{"entity":{"id":"dipss-mipss70","kind":"term","name":"DIPSS, DIPSS-plus and MIPSS70 (myelofibrosis risk scores)","aka":["DIPSS","DIPSS-plus","IPSS for myelofibrosis","MIPSS70","MIPSS70-plus","MIPSS70+ v2","MIPSS70-plus version 2","GIPSS","MYSEC-PM","high-molecular-risk mutations","HMR mutations","myelofibrosis risk score","intermediate-2 myelofibrosis","high-risk myelofibrosis"],"tldr":"Myelofibrosis risk scores decide the biggest question in the disease, whether to go for a stem-cell transplant: DIPSS uses age, blood counts, blasts and symptoms, DIPSS-plus adds chromosomes, transfusions and platelets, and MIPSS70 adds the mutations that mark a dangerous clone.","summary":"What is measured: expected survival in primary myelofibrosis, and so the case for a transplant. How: IPSS (2009, at diagnosis) and DIPSS (dynamic, at any time) score age over 65, haemoglobin under 100 g/L, white cells over 25, circulating blasts of 1 percent or more and constitutional symptoms; DIPSS-plus adds an unfavourable karyotype, platelets under 100 and transfusion dependence, giving low, intermediate-1, intermediate-2 and high risk with median survivals of about 15, 6.5, 3 and 1.3 years. MIPSS70, for transplant-age patients, adds high-molecular-risk mutations (ASXL1, SRSF2, EZH2, IDH1, IDH2, U2AF1 Q157), the absence of a type 1 CALR mutation, two or more such mutations and marrow fibrosis grade 2 or more; MIPSS70-plus version 2 adds a very-high-risk karyotype and sex-adjusted haemoglobin; GIPSS is genetics only, and MYSEC-PM serves myelofibrosis after polycythaemia vera or essential thrombocythaemia. Inputs: blood count and film, marrow biopsy with fibrosis grade, karyotype and a myeloid sequencing panel. What a result changes: intermediate-2 or high risk in a fit patient is the indication for allogeneic transplant, the only cure; lower-risk disease is watched or treated for symptoms and spleen with JAK inhibitors (ruxolitinib, fedratinib, pacritinib when platelets are low, momelotinib when anaemic); the scores set trial entry. Where it matters: primary myelofibrosis.","asOf":"2026-09-17","links":[],"tags":[],"related":["mpn-driver-mutations","cytogenetics","blasts","performance-status","allogeneic-transplant","ruxolitinib","fedratinib","pacritinib","momelotinib"],"cancers":["primary-myelofibrosis"],"sections":[],"technologies":[],"targets":[],"drugs":[],"companies":[],"institutions":[],"pathways":[],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"category":"Biomarkers"},"route":"/terms/dipss-mipss70/","neighbours":{"term":[{"id":"allogeneic-transplant","kind":"term","name":"Allogeneic stem cell transplant (allo-SCT)","route":"/terms/allogeneic-transplant/"},{"id":"blasts","kind":"term","name":"Blasts (leukaemic blast cells)","route":"/terms/blasts/"},{"id":"cytogenetics","kind":"term","name":"Cytogenetics and karyotype","route":"/terms/cytogenetics/"},{"id":"mpn-driver-mutations","kind":"term","name":"MPN driver mutations (JAK2 V617F, CALR, MPL) and allele burden","route":"/terms/mpn-driver-mutations/"},{"id":"performance-status","kind":"term","name":"Performance status (ECOG, Karnofsky)","route":"/terms/performance-status/"}],"drug":[{"id":"fedratinib","kind":"drug","name":"Fedratinib","route":"/drugs/fedratinib/"},{"id":"momelotinib","kind":"drug","name":"Momelotinib","route":"/drugs/momelotinib/"},{"id":"pacritinib","kind":"drug","name":"Pacritinib","route":"/drugs/pacritinib/"},{"id":"ruxolitinib","kind":"drug","name":"Ruxolitinib","route":"/drugs/ruxolitinib/"}],"cancer":[{"id":"primary-myelofibrosis","kind":"cancer","name":"Primary myelofibrosis","route":"/cancers/primary-myelofibrosis/"}]}}