completely inhibit the mutant JAK2 enzyme. While they may prove to be effective in controlling hyperproliferation of hematopoietic cells in PV and ET, they may not be able to eliminate mutant clones. On the other hand, JAK inhibitors may have great therapeutic benefit by controlling the disease for patients with MPNs who suffer from debilitating signs (eg, splenomegaly) or constitutional symptoms (which presumably result from high levels of circulating cytokines that signal through JAK enzymes). Indeed, the primary clinical benefits observed so far in MF patients have been significant reduction is splenomegaly, elimination of debilitating disease-related symptoms, and weight gain. Most importantly, patients with and without the JAK2V617F mutation appear to benefit to the same extent. In this review we summarize current clinical experience with JAK2 inhibitors in MPNs.
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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.