{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T15:47:15Z","timestamp":1790264835947,"version":"4.1.0"},"reference-count":33,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2017,5,18]],"date-time":"2017-05-18T00:00:00Z","timestamp":1495065600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100005189","name":"Leukemia and Lymphoma Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005189","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2017,7,15]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND<\/jats:title>\n                    <jats:p>Although recombinant interferon\u2010\u03b1 (rIFN\u03b1) effectively treats patients with early myelofibrosis, the effect of driver and high molecular risk (HMR) mutations has not been considered. In this phase 2 study, for the first time, the authors correlate response to rIFN\u03b1 treatment with driver and HMR mutations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>Patients were diagnosed using World Health Organization or International Working Group for Myeloproliferative Neoplasms Research and Treatment criteria. Only patients who had low or intermediate\u20101 Dynamic International Prognostic Scoring System scores with \u226515% hematopoietic bone marrow foci were included. History, symptom assessment, physical examination, and blood and bone marrow studies were performed. Genomic DNA was extracted from frozen cells, and next\u2010generation targeted sequencing of 45 genes was performed. Either rIFN\u03b1\u20102b (0.5 million units subcutaneously 3 times weekly) or pegylated rIFN\u03b1\u20102a (45 \u03bcg weekly) with escalation was initiated. All patients were followed at the authors' institution, and regular bone marrow biopsies were encouraged. International Working Group for Myeloproliferative Neoplasms Research and Treatment and European LeukemiaNet treatment response criteria were used.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      Of 30 patients (16 women and 14 men; median age, 58 years), 22 were classified as low risk, and 8 were classified as intermediate\u20101 risk. Two patients achieved complete remission, 9 achieved partial remission, 4 had clinical improvement, 7 had stable disease; 3 had progressive disease, 1 relapsed, and 4 died. There were 22 patients with\n                      <jats:italic>JAK<\/jats:italic>\n                      mutations, 6 with\n                      <jats:italic>CALR<\/jats:italic>\n                      mutations, and 2 with\n                      <jats:italic>MPL<\/jats:italic>\n                      mutations. Seventy\u2010three percent of patients improved or remained stable with acceptable toxicity, including 37% who achieved complete or partial remission. There was no correlation between treatment response and baseline driver mutations or Dynamic International Prognostic Scoring System scores. Of 8 poor responders, 3 had\n                      <jats:italic>ASXL1<\/jats:italic>\n                      or\n                      <jats:italic>SRSF2<\/jats:italic>\n                      mutations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>\n                      Early treatment with rIFN\u03b1 in patients without HMR mutations may prevent the development of marked splenomegaly, anemia, and florid myelofibrosis. Molecular profiling at the time of diagnosis may predict prognosis and treatment response.\n                      <jats:bold>\n                        <jats:italic>Cancer<\/jats:italic>\n                        2017;123:2680\u201087\n                      <\/jats:bold>\n                      . \u00a9\n                      <jats:italic>2017 American Cancer Society<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cncr.30679","type":"journal-article","created":{"date-parts":[[2017,5,18]],"date-time":"2017-05-18T11:09:03Z","timestamp":1495105743000},"page":"2680-2687","source":"Crossref","is-referenced-by-count":63,"title":["The effect of initial molecular profile on response to recombinant interferon\u2010\u03b1 (rIFN\u03b1) treatment in early myelofibrosis"],"prefix":"10.1002","volume":"123","author":[{"given":"Richard T.","family":"Silver","sequence":"first","affiliation":[{"name":"Richard T Silver, MD Myeloproliferative Neoplasms Center, Division of Hematology\u2010Medical Oncology Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ariella C.","family":"Barel","sequence":"additional","affiliation":[{"name":"Richard T Silver, MD Myeloproliferative Neoplasms Center, Division of Hematology\u2010Medical Oncology Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Lascu","sequence":"additional","affiliation":[{"name":"Richard T Silver, MD Myeloproliferative Neoplasms Center, Division of Hematology\u2010Medical Oncology Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen K.","family":"Ritchie","sequence":"additional","affiliation":[{"name":"Richard T Silver, MD Myeloproliferative Neoplasms Center, Division of Hematology\u2010Medical Oncology Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gail J.","family":"Roboz","sequence":"additional","affiliation":[{"name":"Richard T Silver, MD Myeloproliferative Neoplasms Center, Division of Hematology\u2010Medical Oncology Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J.","family":"Christos","sequence":"additional","affiliation":[{"name":"Division of Biostatistics and Epidemiology, Department of Healthcare Policy and Research Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Attilio","family":"Orazi","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Duane C.","family":"Hassane","sequence":"additional","affiliation":[{"name":"Institute for Computational Biomedicine, Division of Hematology and Medical Oncology, Department of Medicine Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wayne","family":"Tam","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Weill Cornell Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas C. 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