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Primary Myelofibrosis

Primary Myelofibrosis (PMF): Disease Characteristics Research Report

2026-04-05
Falcon MONDO:0009692 Model: Edison Scientific Literature 45 citations

Primary Myelofibrosis (PMF): Disease Characteristics Research Report

Target Disease

1. Disease Information

1.1 Concise overview (current understanding)

Primary myelofibrosis is a clonal hematopoietic stem/progenitor cell neoplasm characterized by atypical megakaryocytic (and granulocytic) proliferation, progressive bone marrow (BM) fibrosis, and extramedullary hematopoiesis (EMH), which collectively drive cytopenias, splenomegaly, constitutional symptoms, and risk of leukemic transformation (martino2024treatmentstrategiesused pages 1-2, wang2025currentadvancesin pages 5-7). A recent pathologic review describes PMF as a Ph-negative MPN featuring “clonal proliferation of atypical megakaryocytes and myeloid cells, fibrosis of the bone marrow, extramedullary hematopoiesis, and increased risk of leukemic transformation to acute myeloid leukemia (AML)” (abstract) (https://doi.org/10.3390/cancers18010050; 2025-12) (shao2025areviewof pages 4-6).

PMF includes a prefibrotic/early PMF stage (hypercellular marrow with minimal fibrosis) and overt/fibrotic-stage PMF with advanced fibrosis and leukoerythroblastosis (wang2025currentadvancesin pages 4-5, wang2025currentadvancesin pages 5-7).

1.2 Key identifiers and classifications

Because the current tool runs retrieved mostly primary literature and guideline-style reviews, ontology/administrative identifiers (ICD-10/ICD-11, MeSH, OMIM, Orphanet, MONDO) are not fully populated from the evidence captured here.

What can be stated from evidence: - Classification systems used clinically: WHO and ICC frameworks (WHO 5th edition/WHO-HAEM5; ICC 2022) are explicitly referenced in multiple sources for PMF/pre-PMF diagnosis and classification (https://doi.org/10.1007/s00277-025-06191-7; 2025-01) (wang2025currentadvancesin pages 5-7), and are discussed as contemporaneous classification systems (https://doi.org/10.1186/s13045-024-01571-4; 2024-07) (stuckey2025myelofibrosistreatmentoptions pages 8-10).

1.3 Common synonyms / alternative names

1.4 Evidence provenance: individual vs aggregated resources

2. Etiology

2.1 Disease causal factors (genetic/mechanistic)

PMF is driven by constitutive activation of the JAK–STAT signaling axis, typically via somatic driver mutations in JAK2, CALR, or MPL (chifotides2023associationofmyelofibrosis pages 2-4, wang2025currentadvancesin pages 5-7). A 2022 ASH Education review states MF is “universally driven by Jak/STAT pathway activation” (https://doi.org/10.1182/hematology.2022000340; 2022-12) (reynolds2022newapproachesto pages 1-3).

2.2 Risk factors

Genetic risk factors

Environmental/host risk factors

Specific exogenous environmental causes (toxins, infections, etc.) were not identified in the retrieved evidence snippets. Host factors associated with outcomes/complications in real-world datasets include age and blood count abnormalities (martino2024treatmentstrategiesused pages 1-2, reynolds2022newapproachesto pages 1-3).

2.3 Protective factors

No specific genetic or environmental protective factors were captured in the current evidence set.

2.4 Gene–environment interactions

No PMF-specific gene–environment interaction evidence was captured in the current evidence set.

3. Phenotypes

3.1 Core clinical manifestations and laboratory abnormalities

PMF exhibits heterogeneous presentation; ~25–33% can be asymptomatic initially (shao2025areviewof pages 4-6). Common manifestations include: - Splenomegaly (often marked), due to EMH (shao2025areviewof pages 4-6, wang2025currentadvancesin pages 5-7) - Anemia and progressive cytopenias (shao2025areviewof pages 4-6, wang2025currentadvancesin pages 5-7) - Leukoerythroblastosis and teardrop RBCs (peripheral smear) (shao2025areviewof pages 4-6) - Constitutional symptoms (fever, weight loss, night sweats) and cachexia (wang2025currentadvancesin pages 5-7) - Thrombosis/bleeding: a pathology review reports “Thromboembolic events occur in ~10–20% of patients” (https://doi.org/10.3390/cancers18010050; 2025-12) (shao2025areviewof pages 4-6).

