ReviewLeukemia2023
Biological drivers of clinical phenotype in myelofibrosis.
Review in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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
35 citing papers in PubMed, 52 citations in OpenAlex.
- POIESIS: a phase III study of add-on navtemadlin in JAK inhibitor-naïve myelofibrosis patients with a suboptimal response to ruxolitinib.Future oncology (London, England) · 2026Trial
- Spleen-derived circulating intercellular adhesion molecule 2 promotes osteosclerosis in chronic myelofibrosis.Bone research · 2026Article
- Targeting nuclear export and Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signalling in myelofibrosis: A novel combinatorial strategy that impacts intrinsic and microenvironment-related pathways.British journal of haematology · 2026Article
- Allogeneic Hematopoietic Stem Cell Transplantation in Myelofibrosis: Evolving Indications, Conditioning Strategies, and Outcomes.Hematology reports · 2026Review
- Clonal Metamorphosis: Deconstructing MPN Evolution with Single-Cell and Spatial Multi-Omics.Clinical and experimental medicine · 2026Review
- Clinical and prognostic significance of concomitant autoimmune disease in patients with myelofibrosis.Annals of hematology · 2026Article
- Hepcidin as a Molecular Hub of Iron Homeostasis: From BMP-SMAD Signaling to Therapeutic Modulation.Biomolecules · 2026Review
- Selinexor plus ruxolitinib in JAK inhibitor-naïve patients with myelofibrosis: a multicenter, open-label, phase 1 study.Blood advances · 2026Article
- Prospects of Chimeric Antigen Receptor T-Cell Therapy in Myelofibrosis: From Immunopathogenesis to Therapeutic Strategies.Cancers · 2026Review
- High-dose ruxolitinib (25 mg twice daily) in myelofibrosis: feasibility, safety, and long-term treatment exposure in a real-world cohort.Annals of hematology · 2026Article
- Comparison of the enzymatic and cellular profiles of clinical JAK inhibitors for the treatment of myelofibrosis.Blood neoplasia · 2026Article
- Platelets Outperform Leukocytes in Transcriptomic Liquid Biopsy Profiling of Myeloproliferative Neoplasms.bioRxiv : the preprint server for biology · 2026Article
- Immune and cytokine landscape differs between cytopenic and proliferative phenotypes in primary myelofibrosis.Therapeutic advances in hematology · 2026Article
- PD-1/PD-L1-CXCR3 Coexpression and CXCR3 on Intermediate Monocytes Predict Fibrosis, Leukemic Transformation, and Survival in Egyptian Philadelphia-Negative Myeloproliferative Neoplasms.Clinical Medicine Insights. Oncology · 2026Article
- Quantitative MRI Assessment of Bone Marrow Disease in Myelofibrosis: A Prospective Study.Radiology. Imaging cancer · 2025Observational
- Emerging Therapeutic Approaches for Anemia in Myelofibrosis.Current hematologic malignancy reports · 2025Review
- Article
- Selinexor plus ruxolitinib in JAK inhibitor treatment-naïve myelofibrosis: SENTRY Phase 3 study design.Future oncology (London, England) · 2025Article
- The Ongoing Challenges of Managing Cytopenic Myelofibrosis in 2025: The Emergence of Non-JAK Inhibitor Therapies.Blood and lymphatic cancer : targets and therapy · 2025Review
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 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
12 authors at 10 institutions in 6 countries.
Funding
Abstract
Myelofibrosis (MF) is a myeloproliferative disorder that exhibits considerable biological and clinical heterogeneity. At the two ends of the disease spectrum are the myelodepletive or cytopenic phenotype and the myeloproliferative phenotype. The cytopenic phenotype has a high prevalence in primary MF (PMF) and is characterized by low blood counts. The myeloproliferative phenotype is typically associated with secondary MF (SMF), mild anemia, minimal need for transfusion support, and normal to mild thrombocytopenia. Differences in somatic driver mutations and allelic burden, as well as the acquisition of non-driver mutations further influences these phenotypic differences, prognosis, and response to therapies such as JAK2 inhibitors. The outcome of patients with the cytopenic phenotype are comparatively worse and frequently pose a challenge to treat given the inherent exacerbation of cytopenias. Recent data indicate that an innate immune deregulated state that hinges on the myddosome-IRAK-NFκB axis favors the cytopenic myelofibrosis phenotype and offers opportunity for novel treatment approaches. We will review the biological and clinical features of the MF disease spectrum and associated treatment considerations.
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What OpenQuestion 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 OpenQuestion graph.