2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T72d,In this study, we hypothesized that transcriptomic features among disease-driving hematopoietic stem and progenitor cells (HSPC) could improve current paradigms for risk stratification in myelofibrosis (MF). Therefore, we performed bulk RNA sequencing (RNA-seq) of blood from 358 patients with MF, split into training and test cohorts. Single-cell RNA-seq data from Lin-CD34+ MF HSPCs were used to guide the development of a prognostic model trained on the bulk RNA-seq data. A NanoString assay was used to validate our final model in 2 independent cohorts of patients with MF. We identified a 24-gene weighted-sum expression score (MPN24) that was prognostic of overall survival (OS). In 2 independent cohorts of 170 and 100 patients with MF, MPN24-high scoring patients had worse 5-year OS compared with MPN24-low scoring patients (25.5% vs 86.9%, hazard ratio [HR] = 9.81, P = 4.0e-11 and 23.5% vs 75.9%, HR, 6.40, P = 1.8e-7, respectively). MPN24-high was also associated with clinical, mutation and karyotypic features known to confer adverse risk in MF. The MPN24 score retained independent prognostic significance in multivariable analysis incorporating these covariates and existing risk stratification models including Dynamic International Prognostic Scoring System (DIPSS), DIPSS plus, Mutation-Enhanced International Prognostic Score System (MIPSS70), and MIPSS70 plus version 2.0, adding significant prognostic value to these risk stratification models (P = 1.6e-5, 4.0e-6, 1.5e-6, and 5.4e-4, respectively). The MPN24 score was particularly useful in improving risk-stratification of DIPSS-intermediate, and MIPSS70-intermediate and high-risk patients. MPN24 is an HSPC-derived gene expression score that is associated with OS independent of clinical and genomic prognostic variables and improves risk stratification in MF.31:T7bf, Abstract In this study, we hypothesized that transcriptomic features among disease-driving hematopoietic stem and progenitor cells (HSPC) could improve current paradigms for risk stratification in myelofibrosis (MF). Therefore, we performed bulk RNA sequencing (RNA-seq) of blood from 358 patients with MF, split into training and test cohorts. Single-cell RNA-seq data from Lin–CD34+ MF HSPCs were used to guide the development of a prognostic model trained on the bulk RNA-seq data. A NanoString assay was used to validate our final model in 2 independent cohorts of patients with MF. We identified a 24-gene weighted-sum expression score (MPN24) that was prognostic of overall survival (OS). In 2 independent cohorts of 170 and 100 patients with MF, MPN24-high scoring patients had worse 5-year OS compared with MPN24-low scoring patients (25.5% vs 86.9%, hazard ratio [HR] = 9.81, P = 4.0e−11 and 23.5% vs 75.9%, HR, 6.40, P = 1.8e−7, respectively). MPN24-high was also associated with clinical, mutation and karyotypic features known to confer adverse risk in MF. The MPN24 score retained independent prognostic significance in multivariable analysis incorporating these covariates and existing risk stratification models including Dynamic International Prognostic Scoring System (DIPSS), DIPSS plus, Mutation-Enhanced International Prognostic Score System (MIPSS70), and MIPSS70 plus version 2.0, adding significant prognostic value to these risk stratification models (P = 1.6e−5, 4.0e−6, 1.5e−6, and 5.4e−4, respectively). The MPN24 score was particularly useful in improving risk-stratification of DIPSS-intermediate, and MIPSS70-intermediate and high-risk patients. MPN24 is an HSPC-derived gene expression score that is associated with OS independent of clinical and genomic prognostic variables and improves risk stratification in MF. 32:T5d7,Somatic frameshift mutations in the gene encoding calreticulin (CALR) give rise to myelofibrosis and are classified as Type 1 (del52) or Type 2 (ins5) according to the degree of wildtype sequence retained adjacent to the neopeptide, with each type conferring different clinical outcomes. Targeting strategies specific for Type 1 vs Type 2 mutations would have enormous clinical utility in the treatment and prevention of myelofibrosis as responses to tyrosine kinase inhibitors are not durable nor mutation-specific. Here we show that dual targeting of Type 1 (del52) mutant CALR with two monoclonal antibodies directed against distinct epitopes in CALR