Home / Deep Research / Myeloproliferative Neoplasm, Unclassifiable

Myeloproliferative Neoplasm, Unclassifiable

1. Disease Information

2026-05-11
Falcon MONDO:0019452 Model: Edison Scientific Literature 43 citations

1. Disease Information

Overview / definition

Myeloproliferative neoplasm, unclassifiable (MPN-U) is defined as a myeloproliferative neoplasm with clinical/hematologic/morphologic features of an MPN that does not fulfill diagnostic criteria for any other defined MPN entity; it is described as rare, heterogeneous, and often requiring “dynamic review over time” because some cases may later become classifiable as PV/ET/PMF or another MPN. (mclornan2022howimanage pages 1-1, mclornan2022howimanage pages 1-2)

Current classification terminology (WHO vs ICC)

Both WHO-HAEM5 and the International Consensus Classification (ICC) retain a “catch-all” entity for otherwise unclassifiable MPNs, but with different names: MPN-NOS in WHO-HAEM5 versus MPN-unclassifiable in the ICC. (xiao2024apracticalapproach pages 2-4)

Synonyms / alternative names

Commonly used names include “myeloproliferative neoplasm, unclassifiable” and “MPN not otherwise specified (NOS)” in WHO-era usage. (mclornan2022howimanage pages 1-1, xiao2024apracticalapproach pages 2-4, pizzi2021theclassificationof pages 7-8)

Key identifiers (available in retrieved sources)

Identifiers not found in retrieved corpus: MONDO ID, Orphanet ID, and MeSH term mappings were not present in the excerpts retrieved for this run.

Evidence type note (patient-level vs aggregated)

Evidence spans (i) aggregated cohort/registry studies (UK tertiary-center cohort; population-based Danish and Swedish studies) and (ii) expert review/survey synthesis. (deschamps2021clinicopathologicalcharacterisationof pages 2-3, hargreaves2022diagnosticandmanagement pages 6-7, landtblom2018secondmalignanciesin pages 3-4, pedersen2020twofoldriskof pages 1-2)

2. Etiology

Disease causal factors (current understanding)

MPN-U is best understood as a clonal hematopoietic stem/progenitor cell disorder that manifests as myeloproliferation but lacks sufficient integrated clinicopathologic criteria to be assigned to a specific MPN subtype at a given timepoint. Clonality is commonly supported by canonical MPN “driver” mutations (JAK2/CALR/MPL) and/or other myeloid neoplasm–associated mutations and cytogenetic abnormalities. (gianelli2023internationalconsensusclassification pages 13-14, pizzi2021theclassificationof pages 7-8)

Risk factors

Smoking (lifestyle/environmental): In a Danish general-population cohort (DANHES), smoking was associated with higher risk of incident MPN overall and particularly high relative risks for MPN-U. Multivariable HR for any MPN was 2.5 (95% CI 1.3–5.0) for daily smokers versus never-smokers; subtype analysis showed MPN-U HR 6.2 (1.5–25) for daily smokers and MPN-U HR 6.2 (1.8–21) for occasional/ex-smokers. (pedersen2018smokingisassociated pages 1-2)

Other environmental/occupational risk factors were mentioned only qualitatively as conflicting/limited in the retrieved excerpts; no robust, MPN-U-specific quantitative estimates beyond smoking were retrieved. (pedersen2018smokingisassociated pages 5-6)

Protective factors

No protective genetic or environmental factors were identified in the retrieved evidence set.

Gene–environment interactions

No explicit gene–environment interaction evidence (e.g., JAK2 genotype-by-smoking) was available in the retrieved excerpts.

3. Phenotypes (clinical features) and HPO suggestions

Typical phenotype spectrum

MPN-U shows a broad phenotype that can include constitutional symptoms, hepatosplenomegaly, thrombosis (including splanchnic vein thrombosis), and variable blood-count abnormalities; cases may represent a prodromal/pre-proliferative stage of classical MPN. (mclornan2022howimanage pages 2-2)

Quantified phenotype frequencies from a contemporary cohort (UK tertiary center)

In a single-center cohort of 82 MPN-U patients (median age 49.7 years; 56% female): splenomegaly 27%, pruritus 36%, constitutional symptoms 29%, transfusion dependency 2.4%; thrombocytosis 78% (median platelets 650×10^9/L); LDH elevated 72%; peripheral blood film features included teardrop cells (18.3%), leukoerythroblastosis (7%), and prominent large granular lymphocytes (19.7%). (deschamps2021clinicopathologicalcharacterisationof pages 2-3)

Thrombotic phenotype (including timing)

In the same cohort, thrombosis occurred in ~21% (arterial 10; portal vein 4; other venous 3), with median time from diagnosis to thrombotic event 0.2 months (0–208.3); 47% of those with thrombosis presented with a “heralding” thrombosis (9.9% of the whole cohort). (deschamps2021clinicopathologicalcharacterisationof pages 2-3)

