{"entity":{"id":"myeloproliferative-neoplasms","kind":"cancer","name":"Myeloproliferative neoplasms (PV, ET, myelofibrosis)","aka":["MPN","Polycythaemia vera","Essential thrombocythaemia","Primary myelofibrosis"],"tldr":"Myeloproliferative neoplasms are slow-growing blood cancers in which the marrow overproduces red cells (polycythaemia vera), platelets (essential thrombocythaemia) or scar tissue (myelofibrosis). Almost all carry a mutation in JAK2, CALR or MPL; treatment aims to prevent clots and control symptoms, and only transplant cures myelofibrosis.","summary":"The classical BCR-ABL1-negative MPNs (polycythaemia vera, essential thrombocythaemia, primary myelofibrosis) are clonal diseases driven by JAK-STAT activation: JAK2 V617F in ~95% of PV and ~60% of ET/PMF, CALR in ~25% of ET/PMF, MPL in ~5%. Risk in PV/ET is thrombosis (managed with aspirin, phlebotomy, hydroxyurea or interferon); in myelofibrosis it is cytopenias, splenomegaly, constitutional symptoms and leukaemic transformation (about 10-20%), risk-scored by DIPSS-plus, MIPSS70 and MIPSS70+ v2.0.\n\nRuxolitinib (COMFORT-I/II, 2011) was the first JAK inhibitor; fedratinib (2019), pacritinib (2022, for platelets <50) and momelotinib (2023, for anaemic patients) followed. None is disease-modifying: allogeneic transplant remains the only cure for myelofibrosis. Ropeginterferon alfa-2b (2021) is the first approved interferon for PV with evidence of molecular response, and rusfertide (2026), a hepcidin mimetic, is the first drug to control PV erythrocytosis without phlebotomy (VERIFY). CALR-directed antibodies and JAK2 V617F-selective inhibitors are the disease-modifying hope; pelabresib (BET inhibitor) plus ruxolitinib improved spleen response but not symptoms in MANIFEST-2.","asOf":"2026-09-08","wikipedia":"https://en.wikipedia.org/wiki/Myeloproliferative_neoplasm","links":[{"label":"NCCN Guidelines: MPN","url":"https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1477"},{"label":"NCI PDQ: chronic MPN","url":"https://www.cancer.gov/types/myeloproliferative/patient/chronic-treatment-pdq"},{"label":"MPN Research Foundation","url":"https://www.mpnresearchfoundation.org/"}],"tags":["gap-fill","haematologic"],"related":[],"cancers":[],"sections":[],"technologies":["kinase-inhibitors","allogeneic-hsct","cytokine-therapy","ngs-mrd-clonoseq"],"targets":["jak2","bcl2"],"drugs":["ruxolitinib","fedratinib","pacritinib","momelotinib","hydroxyurea","ropeginterferon-alfa-2b","rusfertide","luspatercept","anagrelide"],"companies":["novartis","bms","gsk","incyte"],"institutions":[],"pathways":["pi3k-akt-mtor"],"terms":["eln-risk"],"trials":["nct06093672","nct06351631","nct04468984","nct06468033","nct04717414","nct04562389","verify","nct07429266","nct05481151","nct06033586","nct04064060","impactmf","nct04285086","nct04655092"],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"group":"haematologic","burden":"Combined incidence around 2-3 per 100,000 per year; PV and ET are chronic diseases lived with for decades, myelofibrosis has a median survival of about six years.","subtypes":["Polycythaemia vera (PV)","Essential thrombocythaemia (ET)","Prefibrotic and overt primary myelofibrosis (PMF)","Post-PV / post-ET myelofibrosis","MPN in blast phase","Triple-negative MPN"],"biomarkers":["JAK2 V617F and exon 12","CALR type 1/2","MPL W515","High-molecular-risk mutations (ASXL1, EZH2, SRSF2, IDH1/2, U2AF1)","DIPSS-plus / MIPSS70+ v2.0","Haematocrit target <45% (CYTO-PV)","Platelet count (pacritinib eligibility)"],"standardOfCare":[{"setting":"PV","approach":"Low-dose aspirin, phlebotomy to haematocrit <45%; cytoreduction (hydroxyurea or ropeginterferon alfa-2b) for high-risk; ruxolitinib after hydroxyurea failure (RESPONSE); rusfertide to eliminate phlebotomy need (VERIFY, 2026).","refs":["hydroxyurea","ropeginterferon-alfa-2b","ruxolitinib","rusfertide"],"guideline":{"nccn":"Category 1 (ropeginterferon, hydroxyurea)","version":"NCCN