ReviewHemaSphere2020
JAK Inhibition for the Treatment of Myelofibrosis: Limitations and Future Perspectives.
Review in HemaSphere, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Clinical Practice Recommendations for Myelofibrosis Management in the Asia-Pacific Region: The APAC-MF Alliance.JCO oncology practice · 2026Pooled it
- Pelabresib plus ruxolitinib for JAK inhibitor-naive myelofibrosis: a randomized phase 3 trial.Nature medicine · 2025Trial
- Addition of Navitoclax to Ongoing Ruxolitinib Therapy for Patients With Myelofibrosis With Progression or Suboptimal Response: Phase II Safety and Efficacy.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022Trial
- KT-253, a highly potent and selective MDM2 protein degrader, eliminates malignant myelofibrosis stem/progenitor cells.Leukemia · 2026Article
- Myelofibrosis and anemia: a German claims data analysis to describe treatment sequencing, survival outcomes, and healthcare resource utilization.Annals of hematology · 2026Article
- Review
- RSK signaling in myeloid malignancies: biology, disease dependency, and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Emerging Therapeutic Approaches for Anemia in Myelofibrosis.Current hematologic malignancy reports · 2025Review
- Article
- FDA-approved drugs featuring macrocycles or medium-sized rings.Archiv der Pharmazie · 2025Review
- Spatial-transcriptomic profiling: a new lens for understanding myelofibrosis pathophysiology.Cell communication and signaling : CCS · 2024Review
- Validation and molecular integration of the RR6 model to predict survival after 6 months of therapy with ruxolitinib.Haematologica · 2024Article
- Patchouli Alcohol Protects the Heart against Diabetes-Related Cardiomyopathy through the JAK2/STAT3 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Article
- Type II mode of JAK2 inhibition and destabilization are potential therapeutic approaches against the ruxolitinib resistance driven myeloproliferative neoplasms.Frontiers in oncology · 2024Article
- A phase I trial of pevonedistat in combination with ruxolitinib for the treatment of myelofibrosis.Therapeutic advances in hematology · 2024Article
- JAK Inhibitors in Cytokine Storm Syndromes.Advances in experimental medicine and biology · 2024Review
- Molecular biomarkers of leukemia: convergence-based drug resistance mechanisms in chronic myeloid leukemia and myeloproliferative neoplasms.Frontiers in pharmacology · 2024Review
- Review
- Precision medicine in nasopharyngeal carcinoma: comprehensive review of past, present, and future prospect.Journal of translational medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 2011 approval of ruxolitinib ushered in the Janus kinase (JAK) inhibitor era in the treatment of myelofibrosis (MF), and 2019 saw the US approval of fedratinib. The first therapeutic agents approved by regulatory authorities for MF, these drugs attenuate the overactive JAK-signal transducer and activator of transcription (STAT) signaling universally present in these patients, translating into major clinical benefits in terms of spleen shrinkage and symptom improvement. These, in turn, confer a survival advantage on patients with advanced disease, demonstrated in the case of ruxolitinib, for which long-term follow-up data are available. However, JAK inhibitors do not improve cytopenias in most patients, have relatively modest effects on bone marrow fibrosis and driver mutation allele burden, and clinical resistance eventually develops. Furthermore, they do not modify the risk of transformation to blast phase; indeed, their mechanism of action may be more anti-inflammatory than truly disease-modifying. This has spurred interest in rational combinations of JAK inhibitors with other agents that may improve cytopenias and drugs that could potentially modify the natural history of MF. Newer JAK inhibitors that are distinguished from ruxolitinib and fedratinib by their ability to improve anemia (eg, momelotinib) or safety and efficacy in severely thrombocytopenic patients (eg, pacritinib) are in phase 3 clinical trials. There is also interest in developing inhibitors that are highly selective for mutant JAK2, as well as "type II" JAK2 inhibitors. Overall, although current JAK inhibitors have limitations, they will likely continue to form the backbone of MF therapy for the foreseeable future.
Identifiers
What Socratic holds
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 Socratic graph.