Suggested HPO terms (non-exhaustive; mapping requires ontology validation)

Quality-of-life: MPN-SAF symptom scores ranged 0–73/100 in a subset, indicating wide symptom-burden variability, but no standardized QoL instruments (EQ-5D/SF-36) or comparative QoL statistics were available in retrieved excerpts. (deschamps2021clinicopathologicalcharacterisationof pages 3-5)

4. Genetic/Molecular Information

Molecular hallmarks and clonality support

Diagnosis requires exclusion of reactive conditions (infection/toxin/drug-related) and can be supported by detection of canonical MPN driver mutations or other myeloid neoplasm–associated mutations (e.g., ASXL1, EZH2, TET2, IDH1/2, SRSF2, SF3B1) and/or cytogenetic abnormalities. (gianelli2023internationalconsensusclassification pages 13-14, pizzi2021theclassificationof pages 7-8)

Driver mutation frequencies (cohort data)

In the 82-patient UK cohort: * JAK2 V617F: 53.7% (44/82) * JAK2 exon 12: 2.4% (2/82) * CALR type 1: 8.5% (7/82) * CALR type 2: 4.8% (4/82) * MPL: 6.1% (5/82) * Triple-negative (JAK2/CALR/MPL negative): 24% (20/82) No PDGFRA/B, CSF3R, BCR/ABL1, FGFR1, or PCM1-JAK2 rearrangements were detected in that series. (deschamps2021clinicopathologicalcharacterisationof pages 1-2)

Additional somatic mutations / cytogenetics

Extended molecular testing identified additional non-driver mutations in 24% (7/29) of those tested in the UK cohort. (deschamps2021clinicopathologicalcharacterisationof pages 1-2) Reviews summarize cytogenetic abnormalities in ~20–30% (or ~30%) of MPN-U cases; in the UK cohort with available cytogenetics, 88.5% were normal (suggesting cohort and testing differences). (gianelli2023internationalconsensusclassification pages 13-14, deschamps2021clinicopathologicalcharacterisationof pages 1-2)

Variant classification / allele frequency / germline vs somatic

Not available in the retrieved excerpts (no ClinVar/gnomAD-style allele frequency reporting was present).

Epigenetics / transcriptomics / proteomics / metabolomics

Not available in the retrieved excerpts.

5. Environmental Information

Beyond smoking (Section 2), no specific toxins/radiation/pollution or infectious triggers with reproducible quantitative evidence specific to MPN-U were available in the retrieved excerpts. (pedersen2018smokingisassociated pages 5-6)

6. Mechanism / Pathophysiology (high-level)

Mechanistically, MPN-U is interpreted as clonal myeloid proliferation driven by canonical MPN signaling lesions (JAK2/CALR/MPL) in many cases, with additional cooperating mutations in epigenetic regulators and splicing factors in subsets; however, the defining feature of MPN-U is not a unique pathway but rather failure to meet integrated diagnostic thresholds for a specific MPN subtype at the time of evaluation. (gianelli2023internationalconsensusclassification pages 13-14, pizzi2021theclassificationof pages 7-8)

Mechanistic details (e.g., JAK-STAT pathway activation, inflammatory cytokine loops) were not available as primary mechanistic experiments in this evidence set; only epidemiologic/mechanistic plausibility statements linking smoking to inflammatory signaling were present. (pedersen2018smokingisassociated pages 5-6)

Suggested GO biological-process terms (hypothesis-driven; requires validation): * “myeloid cell proliferation” (GO:0008283 related), “hematopoietic stem cell proliferation” (GO terms vary)

Suggested CL cell types (hypothesis-driven; requires validation): * Hematopoietic stem cell (CL:0000037), myeloid progenitor (CL:0000763), megakaryocyte (CL:0000554)

7. Anatomical Structures Affected

Primary anatomic sites include: * Bone marrow (hypercellularity; megakaryocytic clustering/pleomorphism; variable fibrosis) (deschamps2021clinicopathologicalcharacterisationof pages 2-3) * Spleen (splenomegaly; extramedullary hematopoiesis mentioned in reviews) (deschamps2021clinicopathologicalcharacterisationof pages 2-3, mclornan2022howimanage pages 2-2) * Splanchnic vasculature (portal vein thrombosis and broader SVT association; a major clinical presentation route) (deschamps2021clinicopathologicalcharacterisationof pages 2-3, pizzi2021theclassificationof pages 7-8)

Suggested UBERON terms (requires validation): * Bone marrow — UBERON:0002371 * Spleen — UBERON:0002106 * Portal vein — UBERON:0001189

Subcellular localization was not addressed in retrieved excerpts.