have significant advantages compared to single agent treatment in the eradication of primary megakaryocyte progenitors in vitro and in a humanized ossicle microenvironment leading to improved survival in xenograft models. Dual targeting was superior in blocking constitutive STAT5 and ERK phosphorylation induced by del52 and prevented accumulation of JAK2 phosphorylation, overcoming ruxolitinib resistance. In contrast, Type 2 mutations showed increased CALR dimerization and were partially resistant to antibody targeting but could be impacted by ruxolitinib triple combination. Together, our data demonstrate an ultra-precision medicine approach tailored to either Type 1 OR Type 2 mutation classes will be required for maximal efficacy and complete blockade of JAK/STAT signalling, with far-reaching implications for patient management.33:T5e8,Somatic frameshift mutations in the gene encoding calreticulin (CALR) give rise to myelofibrosis and are classified as Type 1 (del52) or Type 2 (ins5) according to the degree of wildtype sequence retained adjacent to the neopeptide, with each type conferring different clinical outcomes. Targeting strategies specific for Type 1 vs Type 2 mutations would have enormous clinical utility in the treatment and prevention of myelofibrosis as responses to tyrosine kinase inhibitors are not durable nor mutation-specific. Here we show that dual targeting of Type 1 (del52) mutant CALR with two monoclonal antibodies directed against distinct epitopes in CALR have significant advantages compared to single agent treatment in the eradication of primary megakaryocyte progenitors in vitro and in a humanized ossicle microenvironment leading to improved survival in xenograft models. Dual targeting was superior in blocking constitutive STAT5 and ERK phosphorylation induced by del52 and prevented accumulation of JAK2 phosphorylation, overcoming ruxolitinib resistance. In contrast, Type 2 mutations showed increased CALR dimerization and were partially resistant to antibody targeting but could be impacted by ruxolitinib triple combination. Together, our data demonstrate an ultra-precision medicine approach tailored to either Type 1 OR Type 2 mutation classes will be required for maximal efficacy and complete blockade of JAK/STAT signalling, with far-reaching implications for patient management.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Myeloproliferative Neoplasm: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Myeloproliferative Neoplasm (condition). Clinician-written summaries and actionable practice insights. Updated daily.\",\"url\":\"https://www.reachrx.ai/hub/tag/condition/Myeloproliferative%20Neoplasm\",\"breadcrumb\":{\"@type\":\"BreadcrumbList\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https://www.reachrx.ai\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Research Hub\",\"item\":\"https://www.reachrx.ai/hub\"},{\"@type\":\"ListItem\",\"position\":3,\"name\":\"Conditions\",\"item\":\"https://www.reachrx.ai/hub/tag/condition\"},{\"@type\":\"ListItem\",\"position\":4,\"name\":\"Myeloproliferative Neoplasm\",\"item\":\"https://www.reachrx.ai/hub/tag/condition/Myeloproliferative%20Neoplasm\"}]}}"}}]],["$","$L2f",null,{"title":"Myeloproliferative Neoplasm: Research & Clinical Takeaways","description":"Discover peer-reviewed research on Myeloproliferative Neoplasm with concise clinician summaries and next-step guidance.","papers":[{"doi":"10.1182/blood.2025032631","pmid":"42345360","title":"Galectin-1 Fuels Monocyte Hyperinflammation and Represents a Novel Therapeutic Target in Myeloproliferative Neoplasms","journal_title":"Blood Journal","journal_issn":"0006-4971","published_at":"2026-06-23T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025032631","source_score":8,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-29T13:22:48.475Z","updated_at":"2026-06-29T13:22:48.475Z","tags":[{"paper_doi":"10.1182/blood.2025032631","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"brand","value":"OTX008","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"condition","value":"Essential Thrombocythemia","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"condition","value":"Myelofibrosis","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"condition","value":"Myeloproliferative Neoplasm","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"condition","value":"Polycythemia