Guidelines: MPN","url":"https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1477"}},{"setting":"ET","approach":"Risk-adapted (IPSET-thrombosis): observation or aspirin in low risk; hydroxyurea or interferon in high risk; anagrelide second line.","refs":["hydroxyurea","ropeginterferon-alfa-2b"],"guideline":{"version":"NCCN Guidelines: MPN"}},{"setting":"Myelofibrosis, intermediate-2/high risk","approach":"JAK inhibitor for spleen and symptoms: ruxolitinib (COMFORT), fedratinib, pacritinib if platelets <50×10⁹/L, momelotinib if anaemic (MOMENTUM); allogeneic HSCT for eligible patients (the only cure).","refs":["ruxolitinib","fedratinib","pacritinib","momelotinib","allogeneic-hsct","comfort-i","comfort-ii"],"guideline":{"nccn":"Category 1 (ruxolitinib, fedratinib); 2A (pacritinib, momelotinib)","version":"NCCN Guidelines: MPN"}},{"setting":"Anaemia of myelofibrosis","approach":"Momelotinib, luspatercept (INDEPENDENCE), ESA, danazol, transfusion.","refs":["momelotinib","luspatercept"]}],"stateOfArt":["Four approved JAK inhibitors cover spleen, symptoms, thrombocytopenia and anaemia, but none reverses fibrosis or clears the clone.","Interferon is the only drug with consistent molecular responses in PV/ET, and ropeginterferon made it practical.","Rusfertide (2026) is the first mechanistically new PV drug in a decade and removes the need for phlebotomy in most patients.","The next wave targets the clone itself: mutant-CALR antibodies (e.g. INCA033989), JAK2 V617F-selective inhibitors, and navitoclax/pelabresib combinations with mixed phase 3 results."],"history":[{"year":1951,"title":"Dameshek groups the MPNs","note":"Proposes that PV, ET, CML and myelofibrosis are related myeloproliferative disorders.","refs":[]},{"year":2005,"title":"JAK2 V617F discovered","note":"Four groups report the mutation in most PV and half of ET/PMF; the first molecular marker for BCR-ABL1-negative MPN.","refs":["jak2"]},{"year":2011,"title":"Ruxolitinib approved","note":"COMFORT-I/II: spleen and symptom benefit in myelofibrosis; the first JAK inhibitor.","refs":["ruxolitinib"]},{"year":2013,"title":"CALR mutations","note":"Klampfl and Nangalia find CALR exon 9 mutations in most JAK2-negative ET/PMF.","refs":[]},{"year":2013,"title":"Haematocrit target proven","note":"CYTO-PV: keeping haematocrit <45% cuts cardiovascular death and major thrombosis in PV.","refs":[]},{"year":2019,"title":"Fedratinib approved","note":"JAKARTA; the second JAK inhibitor after an eight-year gap.","refs":["fedratinib"]},{"year":2021,"title":"Ropeginterferon alfa-2b approved for PV","note":"PROUD/CONTINUATION-PV: superior long-term haematologic and molecular response versus hydroxyurea.","refs":["ropeginterferon-alfa-2b"]},{"year":2022,"title":"Pacritinib for severe thrombocytopenia","refs":["pacritinib"]},{"year":2023,"title":"Momelotinib for anaemic myelofibrosis","note":"MOMENTUM: symptom, spleen and transfusion-independence benefit versus danazol.","refs":["momelotinib"]},{"year":2026,"title":"Rusfertide approved for PV","note":"VERIFY: hepcidin mimetic controls erythrocytosis without phlebotomy; FDA approval August 2026.","refs":["rusfertide"]}],"pipeline":["rusfertide","momelotinib","luspatercept","allogeneic-hsct","givinostat","bomedemstat","navitoclax","krt-232","flonoltinib","jbi-802"],"openProblems":["No disease-modifying therapy in myelofibrosis short of transplant.","MPN in blast phase: outcomes as poor as secondary AML.","Whether interferon-induced molecular response prevents progression.","Sequencing and combining JAK inhibitors with BET, BCL-XL or CALR-directed agents."]},"route":"/cancers/myeloproliferative-neoplasms/","neighbours":{"technology":[{"id":"allogeneic-hsct","kind":"technology","name":"Allogeneic stem cell transplantation","route":"/technologies/allogeneic-hsct/"},{"id":"cytokine-therapy","kind":"technology","name":"Cytokines & engineered 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