8. Temporal Development

MPN-U is commonly conceptualized as including: * Early/prodromal phase with incompletely developed subtype-specific morphology (often overlapping ET/pre-PMF) and fewer organomegaly features (gianelli2023internationalconsensusclassification pages 13-14, pizzi2021theclassificationof pages 7-8) * Advanced fibrotic phase with cytopenias, organomegaly, fibrosis-related marrow changes, and higher transformation risk (pizzi2021theclassificationof pages 7-8)

In the UK cohort, transformation to accelerated/blast phase occurred in 7/82 (8.5%) with median time to transformation 88.2 months (15.6–183.9). (deschamps2021clinicopathologicalcharacterisationof pages 2-3)

9. Inheritance and Population

Inheritance

MPN-U is generally discussed as a somatic clonal neoplasm; explicit Mendelian inheritance patterns were not described in the retrieved excerpts.

Epidemiology (proportion among MPNs)

MPN-U is estimated at ~5–10% of MPNs in reviews/classification discussions. (pizzi2021theclassificationof pages 7-8, gianelli2023internationalconsensusclassification pages 11-13) In a UK tertiary registry, MPN-U constituted 82/1512 = 5.4% of MPN patients. (deschamps2021clinicopathologicalcharacterisationof pages 1-2)

Age/sex distribution

In the UK cohort: median age 49.7 years (range 13–79) and 56% female. (deschamps2021clinicopathologicalcharacterisationof pages 2-3)

10. Diagnostics (limited to retrieved evidence)

Diagnostic framing

Diagnosis is clinicopathologic and by exclusion: “features of an MPN are present” but criteria for defined entities are not met, and exclusionary rearrangements/fusions (e.g., BCR::ABL1, PCM1-JAK2; PDGFRA/B; FGFR1) must be absent; reactive drivers such as infection/toxin/drug exposure should be ruled out. (gianelli2023internationalconsensusclassification pages 13-14, mclornan2022howimanage pages 1-2)

WHO vs ICC placement

WHO-HAEM5 uses MPN-NOS; ICC uses MPN-unclassifiable. (xiao2024apracticalapproach pages 2-4)

Molecular testing sensitivity / contemporary updates

ICC-focused review text recommends highly sensitive molecular techniques for identifying JAK2/CALR/MPL driver mutations, with “minimal level of VAF 1%” as a recommended diagnostic backbone (in the ICC MPN classification paper’s conclusion). (gianelli2023internationalconsensusclassification pages 14-15)

Differential diagnosis (high-level)

Key exclusions include entities defined by specific lesions (e.g., BCR::ABL1; eosinophilia with tyrosine kinase fusions), and careful separation from MDS/MPN overlap neoplasms when dysplasia predominates. (gianelli2023internationalconsensusclassification pages 13-14)

Not available in retrieved evidence: complete WHO-HAEM5/ICC “major/minor criteria” tables for MPN-NOS/MPN-U, SNOMED/LOINC mappings, and structured genetic testing panel recommendations beyond general statements.

11. Outcome / Prognosis

Cohort-based survival estimates

In the UK cohort (n=82): * Median event-free survival (EFS) 11.25 years (95% CI 9.3–not reached) * Median OS not reached; 10-year OS 88.8% (95% CI 77.7–100.0%) (deschamps2021clinicopathologicalcharacterisationof pages 2-3)

Transformation/progression

Prognostic factors (EFS)

Lower platelets and leukocytosis stratified higher-risk groups: low platelet quartile HR 3.45 (95% CI 1.43–8.32) and leukocytosis HR 2.91 (95% CI 1.11–7.64) in multivariable analysis. (deschamps2021clinicopathologicalcharacterisationof pages 5-6, deschamps2021clinicopathologicalcharacterisationof media cb1fee4a)

Complications and comorbidity burden (population-based)

  • Pneumonia and respiratory mortality: In a Danish cohort, myelofibrosis/unclassifiable MPN had HR 3.03 (95% CI 1.86–4.93) for pneumonia and HR 2.40 (95% CI 1.11–5.19) for respiratory death (subtypes combined). (pedersen2020twofoldriskof pages 1-2)
  • Second malignancies: In a Swedish population cohort (9379 MPN patients; 1113 MPN-U), the hazard ratio for non-hematologic second malignancies in MPN-U was HR 1.9 (95% CI 1.5–2.5) versus controls. (landtblom2018secondmalignanciesin pages 3-4)

12. Treatment (evidence-limited; phenotype-driven)

There are no licensed, MPN-U-specific therapies highlighted in the retrieved evidence; management is explicitly described as challenging due to “lack of agreed guidelines” and is generally phenotype- and complication-driven (treating cytoses, symptoms/splenomegaly, and thrombosis risk similarly to classical MPNs). (hargreaves2022diagnosticandmanagement pages 6-7, hargreaves2022diagnosticandmanagement pages 3-6)