Vera","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"generic","value":"galectin-1 inhibitor OTX008","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"modality","value":"Galectin Inhibitor","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"sample_size","value":"n=34","value_numeric":34},{"paper_doi":"10.1182/blood.2025032631","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"study_design","value":"Translational Study (scRNA-seq, CyTOF, In Vitro, In Vivo Mouse Model)","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"warning","value":"Sample size for human plasma ELISA (n=34 MPN, n=7 HI) is small; subgroup analyses by MPN subtype (PV n=8, ET n=13, MF n=13) are underpowered.","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"warning","value":"Study design is predominantly preclinical and translational; no randomized clinical trial data are included — 'practice_changing' impact flag reflects novelty of therapeutic target, not clinical trial evidence.","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"warning","value":"Study design tag reflects a multi-method translational study; no single canonical design label applies cleanly.","value_numeric":null},{"paper_doi":"10.1182/blood.2025032631","tag_type":"warning","value":"TLR4–Gal-1 protein interaction is inferred by computational docking and co-immunoprecipitation only; direct structural confirmation is lacking.","value_numeric":null}],"summaries":{"what_studied":"This study investigated the role of galectin-1 (Gal-1/LGALS1) in monocyte-driven inflammation in myeloproliferative neoplasms (MPNs), using scRNA-seq, CyTOF, and functional assays in human MPN samples (n=34 patients) and a MPLW515L murine transplant model, with Lgals1 genetic knockout and pharmacological inhibition (OTX008).","key_result":"Gal-1 was elevated in MPN monocytes and plasma (vs. healthy controls, n=7 HI vs. n=34 MPN by ELISA); recombinant Gal-1 markedly increased inflammatory cytokine transcription and secretion in CD14+ MPN monocytes via TLR4/NF-κB signaling; Lgals1 knockout in the MPLW515L mouse model ameliorated leukocytosis and splenomegaly, and Gal-1 inhibition suppressed carrageenan-induced thrombosis and inflammation in vivo.","limitations":"- Murine MPLW515L transplant model may not fully recapitulate human MPN biology.\n- Human cohort is relatively small (n=34 MPN), limiting generalizability across MPN subtypes and mutational contexts.\n- Mechanistic TLR4–Gal-1 interaction is supported by computational docking and co-immunoprecipitation but lacks structural confirmation (e.g., crystallography).","practice_takeaway":"Gal-1 drives monocyte hyperinflammation in MPNs through TLR4/NF-κB signaling and may represent a druggable target; the Gal-1 inhibitor OTX008 warrants clinical investigation in MPN, particularly for patients with high monocyte counts or inflammatory burden."}},{"doi":"10.1182/blood.2026033951","pmid":"42233405","title":"Type I interferon-activated NK cells control polycythemia vera in vivo","journal_title":"Blood Journal","journal_issn":"0006-4971","published_at":"2026-06-02T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2026033951","source_score":21,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:24:31.500Z","updated_at":"2026-06-10T14:24:31.500Z","tags":[{"paper_doi":"10.1182/blood.2026033951","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"condition","value":"Essential Thrombocythemia","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"condition","value":"Myeloproliferative Neoplasm","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"condition","value":"Polycythemia Vera","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"generic","value":"interferon alfa","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"modality","value":"Interferon","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"modality","value":"NK Cell Therapy","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"study_design","value":"Translational Study (In Vivo/In Vitro with Patient Cohort)","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"warning","value":"Study design label is non-standard — the paper combines in vivo animal work, in vitro experiments, and a patient cohort, which does not map cleanly to a single canonical design category.","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"warning","value":"Study design mixes transgenic mouse model