3.2 Phenotype subtypes (proliferative vs cytopenic)

Two clinically meaningful ends of a spectrum are highlighted: - Myeloproliferative phenotype: larger spleens, leukocytosis, normal/higher counts or mild anemia; fewer non-driver mutations and higher JAK2 allele burden; generally better response to ruxolitinib (chifotides2023associationofmyelofibrosis pages 2-4). - Myelodepletive/cytopenic phenotype: ≥2 cytopenias, transfusion dependence, modest splenomegaly; more HMR mutations and genomic complexity; inferior outcomes; emphasizes less myelosuppressive JAK inhibitors (momelotinib/pacritinib) (chifotides2023associationofmyelofibrosis pages 2-4, reynolds2022newapproachesto pages 1-3).

3.3 Phenotype characteristics (age of onset, progression, frequency)

3.4 Quality-of-life impact

Quality of life is impacted by anemia, constitutional symptoms, and splenomegaly; treatment goals emphasize symptom and spleen improvement (martino2024treatmentstrategiesused pages 1-2, wang2025currentadvancesin pages 5-7).

3.5 Suggested HPO terms (examples)

4. Genetic / Molecular Information

4.1 Causal genes (somatic driver genes)

4.2 Pathogenic variants (typical PMF)

4.3 Modifier/cooperating mutations and prognostic genomics

4.4 Epigenetic information

The current evidence set supports that epigenetic regulators (e.g., ASXL1, DNMT3A, EZH2, TET2) are common co-mutations and carry prognostic relevance, but does not provide direct disease-specific methylation/histone profiling datasets (mora2024prognosticandpredictive pages 1-2).

4.5 Chromosomal abnormalities

A pathology review notes karyotypic abnormalities in up to ~45% of cases; common abnormalities include del(20q), del(13q), +8, +9 (shao2025areviewof pages 4-6). Another review gives a similar range (~30–50%) and lists del(13q), del(20q), +8, +9, del(12p), trisomy 1q (ozygała2024biologicalmarkersof pages 10-12).

5. Environmental Information

6. Mechanism / Pathophysiology

6.1 Core causal chain (integrated)

1) Somatic driver mutation (JAK2/CALR/MPL) in hematopoietic stem/progenitor cells → constitutive JAK–STAT signaling (chifotides2023associationofmyelofibrosis pages 2-4, reynolds2022newapproachesto pages 1-3).
2) Expansion/dysregulation of myeloid lineages with atypical megakaryocytes → secretion of pro-inflammatory/pro-fibrotic mediators (IL-1β, TGF-β; PDGF, VEGF, b-FGF) (wang2025currentadvancesin pages 5-7).
3) Bone marrow microenvironment remodeling and activation of stromal programs → progressive reticulin/collagen fibrosis and ineffective hematopoiesis (martino2024treatmentstrategiesused pages 1-2, wang2025currentadvancesin pages 5-7).
4) BM failure drives EMH in spleen/liver and systemic symptoms (shao2025areviewof pages 4-6, wang2025currentadvancesin pages 5-7).

6.2 Fibrosis biology and cell types

A pathology review states fibrosis is driven by profibrotic cytokines including “TGF-β, PDGF, VEGF” and implicates Gli1+ and Lepr+ mesenchymal stem cell populations in fibrotic remodeling, alongside pathways such as BMP/Wnt (shao2025areviewof pages 4-6).

6.3 Anemia biology and hepcidin/ACVR1 axis (therapeutically actionable)

Anemia is a hallmark and negative prognostic factor (mora2024prognosticandpredictive pages 1-2, reynolds2022newapproachesto pages 1-3). ACVR1 (ALK2) inhibition is used therapeutically to suppress hepcidin signaling and improve iron-restricted anemia; momelotinib is a JAK1/2 and ACVR1 inhibitor whose “dual inhibition mechanism addresses anemia by suppressing hepcidin production” (review abstract) (https://doi.org/10.3389/fonc.2024.1411972; 2024-06) (chifotides2023associationofmyelofibrosis pages 2-4).