Real-world approaches are summarized in the management artifact (cytoreduction, antithrombotics, ruxolitinib off-label, allo-HCT escalation, and key MPN registries/trials). | Management domain | Therapy/approach | Real-world implementation in MPN-U / MPN-NOS | Quantitative details | Citation | |---|---|---|---|---| | Cytoreduction | Any cytoreductive therapy | Commonly used in practice, but indications are phenotype-driven rather than guideline-standardized | In the UK cohort, 51/82 patients (62.2%) received cytoreductive therapy; in the survey, 66% of centres would offer cytoreduction for thrombocytosis | (deschamps2021clinicopathologicalcharacterisationof pages 1-2, hargreaves2022diagnosticandmanagement pages 6-7) | | Cytoreduction | Hydroxycarbamide / hydroxyurea | Most commonly used first-line cytoreductive agent in cohort and survey practice | UK cohort: 40/82 (48.8%) received hydroxycarbamide; survey: 14 centres (41%) targeted platelets around 400 × 10^9/L, and 20 centres (59%) combined hydroxycarbamide with extended postoperative thromboprophylaxis | (deschamps2021clinicopathologicalcharacterisationof pages 1-2, hargreaves2022diagnosticandmanagement pages 6-7, hargreaves2022diagnosticandmanagement pages 3-6) | | Cytoreduction | Interferon / pegylated interferon | Used in a minority overall; may be considered in selected settings such as pregnancy or younger patients, but not a common first-choice agent in survey responses | UK cohort: 14/82 (17.1%) received interferon; survey of thrombocytosis management: no centres selected interferon as agent of choice; pregnancy-focused recommendations note interferon-based approaches at some centres | (deschamps2021clinicopathologicalcharacterisationof pages 1-2, hargreaves2022diagnosticandmanagement pages 6-7, hargreaves2022diagnosticandmanagement pages 3-6, mclornan2022howimanage pages 4-5) | | Cytoreduction | Anagrelide | Used infrequently for platelet control in selected patients | UK cohort: 8/82 (9.8%) received anagrelide | (deschamps2021clinicopathologicalcharacterisationof pages 1-2) | | Symptom/spleen-directed therapy | Ruxolitinib / JAK inhibitor | Off-label, phenotype-driven use for splenomegaly and symptom burden; many centres report little or no use, reflecting uncertainty and lack of approval | UK cohort: 5/82 (6.1%) received a JAK inhibitor; survey/review: about half of centres reported off-label ruxolitinib use for splenomegaly and/or symptoms, while many centres had no MPN-U patients on ruxolitinib | (deschamps2021clinicopathologicalcharacterisationof pages 1-2, hargreaves2022diagnosticandmanagement pages 3-6, mclornan2022howimanage pages 7-7) | | Antithrombotic management | Aspirin | Frequently used, especially with thrombocytosis and in pregnancy; does not eliminate thrombosis risk | Review suggests aspirin 75 mg once daily in selected phenotype-driven strategies; pregnancy recommendations include aspirin throughout pregnancy; cohort noted thromboses still occurred despite low-dose aspirin plus effective cytoreduction | (mclornan2022howimanage pages 8-9, mclornan2022howimanage pages 4-5, deschamps2021clinicopathologicalcharacterisationof pages 3-5) | | Antithrombotic management | LMWH | Used particularly in pregnancy and postpartum; also part of broader thrombosis management strategies extrapolated from other MPNs | Pregnancy guidance: antenatal LMWH plus standard 6-week postpartum prophylaxis | (mclornan2022howimanage pages 4-5) | | Antithrombotic management | VKA / warfarin | Common choice after venous thromboembolism, especially in heterogeneous real-world practice | Survey: most centres preferred warfarin/VKA after VTE; some reserved VKA specifically for splanchnic vein thrombosis | (hargreaves2022diagnosticandmanagement pages 3-6) | | Antithrombotic management | DOACs | Used by some centres; authors cautiously support DOACs in uncomplicated acute SVT, but liver dysfunction may limit use | Review notes VKA vs DOAC decisions are individualized; cohort/international data cited as showing comparable recurrent thrombosis and bleeding rates with DOACs in selected settings | (mclornan2022howimanage pages 5-6, hargreaves2022diagnosticandmanagement pages 3-6) | | Cytoreduction triggers | Thrombosis history | Many centres start cytoreduction after arterial or venous thrombosis, despite lack of MPN-U-specific evidence | 81% of surveyed centres initiate cytoreduction after venous or arterial thrombosis | (mclornan2022howimanage pages 7-7) | | Cytoreduction triggers | Blood count thresholds | Centres variably use platelet/WBC thresholds to start therapy | Survey: platelet threshold >450 × 10^9/L in 20% of centres, >1500 × 10^9/L in 72%, WBC >15 × 10^9/L in 45% | (mclornan2022howimanage pages 7-7) | | Response in cohort | Cytoreductive treatment outcomes | Outcomes are mixed, reinforcing need for better prognostic tools and standardized management | Among treated cohort patients, ~50% achieved adequate cytoreduction, 26.9% had stable blood counts, and 19.2% progressed (accelerated/transformation or fibrosis) | (deschamps2021clinicopathologicalcharacterisationof pages 3-5) | | Transplant | Allogeneic hematopoietic cell transplantation | Rare but considered for accelerated, blast-phase, fibrotic, or otherwise aggressive disease; early referral is recommended in suitable patients | UK cohort: 5/82 (6.1%) considered for allo-HCT and 2/82 (2.4%) transplanted; survey: observation 7%, HMA with planned allo-SCT 61%, induction chemotherapy then allo-SCT 7%, upfront allo-SCT 24% for progressive/accelerating disease | (deschamps2021clinicopathologicalcharacterisationof pages 1-2, hargreaves2022diagnosticandmanagement pages 6-7, mclornan2022howimanage pages 6-7, deschamps2021clinicopathologicalcharacterisationof pages 3-5) | | Transplant outcomes | Allo-HCT registry data | Best evidence comes from retrospective registry series rather than MPN-U-specific trials | Reported 3-year OS after allo-SCT approximately 55% with myeloablative conditioning vs 44% with reduced-intensity conditioning; relapse rates 23% vs 36% | (hargreaves2022diagnosticandmanagement pages 6-7) | | Monitoring/implementation | Practice framework | Management is individualized because there are no agreed guidelines; cases often managed similarly to classical MPNs and re-reviewed over time | Survey explicitly reports “lack of agreed guidelines” and wide heterogeneity in MDT review, genomic testing, anticoagulant choice, pregnancy care, and transplant referral | (hargreaves2022diagnosticandmanagement pages 1-2, hargreaves2022diagnosticandmanagement pages 6-7, hargreaves2022diagnosticandmanagement pages 3-6) | | Relevant trial/registry | NCT07362225 | Large observational registry tracking symptoms, treatments, and disease progression in people with MPNs; relevant because MPN-U patients are commonly excluded from interventional studies but can be captured in broad registries | Recruiting; observational; target enrollment 5000 | (xiao2024apracticalapproach pages 2-4) | | Relevant trial/registry | NCT03618485 | Taiwan MPN registry; observational real-world resource potentially capturing unclassifiable cases under broader MPN umbrella | Active, not recruiting; observational; target enrollment 500 | (xiao2024apracticalapproach pages 2-4) | | Relevant trial/registry | NCT07384039 | Supportive-care/exercise intervention in patients with MPNs; relevant to symptom burden and quality-of-life research though not MPN-U-specific | Not yet recruiting; interventional; target enrollment 80 | (xiao2024apracticalapproach pages 2-4) | | Relevant trial/registry | NCT06661915 | Phase 2 study in advanced MPNs using ASTX727 with or without iadademstat; relevant for transformed/advanced phenotypes that may include unclassifiable MPN biology | Recruiting; phase 2; target enrollment 62 | (xiao2024apracticalapproach pages 2-4) | | Relevant trial/registry | NCT04282187 | Phase 2 study of decitabine with ruxolitinib/fedratinib/pacritinib for accelerated/blast-phase MPN; relevant to aggressive MPN-U scenarios managed as advanced MPN | Recruiting; phase 2; target enrollment 25 | (xiao2024apracticalapproach pages 2-4) | | Relevant trial/registry | NCT03566446 | CALR-mutant peptide vaccine study in CALR-mutant MPN; relevant to molecularly defined subsets that may overlap with some MPN-U cases | Completed; phase 1; enrollment 10 | (xiao2024apracticalapproach pages 2-4) |