data with a human patient cohort; the relative weight of each is unclear from the abstract alone. Patient sample sizes and follow-up duration are not reported in the abstract.","value_numeric":null},{"paper_doi":"10.1182/blood.2026033951","tag_type":"warning","value":"The 'practice_changing' impact flag is assigned based on novel mechanistic findings and a proposed biomarker; clinical validation in larger prospective cohorts has not yet been performed.","value_numeric":null}],"summaries":{"what_studied":"This study investigated the role of NK cells as immune effectors of IFN-α therapy in polycythemia vera (PV), using a transgenic mouse model of PV and patients with PV or ET on IFN-α therapy, examining NK cell expansion, killing of JAK2V617F mutant HSPCs, and disease control in vivo.","key_result":"IFN-α expanded CD27+ NK cells in mouse bone marrow and CD56bright NK cells in patients, with NK cell frequency correlating with molecular response; NK cell depletion abolished IFN-α's therapeutic effect, and NK cells preferentially killed JAK2V617F mutant HSPCs via TNF-α (independent of IFN-γ or NKG2D); mice lacking NK cells or type-I IFN receptor on NK cells showed accelerated disease progression even without exogenous IFN-α.","limitations":"Mechanistic killing data are primarily from in vitro experiments, which may not fully recapitulate the in vivo bone marrow niche; the patient cohort includes both PV and ET, which are distinct disease entities; the specific patient numbers and follow-up duration are not reported in the abstract.","practice_takeaway":"Monitoring CD56bright NK cell frequency may serve as a pharmacodynamic biomarker of IFN-α response in PV and ET. Strategies to activate or expand NK cells could be explored to enhance or complement IFN-α therapy in myeloproliferative neoplasms."}},{"doi":"10.1182/bloodadvances.2025019152","pmid":"41779966","title":"Low serum cholesterol is a biomarker of advanced disease and poor outcomes in myeloproliferative neoplasms","journal_title":"Blood Advances","journal_issn":"2473-9529","published_at":"2026-05-26T00:00:00.000Z","url":"https://doi.org/10.1182/bloodadvances.2025019152","source_score":9,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-31T13:35:46.502Z","updated_at":"2026-05-31T13:35:46.502Z","tags":[{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"condition","value":"Essential Thrombocythemia","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"condition","value":"Myelofibrosis","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"condition","value":"Myeloproliferative Neoplasm","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"condition","value":"Polycythemia Vera","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"generic","value":"hydroxyurea","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"generic","value":"ruxolitinib","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"modality","value":"Biomarker (Serum Cholesterol)","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"sample_size","value":"n=305","value_numeric":305},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"warning","value":"Median age was 69 years with 82.6% White patients from 3 academic centers in the US, which may limit generalizability to more diverse or community-based MPN populations.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"warning","value":"Patients on statins were excluded entirely — this improves cholesterol measurement validity but means findings cannot be applied to statin users, who represent a significant portion of the MPN population.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019152","tag_type":"warning","value":"The MF subgroup analysis (n=87) was likely underpowered; null findings in MF should not be interpreted as absence of effect. The ET/PV results drive the main conclusions.","value_numeric":null}],"summaries":{"what_studied":"This multicenter retrospective cohort study examined whether serum total cholesterol level (categorized as ≥150, 120–149, or <120 mg/dL) predicts MPN disease progression, major adverse cardiovascular events (MACE), and all-cause mortality in 305 adults with ET, PV, or MF who were not on statin therapy, over a median follow-up of 50.8 months.","key_result":"Total cholesterol <120 mg/dL was independently associated with 3× higher risk of MPN disease progression (aSHR 3.00; 95% CI 1.36–6.63), nearly 4× higher risk of heart failure hospitalization (aSHR 3.76; 95% CI 1.77–7.96), and ~2× higher all-cause mortality (aHR 1.87; 95% CI 1.06–3.30) vs. cholesterol ≥150 mg/dL; the association was strongest in ET/PV patients, not statistically significant in the MF subgroup (likely underpowered, n=87).","limitations":"- Retrospective design with selection bias: only MPN patients who underwent TTE were included, enriching for higher CV risk than the general MPN population.