6.4 Suggested ontology terms

GO Biological Process (examples): - “JAK-STAT cascade” (GO term; verify exact ID in implementation) - “Cytokine-mediated signaling pathway” - “Extracellular matrix organization” - “Collagen fibril organization” - “Hepcidin metabolic process” - “Inflammatory response”

Cell Ontology (CL) (examples): - Megakaryocyte (CL:0000554) - Hematopoietic stem cell (CL:0000037) - Mesenchymal stromal cell / mesenchymal stem cell (term exists; verify exact CL ID)

7. Anatomical Structures Affected

7.1 Organ/tissue targets

7.2 Suggested anatomy ontology (UBERON examples)

8. Temporal Development

8.1 Onset

8.2 Progression patterns

9. Inheritance and Population

9.1 Epidemiology

9.2 Inheritance

PMF is principally a somatic clonal neoplasm in the retrieved evidence set; germline Mendelian inheritance patterns are not emphasized in these sources.

10. Diagnostics

10.1 Diagnostic criteria (WHO/ICC-aligned) and key concepts

Multiple sources converge on a major + minor criteria framework: - A 2023 British Society for Haematology guideline states: “Diagnosis requires all three major criteria and at least one minor criterion confirmed in two consecutive determinations.” (https://doi.org/10.1111/bjh.19164; 2023-11) (mclornan2023diagnosisandevaluation pages 6-6). - A 2024 review similarly summarizes diagnostic structure and provides a detailed minor-criteria list (anemia not due to comorbidity, leukocytosis ≥11×10^9/L, palpable splenomegaly, elevated LDH, leukoerythroblastosis) (martino2024treatmentstrategiesused pages 2-4).

Core diagnostic elements supported by evidence: - Bone marrow morphology: megakaryocytic proliferation/atypia and grading of fibrosis (pre-PMF ≤MF-1; overt PMF MF-2/3) (shao2025areviewof pages 4-6, wang2025currentadvancesin pages 5-7). - Clonality evidence: JAK2/CALR/MPL driver mutation or other clonal marker (martino2024treatmentstrategiesused pages 2-4, mclornan2023diagnosisandevaluation pages 6-6). - Exclusion of other myeloid neoplasms (including BCR::ABL1-positive CML) (martino2024treatmentstrategiesused pages 2-4, wang2025currentadvancesin pages 5-7).

10.2 Testing modalities

  • Driver mutation detection and broader NGS panels are integral; ICC-oriented review emphasizes sensitive techniques and notes “high sensitive single target (RT-qPCR, ddPCR) or multi-target next-generation sequencing assays with a minimal sensitivity of VAF 1% are now important for a proper diagnostic identification of MPN cases with low allelic frequencies at initial presentation” (https://doi.org/10.1007/s00428-022-03480-8; 2023-12) (wang2025currentadvancesin pages 5-7).

10.3 Differential diagnosis (high level)

11. Outcome / Prognosis

11.1 Survival and mortality (risk-stratified)

Prognosis is heterogeneous and is commonly modeled using clinical, cytogenetic, and molecular risk systems. - A 2024 prognostic review provides median OS estimates by MF subtype: “Median overall survival (OS) of pre-PMF, overt-PMF and SMF patients is around 14 years, seven and nine years, respectively.” (abstract) (https://doi.org/10.1007/s11899-024-00739-6; 2024-08) (mora2024prognosticandpredictive pages 1-2). - Risk scores (IPSS/DIPSS/DIPSS-plus) span median OS approximately from ~11.3 years (low risk) to ~2.3 years (high risk) in one review summary (mora2024prognosticandpredictive pages 1-2). Another review provides representative medians by IPSS and DIPSS-plus categories (martino2024treatmentstrategiesused pages 2-4).

11.2 Prognostic factors

Common adverse features include older age, leukocytosis, anemia, thrombocytopenia, circulating blasts, constitutional symptoms, unfavorable karyotype, and HMR mutations (martino2024treatmentstrategiesused pages 2-4, mora2024prognosticandpredictive pages 1-2).

11.3 Prognostic models used clinically

12. Treatment

12.1 Treatment goals and real-world implementation

Goals emphasize symptom control and spleen volume reduction; transplantation is reserved for selected higher-risk patients (martino2024treatmentstrategiesused pages 1-2, martino2024treatmentstrategiesused pages 2-4). A 2024 review states: “Current drug therapy for myelofibrosis does not alter the natural course of the disease or prolong survival, and allogeneic stem cell transplantation is the only curative treatment modality.” (abstract) (https://doi.org/10.3390/hematolrep16040067; 2024-10) (martino2024treatmentstrategiesused pages 1-2).