Table: This table summarizes how MPN-U/MPN-NOS is managed in real-world cohorts, surveys, and broader MPN studies. It highlights the absence of standardized guidelines, the phenotype-driven use of cytoreduction and antithrombotic therapy, transplant escalation in advanced disease, and relevant current trial or registry infrastructure.

Suggested MAXO terms (requires ontology validation): * Cytoreductive therapy — e.g., MAXO term for “cytoreductive therapy” * Antiplatelet therapy (aspirin) * Anticoagulation therapy * Allogeneic hematopoietic stem cell transplantation

13. Prevention

No primary-prevention interventions specific to MPN-U were identified. Smoking is a modifiable risk factor associated with MPN risk including MPN-U in one large cohort; smoking cessation is therefore a plausible risk-reduction strategy, although direct evidence for prevention of MPN-U is not established. (pedersen2018smokingisassociated pages 1-2)

Secondary/tertiary prevention in practice focuses on prevention of thrombosis/bleeding and monitoring for disease evolution or transformation, but no consensus prevention protocols were available in the retrieved excerpts. (hargreaves2022diagnosticandmanagement pages 3-6, mclornan2022howimanage pages 7-7)

14. Other Species / Natural Disease

No cross-species naturally occurring MPN-U analogs were identified in the retrieved evidence set.

