ReviewCurrent hematologic malignancy reports2024
JAK Inhibitors for Myelofibrosis: Strengths and Limitations.
Review in Current hematologic malignancy reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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
11 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- A systematic review of 47 published cases of extramedullary hematopoiesis in myelofibrosis: clinical patterns, treatment responses, and prognostic implications.Annals of hematology · 2026Pooled it
- Overall survival with momelotinib vs. best available therapy in patients with ruxolitinib-experienced myelofibrosis: a matching-adjusted indirect comparison.Annals of hematology · 2026Pooled it
- Targeting the JAK/STAT signalling axis in cancer: chemopreventive potential of natural compounds with emerging focus on retinoids.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Myelofibrosis and anemia: a German claims data analysis to describe treatment sequencing, survival outcomes, and healthcare resource utilization.Annals of hematology · 2026Article
- Comparison of the enzymatic and cellular profiles of clinical JAK inhibitors for the treatment of myelofibrosis.Blood neoplasia · 2026Article
- Sequential treatment with ruxolitinib and imetelstat effectively depletes myelofibrosis hematopoietic stem and progenitor cells.Leukemia · 2026Article
- Population Pharmacokinetics and Exposure-Response Analyses of Momelotinib, Its Active Metabolite (M21), and Total Active Moiety in Myelofibrosis.Clinical pharmacology and therapeutics · 2026Article
- Regression of Post-Essential Thrombocythaemia Myelofibrosis with Intermittent Hydroxyurea Therapy: A Case Report.Journal of clinical medicine · 2025Article
- The deacetylases HDAC1/HDAC2 control JAK2Signal transduction and targeted therapy · 2025Article
- Myelofibrosis: Treatment Options After Ruxolitinib Failure.Current oncology (Toronto, Ont.) · 2025Review
- Managing Myelofibrosis: Matching Advances in Treatments With Clinical Unmet Needs.Hematological oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewThe landscape of myelofibrosis (MF) has changed since the discovery of the JAK2 V617F mutation and subsequent development of JAK inhibitors (JAKis). However, treatment with JAKis remain a challenge. In this review we critically analyze the strengths and limitations of currently available JAK inhibitors. RECENT
findingsIn MF patients, JAK inhibitors have been associated with reduced symptom burden and spleen size, as well as improved survival. However, durability of response and development of treatment resistance remain an issue. Recently, there has been increased efforts to optimize treatment with the development of highly selective JAK inhibitors, as well as use of combination agents to counter disease resistance through targeting aberrant signaling pathways. Treatment of MF patients with JAKi therapy can be challenging but the development of more potent and selective JAK inhibitors, as well as combination therapies, represent exciting treatment advances in this field.
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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.