12.2 Pharmacotherapy (JAK inhibitors and anemia-directed strategies)

Ruxolitinib (JAK1/2 inhibitor)

Momelotinib (JAK1/2 + ACVR1/ALK2 inhibitor; anemia benefit; FDA approval 2023-09-15)

Pacritinib (JAK2/IRAK1/ACVR1; JAK1-sparing; thrombocytopenic MF)

12.3 Allogeneic hematopoietic stem cell transplantation (allo-HSCT)

Allo-HSCT is repeatedly stated as the only curative option, generally for transplant-eligible higher-risk patients (martino2024treatmentstrategiesused pages 1-2, stuckey2025myelofibrosistreatmentoptions pages 8-10). (A detailed 2024 EBMT/ELN transplant guideline was not obtainable in this run, so granular transplant outcome statistics cannot be quoted here.)

12.4 Supportive care and symptom measurement implementation

12.5 MAXO (Medical Action Ontology) suggestions (examples)

  • JAK inhibitor therapy (e.g., ruxolitinib, fedratinib, momelotinib, pacritinib)
  • Allogeneic hematopoietic stem cell transplantation
  • Red blood cell transfusion
  • Symptom assessment/monitoring with validated PRO instruments

13. Prevention

No established primary prevention strategies are identified in the retrieved evidence, consistent with PMF being largely a sporadic somatic neoplasm in most clinical contexts. Secondary/tertiary prevention focuses on monitoring, symptom control, transfusion support, thrombosis/bleeding management, and preventing/mitigating progression via risk-adapted therapy (martino2024treatmentstrategiesused pages 2-4, mclornan2023diagnosisandevaluation pages 6-6).

14. Other Species / Natural Disease

No naturally occurring PMF in non-human species was captured in the retrieved evidence snippets.

15. Model Organisms

The retrieved evidence references stromal-cell involvement and fibrosis pathways (e.g., Gli1+ and Lepr+ mesenchymal stem cells) as part of mechanistic understanding, but does not provide specific PMF model organism systems in the captured snippets (shao2025areviewof pages 4-6).

Recent developments (2023–2024 highlights)

1) Expanded therapeutic landscape for cytopenic/anemic MF: momelotinib approval (2023-09-15) and anemia-focused evidence (SIMPLIFY-2 subgroup TI improvements) (chifotides2023associationofmyelofibrosis pages 2-4, wang2025currentadvancesin pages 5-7).
2) Real-world data scaling using EHR networks: TriNetX-based MF studies spanning >64,000 MF patients to validate risk factors and simplified IPSS approaches (https://doi.org/10.3390/cancers16071416; 2024-04) (martino2024treatmentstrategiesused pages 1-2).
3) Modern prognostication: emphasis on mutation-informed models (MIPSS70+ v2.0) and integrated risk modeling (mora2024prognosticandpredictive pages 1-2, mclornan2023diagnosisandevaluation pages 6-6).
4) Recognition of phenotypic heterogeneity (proliferative vs cytopenic): linking clinical phenotype with allele burden and co-mutation architecture to tailor therapy (chifotides2023associationofmyelofibrosis pages 2-4, reynolds2022newapproachesto pages 1-3).

Key statistics (selected, recent)