15. Model Organisms

The retrieved evidence set did not include dedicated model-organism studies for MPN-U. Mechanistic model systems for canonical MPN driver mutations (e.g., JAK2/CALR/MPL) are widely used in the broader MPN field, but explicit, citable details were not present in the retrieved excerpts and therefore are not asserted here.

“Expert opinion” synthesis (authoritative-source analysis)

Across expert reviews and international survey data, a consistent expert conclusion is that MPN-U is a heterogeneous, diagnosis-of-exclusion category with meaningful thrombotic and transformation risks but insufficient evidence for standardized, disease-specific guidelines, leading to high inter-center practice variability and reliance on extrapolation from classical MPN management and individualized risk assessment. (mclornan2022howimanage pages 1-2, hargreaves2022diagnosticandmanagement pages 6-7, hargreaves2022diagnosticandmanagement pages 3-6)

References (URLs and publication dates from retrieved sources)

PMIDs: Not available in the retrieved excerpts for the above sources in this run; therefore PMID numbers cannot be reliably provided from the current evidence context.

References

  1. (mclornan2022howimanage pages 1-1): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  2. (mclornan2022howimanage pages 1-2): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  3. (xiao2024apracticalapproach pages 2-4): Wenbin Xiao, Valentina Nardi, Eytan Stein, and Robert P. Hasserjian. A practical approach on the classifications of myeloid neoplasms and acute leukemia: who and icc. Journal of Hematology & Oncology, Jul 2024. URL: https://doi.org/10.1186/s13045-024-01571-4, doi:10.1186/s13045-024-01571-4. This article has 40 citations and is from a domain leading peer-reviewed journal.

  4. (hargreaves2022diagnosticandmanagement pages 1-2): Rupen Hargreaves, Claire N Harrison, and Donal P McLornan. Diagnostic and management strategies for myeloproliferative neoplasm-unclassifiable (mpn-u): an international survey of contemporary practice. Current Research in Translational Medicine, 70:103338, Jul 2022. URL: https://doi.org/10.1016/j.retram.2022.103338, doi:10.1016/j.retram.2022.103338. This article has 6 citations and is from a peer-reviewed journal.

  5. (deschamps2021clinicopathologicalcharacterisationof pages 1-2): Paul Deschamps, Mufaddal Moonim, Deepti Radia, Natalia Curto‐Garcia, Claire Woodley, Sarah Bassiony, Jennifer O'Sullivan, Patrick Harrington, Kavita Raj, Yvonne Francis, Shahram Kordasti, Sahra Ali, Claire N. Harrison, and Donal P. McLornan. Clinicopathological characterisation of myeloproliferative neoplasm‐unclassifiable (mpn‐u): a retrospective analysis from a large uk tertiary referral centre. British Journal of Haematology, 193:792-797, Mar 2021. URL: https://doi.org/10.1111/bjh.17375, doi:10.1111/bjh.17375. This article has 19 citations and is from a domain leading peer-reviewed journal.

  6. (pizzi2021theclassificationof pages 7-8): Marco Pizzi, Giorgio Alberto Croci, Marco Ruggeri, Silvia Tabano, Angelo Paolo Dei Tos, Elena Sabattini, and Umberto Gianelli. The classification of myeloproliferative neoplasms: rationale, historical background and future perspectives with focus on unclassifiable cases. Cancers, 13:5666, Nov 2021. URL: https://doi.org/10.3390/cancers13225666, doi:10.3390/cancers13225666. This article has 46 citations.

  7. (mclornan2022howimanage pages 2-2): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  8. (gianelli2023internationalconsensusclassification pages 13-14): Umberto Gianelli, Jürgen Thiele, Attilio Orazi, Naseema Gangat, Alessandro M. Vannucchi, Ayalew Tefferi, and Hans Michael Kvasnicka. International consensus classification of myeloid and lymphoid neoplasms: myeloproliferative neoplasms. Virchows Archiv, 482:53-68, Dec 2023. URL: https://doi.org/10.1007/s00428-022-03480-8, doi:10.1007/s00428-022-03480-8. This article has 61 citations and is from a peer-reviewed journal.

