{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,6]],"date-time":"2025-12-06T04:14:57Z","timestamp":1764994497902,"version":"3.46.0"},"reference-count":25,"publisher":"BMJ","issue":"8","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Clin Pathol"],"accepted":{"date-parts":[[2015,12,14]]},"published-print":{"date-parts":[[2016,8]]},"abstract":"<jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>\n                      Marked thrombocytosis is uncommon in chronic myelogenous leukaemia (CML) but may be associated with mutation of\n                      <jats:italic>JAK2<\/jats:italic>\n                      V617F, calreticulin (\n                      <jats:italic>CALR<\/jats:italic>\n                      ) and\/or phospho-STAT5 (p-STAT5) activation in other myeloproliferative neoplasms (MPNs), particularly essential thrombocythaemia (ET). We investigated the\n                      <jats:italic>JAK2<\/jats:italic>\n                      V617F,\n                      <jats:italic>CALR<\/jats:italic>\n                      and STAT5 activation status in patients with CML and thrombocytosis (CML-T) that mimicked ET, trying to identify a common mechanism for thrombocytosis in MPN.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Blood and bone marrow morphological findings were reviewed from seven CML-T, four otherwise typical CML and one CML in blast phase. All cases were analysed for\n                      <jats:italic>BCR-ABL1<\/jats:italic>\n                      ,\n                      <jats:italic>JAK2<\/jats:italic>\n                      V617F and\n                      <jats:italic>CALR<\/jats:italic>\n                      exon 9 mutation and p-STAT5 expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Four of seven cases of CML-T had marked thrombocytosis (&gt;1000\u00d710\n                      <jats:sup>9<\/jats:sup>\n                      \/L). Eleven of 12 cases had megakaryocyte morphology typical for CML. All cases were\n                      <jats:italic>BCR-ABL1<\/jats:italic>\n                      positive. Eleven of 12 cases were negative for\n                      <jats:italic>JAK2<\/jats:italic>\n                      V617F, while STAT5 was activated in six of seven CML-T and in four of five CML cases. No case had a detectable\n                      <jats:italic>CALR<\/jats:italic>\n                      exon 9 mutation. One case of CML developed ET-like morphology and had\n                      <jats:italic>JAK2<\/jats:italic>\n                      V617F detected while in molecular remission for CML.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Detection of\n                      <jats:italic>BCR-ABL1<\/jats:italic>\n                      is critical in the distinction of ET from CML. Thrombocytosis and STAT5 activation in CML-T are not consistently associated with\n                      <jats:italic>CALR<\/jats:italic>\n                      exon 9 or\n                      <jats:italic>JAK2<\/jats:italic>\n                      V617F mutation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jclinpath-2015-203498","type":"journal-article","created":{"date-parts":[[2016,7,20]],"date-time":"2016-07-20T08:13:24Z","timestamp":1469002404000},"page":"713-719","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Thrombocytosis and STAT5 activation in chronic myelogenous leukaemia are not associated with\n                    <i>JAK2<\/i>\n                    V617F or calreticulin mutations"],"prefix":"10.1136","volume":"69","author":[{"given":"Samir K","family":"Turakhia","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gurunathan","family":"Murugesan","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claudiu V","family":"Cotta","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karl S","family":"Theil","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2016,1,11]]},"reference":[{"key":"2025120518580006000_69.8.713.1","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-10-1613"},{"key":"2025120518580006000_69.8.713.2","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1111\/j.1600-0609.1977.tb01474.x","article-title":"The peripheral blood in chronic granulocytic leukaemia. 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