Embedded summary table: molecular hallmarks

Table (click to expand)
Feature category PMF finding Approximate frequency / definition Clinical or biologic association
Driver mutation JAK2 V617F ~60% of PMF; alternatively described as about two-thirds of PMF (chifotides2023associationofmyelofibrosis pages 2-4, mora2024prognosticandpredictive pages 1-2) Higher allele burden is associated with the myeloproliferative phenotype; lower burden with myelodepletive/cytopenic phenotype (chifotides2023associationofmyelofibrosis pages 2-4)
Driver mutation CALR exon 9 ~25–30% of PMF; another source gives ~25% (chifotides2023associationofmyelofibrosis pages 2-4, mora2024prognosticandpredictive pages 1-2) CALR is a major clonal driver used in diagnosis; type 1/like CALR is incorporated in molecular prognostic models such as MIPSS70 (martino2024treatmentstrategiesused pages 2-4, mora2024prognosticandpredictive pages 1-2)
Driver mutation MPL (classically W515L/K) ~5–10% of PMF; another source gives ~10% (chifotides2023associationofmyelofibrosis pages 2-4, mora2024prognosticandpredictive pages 1-2) Canonical MPN driver used in WHO/ICC-style diagnostic workup (martino2024treatmentstrategiesused pages 2-4, mclornan2023diagnosisandevaluation pages 6-6)
Driver-negative subset Triple-negative PMF ~10% in one review; ~10–15% in another broader MPN review (mora2024prognosticandpredictive pages 1-2, ozygała2024biologicalmarkersof pages 10-12) Generally considered biologically adverse in PMF literature; requires other clonal evidence/exclusion of reactive fibrosis in diagnostic frameworks (mclornan2023diagnosisandevaluation pages 6-6, ozygała2024biologicalmarkersof pages 10-12)
High molecular risk (HMR) definition ASXL1, EZH2, IDH1, IDH2, SRSF2, U2AF1 Q157 HMR genes are the adverse mutation set used in contemporary prognostic models; BSH notes MIPSS70+ v2.0 incorporates HMR genes plus U2AF1 Q157 (chifotides2023associationofmyelofibrosis pages 2-4, mclornan2023diagnosisandevaluation pages 6-6) Associated with worse overall survival, higher blast-phase risk, and more aggressive biology (chifotides2023associationofmyelofibrosis pages 2-4, mora2024prognosticandpredictive pages 1-2)
Common co-mutations ASXL1, DNMT3A, TET2 Co-mutations occur in ~50% of patients; ASXL1, DNMT3A, and TET2 are repeatedly cited as common examples (martino2024treatmentstrategiesused pages 2-4) Reflect clonal complexity and are relevant to prognosis beyond driver status (martino2024treatmentstrategiesused pages 2-4, mora2024prognosticandpredictive pages 1-2)
Additional recurrent co-mutations SRSF2, EZH2, IDH1/2, SF3B1, U2AF1, TP53 About 80% of PMF cases carry non-driver myeloid gene variants in one 2024 review (mora2024prognosticandpredictive pages 1-2) Splicing/epigenetic mutations are enriched in advanced or cytopenic disease and shorten survival (chifotides2023associationofmyelofibrosis pages 2-4, mora2024prognosticandpredictive pages 1-2)
Mutations linked to advanced disease ASXL1, U2AF1-Q157, SRSF2 Not primarily frequency-defined here, but identified as enriched in MF/advanced disease (martino2024treatmentstrategiesused pages 2-4) Poorer survival and adverse-risk enrichment (martino2024treatmentstrategiesused pages 2-4, wang2025currentadvancesin pages 5-7)
Mutations linked to treatment resistance RAS/CBL pathway mutations Defined as non-driver adverse co-mutations rather than frequent drivers (martino2024treatmentstrategiesused pages 2-4, wang2025currentadvancesin pages 5-7) Associated with ruxolitinib resistance/failure (martino2024treatmentstrategiesused pages 2-4, wang2025currentadvancesin pages 5-7)
Phenotype association Myeloproliferative phenotype Molecular profile tends to show higher JAK2 V617F burden and fewer non-driver mutations (chifotides2023associationofmyelofibrosis pages 2-4) Typical features: larger spleen, leukocytosis, normal/mild anemia, lower fibrosis grade, better response to ruxolitinib (chifotides2023associationofmyelofibrosis pages 2-4)
Phenotype association Myelodepletive / cytopenic phenotype More often shows lower JAK2 V617F burden, greater genomic complexity, and more HMR/splicing-epigenetic mutations (chifotides2023associationofmyelofibrosis pages 2-4, reynolds2022newapproachesto pages 1-3) Typical features: ≥2 cytopenias, transfusion dependence, moderate/severe thrombocytopenia, higher fibrosis grade, inferior survival, limited ruxolitinib response; non-myelosuppressive JAK inhibitors (momelotinib/pacritinib) are emphasized for this phenotype (chifotides2023associationofmyelofibrosis pages 2-4, reynolds2022newapproachesto pages 1-3)

Table: This table summarizes the core genetic and molecular hallmarks of primary myelofibrosis, including driver mutation frequencies, adverse co-mutation profiles, and how molecular features map to myeloproliferative versus myelodepletive phenotypes. It is useful as a compact reference for diagnosis, prognosis, and treatment stratification.

Source URLs (selected)

References

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