  9. (deschamps2021clinicopathologicalcharacterisationof pages 2-3): Paul Deschamps, Mufaddal Moonim, Deepti Radia, Natalia Curto‐Garcia, Claire Woodley, Sarah Bassiony, Jennifer O'Sullivan, Patrick Harrington, Kavita Raj, Yvonne Francis, Shahram Kordasti, Sahra Ali, Claire N. Harrison, and Donal P. McLornan. Clinicopathological characterisation of myeloproliferative neoplasm‐unclassifiable (mpn‐u): a retrospective analysis from a large uk tertiary referral centre. British Journal of Haematology, 193:792-797, Mar 2021. URL: https://doi.org/10.1111/bjh.17375, doi:10.1111/bjh.17375. This article has 19 citations and is from a domain leading peer-reviewed journal.

  10. (deschamps2021clinicopathologicalcharacterisationof pages 5-6): Paul Deschamps, Mufaddal Moonim, Deepti Radia, Natalia Curto‐Garcia, Claire Woodley, Sarah Bassiony, Jennifer O'Sullivan, Patrick Harrington, Kavita Raj, Yvonne Francis, Shahram Kordasti, Sahra Ali, Claire N. Harrison, and Donal P. McLornan. Clinicopathological characterisation of myeloproliferative neoplasm‐unclassifiable (mpn‐u): a retrospective analysis from a large uk tertiary referral centre. British Journal of Haematology, 193:792-797, Mar 2021. URL: https://doi.org/10.1111/bjh.17375, doi:10.1111/bjh.17375. This article has 19 citations and is from a domain leading peer-reviewed journal.

  11. (deschamps2021clinicopathologicalcharacterisationof media cb1fee4a): Paul Deschamps, Mufaddal Moonim, Deepti Radia, Natalia Curto‐Garcia, Claire Woodley, Sarah Bassiony, Jennifer O'Sullivan, Patrick Harrington, Kavita Raj, Yvonne Francis, Shahram Kordasti, Sahra Ali, Claire N. Harrison, and Donal P. McLornan. Clinicopathological characterisation of myeloproliferative neoplasm‐unclassifiable (mpn‐u): a retrospective analysis from a large uk tertiary referral centre. British Journal of Haematology, 193:792-797, Mar 2021. URL: https://doi.org/10.1111/bjh.17375, doi:10.1111/bjh.17375. This article has 19 citations and is from a domain leading peer-reviewed journal.

  12. (hargreaves2022diagnosticandmanagement pages 6-7): Rupen Hargreaves, Claire N Harrison, and Donal P McLornan. Diagnostic and management strategies for myeloproliferative neoplasm-unclassifiable (mpn-u): an international survey of contemporary practice. Current Research in Translational Medicine, 70:103338, Jul 2022. URL: https://doi.org/10.1016/j.retram.2022.103338, doi:10.1016/j.retram.2022.103338. This article has 6 citations and is from a peer-reviewed journal.

  13. (hargreaves2022diagnosticandmanagement pages 3-6): Rupen Hargreaves, Claire N Harrison, and Donal P McLornan. Diagnostic and management strategies for myeloproliferative neoplasm-unclassifiable (mpn-u): an international survey of contemporary practice. Current Research in Translational Medicine, 70:103338, Jul 2022. URL: https://doi.org/10.1016/j.retram.2022.103338, doi:10.1016/j.retram.2022.103338. This article has 6 citations and is from a peer-reviewed journal.

  14. (mclornan2022howimanage pages 4-5): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  15. (mclornan2022howimanage pages 7-7): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  16. (mclornan2022howimanage pages 8-9): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  17. (deschamps2021clinicopathologicalcharacterisationof pages 3-5): Paul Deschamps, Mufaddal Moonim, Deepti Radia, Natalia Curto‐Garcia, Claire Woodley, Sarah Bassiony, Jennifer O'Sullivan, Patrick Harrington, Kavita Raj, Yvonne Francis, Shahram Kordasti, Sahra Ali, Claire N. Harrison, and Donal P. McLornan. Clinicopathological characterisation of myeloproliferative neoplasm‐unclassifiable (mpn‐u): a retrospective analysis from a large uk tertiary referral centre. British Journal of Haematology, 193:792-797, Mar 2021. URL: https://doi.org/10.1111/bjh.17375, doi:10.1111/bjh.17375. This article has 19 citations and is from a domain leading peer-reviewed journal.

  18. (mclornan2022howimanage pages 5-6): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  19. (mclornan2022howimanage pages 6-7): Donal P. McLornan, Rupen Hargreaves, Juan Carlos Hernández‐Boluda, and Claire N. Harrison. How i manage myeloproliferative neoplasm‐unclassifiable: practical approaches for 2022 and beyond. British Journal of Haematology, 197:407-416, Feb 2022. URL: https://doi.org/10.1111/bjh.18087, doi:10.1111/bjh.18087. This article has 11 citations and is from a domain leading peer-reviewed journal.