\n- Statin users were excluded, limiting generalizability and preventing assessment of statin effects on outcomes.\n- The MF subgroup was small (n=87), leaving MF-specific analyses underpowered.","practice_takeaway":"In MPN patients not on statins, a total cholesterol <120 mg/dL may signal advanced, high-risk disease and warrant closer monitoring for disease progression and heart failure — consider it a red-flag biomarker alongside spleen size and NLR. Clinicians should also continue to follow guideline-directed statin initiation given the elevated CVD risk in MPN, as prior data suggest potential benefit."}},{"doi":"10.1182/blood.2025030094","pmid":"41481381","title":"A stem and progenitor cell–derived gene expression signature is prognostic for survival in myelofibrosis","journal_title":"Blood","journal_issn":"0006-4971","published_at":"2026-01-02T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025030094","source_score":12,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-12","doi":"10.1182/blood.2025030094","days":"7","issn":"0006-4971","rank":"5","field":"Clinical Medicine","score":"12","category":"Hematology","categories":["Hematology"],"_categories":["Hematology"]},"pubmed":{"doi":"10.1182/blood.2025030094","title":"A stem and progenitor cell-derived gene expression signature is prognostic for survival in myelofibrosis.","journal":"Blood","methods":"","results":"","abstract":"$30","keywords":[],"pubmed_id":"41481381","conclusions":"","publication_date":"2026-01-02T00:00:00"},"crossref":{"DOI":"10.1182/blood.2025030094","URL":"https://doi.org/10.1182/blood.2025030094","ISSN":["0006-4971","1528-0020"],"link":[{"URL":"https://ashpublications.org/blood/article-pdf/147/19/2238/2517431/blood_bld-2025-030094-main.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https://ashpublications.org/blood/article-pdf/147/19/2238/2517431/blood_bld-2025-030094-main.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"2238-2251","type":"journal-article","issue":"19","score":1,"title":["A stem and progenitor cell–derived gene expression signature is prognostic for survival in myelofibrosis"],"author":[{"given":"Jessie J. F.","family":"Medeiros","sequence":"first","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"},{"name":"2Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada"}]},{"given":"Andy G. X.","family":"Zeng","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"},{"name":"2Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada"}]},{"given":"Suraj","family":"Bansal","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Hyerin","family":"Kim","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Michelle","family":"Chan-Seng-Yue","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Tristan","family":"Woo","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Jessica L.","family":"McLeod","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Sagar","family":"Kothari","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Andrea","family":"Arruda","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Hubert","family":"Tsui","sequence":"additional","affiliation":[{"name":"3Division of Hematological Pathology, Department of Laboratory Medicine and Molecular Diagnostics, Precision Diagnostics and Therapeutics Program, Sunnybrook Health Sciences Centre, Toronto, ON, Canada"},{"name":"4Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada"},{"name":"5Department of Laboratory Medicine and Pathobiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada"},{"name":"6Department of Immunology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada"}]},{"given":"Jaime O.","family":"Claudio","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Dawn","family":"Maze","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Hassan","family":"Sibai","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"}]},{"given":"Mark