ArticleCancer research2022
Myelofibrosis: Genetic Characteristics and the Emerging Therapeutic Landscape.
Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Allogeneic Hematopoietic Stem Cell Transplantation in Myelofibrosis: Evolving Indications, Conditioning Strategies, and Outcomes.Hematology reports · 2026Review
- Dissociated Humoral and Cellular Immune Responses to Recombinant Zoster Vaccine in Myeloproliferative Neoplasms Under JAK Inhibition: A Pilot Study.International journal of molecular sciences · 2026Article
- Efficacy and Safety of Momelotinib in Myelofibrosis: A Systematic Review and Meta-Analysis With a Focus on Anemia Outcomes.Journal of hematology · 2025Article
- Selinexor plus ruxolitinib in JAK inhibitor treatment-naïve myelofibrosis: SENTRY Phase 3 study design.Future oncology (London, England) · 2025Article
- Spatial-transcriptomic profiling: a new lens for understanding myelofibrosis pathophysiology.Cell communication and signaling : CCS · 2024Review
- A randomized, double-blind, placebo-controlled phase 3 study to assess efficacy and safety of ropeginterferon alfa-2b in patients with early/lower-risk primary myelofibrosis.Annals of hematology · 2024Article
- Function of serine/arginine-rich splicing factors in hematopoiesis and hematopoietic malignancies.Cancer cell international · 2024Review
- Momelotinib for myelofibrosis: our 14 years of experience with 100 clinical trial patients and recent FDA approval.Blood cancer journal · 2024Article
- Momelotinib (JAK1/JAK2/ACVR1 inhibitor): mechanism of action, clinical trial reports, and therapeutic prospects beyond myelofibrosis.Haematologica · 2023Article
- Exploring the Molecular Landscape of Myelofibrosis, with a Focus on Ras and Mitogen-Activated Protein (MAP) Kinase Signaling.Cancers · 2023Review
- Blast phase myeloproliferative neoplasm with prior exposure to ruxolitinib: comparative analysis of mutations and survival.Haematologica · 2023Article
- Lysyl oxidase like-2 in fibrosis and cardiovascular disease.American journal of physiology. Cell physiology · 2023Review
- Role of TGF-beta1 and TNF-alpha1 produced by neoplastic cells in the pathogenesis of fibrosis in patients with hematologic neoplasms.Journal of clinical and experimental hematopathology : JCEH · 2023Article
- Recent advances in therapies for primary myelofibrosis.Faculty reviews · 2023Review
- The clinical relevance of broad mutational screening of myeloproliferative neoplasms at diagnosis.Frontiers in oncology · 2023Article
- Mutations, inflammation and phenotype of myeloproliferative neoplasms.Frontiers in oncology · 2023Review
- Mutant CALR's "sweet tooth".Blood · 2022Article
- Mutations in the miR-142 gene are not common in myeloproliferative neoplasms.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is one of three myeloproliferative neoplasms (MPN) that are morphologically and molecularly inter-related, the other two being polycythemia vera (PV) and essential thrombocythemia (ET). MPNs are characterized by JAK-STAT-activating JAK2, CALR, or MPL mutations that give rise to stem cell-derived clonal myeloproliferation, which is prone to leukemic and, in case of PV and ET, fibrotic transformation. Abnormal megakaryocyte proliferation is accompanied by bone marrow fibrosis and characterizes PMF, while the clinical phenotype is pathogenetically linked to ineffective hematopoiesis and aberrant cytokine expression. Among MPN-associated driver mutations, type 1-like CALR mutation has been associated with favorable prognosis in PMF, while ASXL1, SRSF2, U2AF1-Q157, EZH2, CBL, and K/NRAS mutations have been shown to be prognostically detrimental. Such information has enabled development of exclusively genetic (GIPSS) and clinically integrated (MIPSSv2) prognostic models that facilitate individualized treatment decisions. Allogeneic stem cell transplantation remains the only treatment modality in MF with the potential to prolong survival, whereas drug therapy, including JAK2 inhibitors, is directed mostly at the inflammatory component of the disease and is therefore palliative in nature. Similarly, disease-modifying activity remains elusive for currently available investigational drugs, while their additional value in symptom management awaits controlled confirmation. There is a need for genetic characterization of clinical observations followed by in vitro and in vivo preclinical studies that will hopefully identify therapies that target the malignant clone in MF to improve patient outcomes.
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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.