  20. (deschamps2021clinicopathologicalcharacterisationof media 1f80ac50): Paul Deschamps, Mufaddal Moonim, Deepti Radia, Natalia Curto‐Garcia, Claire Woodley, Sarah Bassiony, Jennifer O'Sullivan, Patrick Harrington, Kavita Raj, Yvonne Francis, Shahram Kordasti, Sahra Ali, Claire N. Harrison, and Donal P. McLornan. Clinicopathological characterisation of myeloproliferative neoplasm‐unclassifiable (mpn‐u): a retrospective analysis from a large uk tertiary referral centre. British Journal of Haematology, 193:792-797, Mar 2021. URL: https://doi.org/10.1111/bjh.17375, doi:10.1111/bjh.17375. This article has 19 citations and is from a domain leading peer-reviewed journal.

  21. (pedersen2018smokingisassociated pages 2-3): Kasper M. Pedersen, Marie Bak, Anders L. Sørensen, Ann‐Dorthe Zwisler, Christina Ellervik, Morten K. Larsen, Hans C. Hasselbalch, and Janne S. Tolstrup. Smoking is associated with increased risk of myeloproliferative neoplasms: a general population‐based cohort study. Cancer Medicine, 7:5796-5802, Oct 2018. URL: https://doi.org/10.1002/cam4.1815, doi:10.1002/cam4.1815. This article has 47 citations and is from a peer-reviewed journal.

  22. (landtblom2018secondmalignanciesin pages 3-4): Anna Ravn Landtblom, Hannah Bower, Therese M.-L. Andersson, Paul W. Dickman, Jan Samuelsson, Magnus Björkholm, Sigurdur Yngvi Kristinsson, and Malin Hultcrantz. Second malignancies in patients with myeloproliferative neoplasms: a population-based cohort study of 9379 patients. Leukemia, 32:2203-2210, Jan 2018. URL: https://doi.org/10.1038/s41375-018-0027-y, doi:10.1038/s41375-018-0027-y. This article has 107 citations and is from a highest quality peer-reviewed journal.

  23. (pedersen2020twofoldriskof pages 1-2): Kasper Mønsted Pedersen, Yunus Çolak, Hans Carl Hasselbalch, Christina Ellervik, Børge Grønne Nordestgaard, and Stig Egil Bojesen. Two-fold risk of pneumonia and respiratory mortality in individuals with myeloproliferative neoplasm: a population-based cohort study. EClinicalMedicine, 21:100295, Apr 2020. URL: https://doi.org/10.1016/j.eclinm.2020.100295, doi:10.1016/j.eclinm.2020.100295. This article has 9 citations and is from a peer-reviewed journal.

  24. (pedersen2018smokingisassociated pages 1-2): Kasper M. Pedersen, Marie Bak, Anders L. Sørensen, Ann‐Dorthe Zwisler, Christina Ellervik, Morten K. Larsen, Hans C. Hasselbalch, and Janne S. Tolstrup. Smoking is associated with increased risk of myeloproliferative neoplasms: a general population‐based cohort study. Cancer Medicine, 7:5796-5802, Oct 2018. URL: https://doi.org/10.1002/cam4.1815, doi:10.1002/cam4.1815. This article has 47 citations and is from a peer-reviewed journal.

  25. (pedersen2018smokingisassociated pages 5-6): Kasper M. Pedersen, Marie Bak, Anders L. Sørensen, Ann‐Dorthe Zwisler, Christina Ellervik, Morten K. Larsen, Hans C. Hasselbalch, and Janne S. Tolstrup. Smoking is associated with increased risk of myeloproliferative neoplasms: a general population‐based cohort study. Cancer Medicine, 7:5796-5802, Oct 2018. URL: https://doi.org/10.1002/cam4.1815, doi:10.1002/cam4.1815. This article has 47 citations and is from a peer-reviewed journal.

  26. (gianelli2023internationalconsensusclassification pages 11-13): Umberto Gianelli, Jürgen Thiele, Attilio Orazi, Naseema Gangat, Alessandro M. Vannucchi, Ayalew Tefferi, and Hans Michael Kvasnicka. International consensus classification of myeloid and lymphoid neoplasms: myeloproliferative neoplasms. Virchows Archiv, 482:53-68, Dec 2023. URL: https://doi.org/10.1007/s00428-022-03480-8, doi:10.1007/s00428-022-03480-8. This article has 61 citations and is from a peer-reviewed journal.

  27. (gianelli2023internationalconsensusclassification pages 14-15): Umberto Gianelli, Jürgen Thiele, Attilio Orazi, Naseema Gangat, Alessandro M. Vannucchi, Ayalew Tefferi, and Hans Michael Kvasnicka. International consensus classification of myeloid and lymphoid neoplasms: myeloproliferative neoplasms. Virchows Archiv, 482:53-68, Dec 2023. URL: https://doi.org/10.1007/s00428-022-03480-8, doi:10.1007/s00428-022-03480-8. This article has 61 citations and is from a peer-reviewed journal.