D.","family":"Minden","sequence":"additional","affiliation":[{"name":"1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada"},{"name":"7Medical Oncology and Hematology, University Health Network, Toronto, ON, Canada"},{"name":"8Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, ON, Canada"}]},{"given":"James A.","family":"Kennedy","sequence":"additional","affiliation":[{"name":"8Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, ON, Canada"},{"name":"9Medical Oncology and Hematology, Sunnybrook Health Sciences Centre, Toronto, ON, Canada"}]},{"given":"Christopher","family":"Famulare","sequence":"additional","affiliation":[{"name":"10Center for Hematologic Malignancies, Memorial Sloan Kettering Cancer Center, New York, NY"}]},{"given":"Raajit K.","family":"Rampal","sequence":"additional","affiliation":[{"name":"11Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY"}]},{"given":"Jean C. 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The score remained independently prognostic and added value beyond DIPSS, DIPSS plus, MIPSS70, and MIPSS70+ v2.0 (P=1.6e‑5, 4.0e‑6, 1.5e‑6, 5.4e‑4).","practice_takeaway":"Use the NanoString‑based MPN24 score alongside existing MF risk models to refine survival risk, particularly for DIPSS‑intermediate and MIPSS70‑intermediate/high categories."}},{"doi":"10.1182/blood.2024027897","pmid":"41481383","title":"Ultraprecision Therapy for Type 1 vs Type 2 CALR+ MPN by Dual Epitope Targeting that Restores Ruxolitinib Sensitivity","journal_title":"Blood Journal","journal_issn":"0006-4971","published_at":"2026-01-02T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2024027897","source_score":24,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-05","doi":"10.1182/blood.2024027897","days":"14","issn":"0006-4971","rank":"9","field":"Clinical 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Sensitivity.","journal":"Blood","methods":"","results":"","abstract":"$32","keywords":[],"pubmed_id":"41481383","conclusions":"","publication_date":"2026-01-02T00:00:00"},"crossref":{"DOI":"10.1182/blood.2024027897","URL":"https://doi.org/10.1182/blood.2024027897","ISSN":["0006-4971","1528-0020"],"link":[{"URL":"https://ashpublications.org/blood/article-pdf/doi/10.1182/blood.2024027897/2478889/blood.2024027897.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https://ashpublications.org/blood/article-pdf/doi/10.1182/blood.2024027897/2478889/blood.2024027897.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Ultraprecision Therapy for Type 1 vs Type 2 CALR+ MPN by Dual Epitope Targeting that Restores Ruxolitinib Sensitivity"],"author":[{"given":"Chloe AL","family":"Thompson-Peach","sequence":"first","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Daniel","family":"Thomas","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Mara","family":"Dottore","sequence":"additional","affiliation":[{"name":"SA Pathology, Adelaide, SA, Australia"}]},{"given":"Kelly","family":"Lim","sequence":"additional","affiliation":[{"name":"University of Adelaide, Adelaide, Australia"}]},{"given":"Frank","family":"Stomski","sequence":"additional","affiliation":[{"name":"University of South Australia, Adelaide, Australia"}]},{"given":"Romana","family":"Panagopoulos","sequence":"additional","affiliation":[{"name":"University of Adelaide"}]},{"given":"Johannes","family":"Foßelteder","sequence":"additional","affiliation":[{"name":"Medical University of Graz, Graz, Austria"}]},{"given":"Andreas","family":"Reinisch","sequence":"additional","affiliation":[{"name":"Medical University of Graz, Graz, Austria"}]},{"given":"Vashe","family":"Chandrakanthan","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Sandra","family":"Jenkner","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Luke","family":"Bland","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Sharon","family":"Paton","sequence":"additional","affiliation":[{"name":"University of Adelaide, Adelaide, Australia"}]},{"given":"Stan","family":"Gronthos","sequence":"additional","affiliation":[{"name":"University of Adelaide, Adelaide, SA, Australia"}]},{"given":"Timothy","family":"Hercus","sequence":"additional","affiliation":[{"name":"Centre for Cancer Biology, SA Pathology, Adelaide, Australia"}]},{"given":"Hannah","family":"Wardill","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Winnie L","family":"Kan","sequence":"additional","affiliation":[{"name":"University of South Australia and SA Pathology, Adelaide, Australia"}]},{"given":"Maha","family":"Kamel","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Paul A","family":"Moretti","sequence":"additional","affiliation":[{"name":"University of South Australia and SA Pathology, Adelaide, Australia"}]},{"given":"Stuart M","family":"Pitson","sequence":"additional","affiliation":[{"name":"University of South Australia and SA Pathology, Adelaide, Australia"}]},{"given":"Kate","family":"Burbury","sequence":"additional","affiliation":[{"name":"Peter MacCallum Cancer Centre, Melbourne, Australia"}]},{"given":"David Morrall","family":"Ross","sequence":"additional","affiliation":[{"name":"SA Pathology, Adelaide, Australia"}]},{"given":"Pramod","family":"Nair","sequence":"additional","affiliation":[{"name":"The University of Adelaide, Adelaide, Australia"}]},{"given":"Angel F.","family":"Lopez","sequence":"additional","affiliation":[{"name":"Centre for Cancer Biology, SA Pathology, Adelaide, SA, Australia"}]},{"given":"Denis","family":"Tvorogov","sequence":"additional","affiliation":[{"name":"University of South Australia and SA Pathology, Adelaide, Australia"}]}],"issued":{"date-parts":[[2026,1,2]]},"member":"234","prefix":"10.1182","source":"Crossref","volume":null,"created":{"date-time":"2026-01-02T17:17:03Z","timestamp":1767374223000,"date-parts":[[2026,1,2]]},"indexed":{"date-time":"2026-01-02T17:25:42Z","timestamp":1767374742979,"date-parts":[[2026,1,2]]},"subject":[],"abstract":"$33","language":"en","relation":{},"resource":{"primary":{"URL":"https://ashpublications.org/blood/article/doi/10.1182/blood.2024027897/557584/Ultraprecision-Therapy-for-Type-1-vs-Type-2-CALR"}},"subtitle":[],"deposited":{"date-time":"2026-01-02T17:17:03Z","timestamp":1767374223000,"date-parts":[[2026,1,2]]},"issn-type":[{"type":"print","value":"0006-4971"},{"type":"electronic","value":"1528-0020"}],"published":{"date-parts":[[2026,1,2]]},"publisher":"American Society of 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Sensitivity","updated":"2026-01-03T00:50:51+00:00","published_date":"2026-01-02","best_oa_location":null}},"created_at":"2026-01-15T20:51:27.064Z","updated_at":"2026-01-17T09:03:27.421Z","tags":[{"paper_doi":"10.1182/blood.2024027897","tag_type":"brand","value":"Jakafi","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"condition","value":"Myeloproliferative Neoplasm","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"generic","value":"ruxolitinib","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"modality","value":"Monoclonal Antibody","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"study_design","value":"Preclinical Study","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"warning","value":"Evidence is preclinical only; no human outcomes are reported.","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"warning","value":"No quantitative data (effect sizes, sample sizes, or timeframes) are provided in the abstract.","value_numeric":null},{"paper_doi":"10.1182/blood.2024027897","tag_type":"warning","value":"Study design classification is approximate for a preclinical mechanistic study.","value_numeric":null}],"summaries":{"what_studied":"Evaluated dual-epitope monoclonal antibody targeting of Type 1 (del52) CALR versus single-antibody therapy, with and without ruxolitinib, across in vitro assays, a humanized ossicle microenvironment, and xenograft models; Type 2 (ins5) CALR responses were also examined.","key_result":"Dual targeting surpassed single antibody by eradicating primary megakaryocyte progenitors in vitro and in the humanized ossicle setting and improved survival in xenografts; it more completely blocked constitutive STAT5/ERK signaling, prevented JAK2 phosphorylation buildup, and restored ruxolitinib sensitivity. Type 2 mutations showed increased CALR dimerization with partial resistance to antibody targeting but were affected by a triple combination including ruxolitinib.","limitations":"Findings are limited to in vitro and xenograft models with no human clinical outcomes. The abstract reports no numerical effect sizes, sample sizes, or timeframes."}}],"initialOffset":5,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Myeloproliferative Neoplasm"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Myeloproliferative Neoplasm"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Myeloproliferative Neoplasm"}}}]]

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