TY - JOUR T1 - Thrombocytosis and STAT5 activation in chronic myelogenous leukaemia are not associated with <em>JAK2</em> V617F or calreticulin mutations JF - Journal of Clinical Pathology JO - J Clin Pathol SP - 713 LP - 719 DO - 10.1136/jclinpath-2015-203498 VL - 69 IS - 8 AU - Samir K Turakhia AU - Gurunathan Murugesan AU - Claudiu V Cotta AU - Karl S Theil Y1 - 2016/08/01 UR - http://jcp.bmj.com/content/69/8/713.abstract N2 - Aims Marked thrombocytosis is uncommon in chronic myelogenous leukaemia (CML) but may be associated with mutation of JAK2 V617F, calreticulin (CALR) and/or phospho-STAT5 (p-STAT5) activation in other myeloproliferative neoplasms (MPNs), particularly essential thrombocythaemia (ET). We investigated the JAK2 V617F, CALR 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.Methods 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 BCR-ABL1, JAK2 V617F and CALR exon 9 mutation and p-STAT5 expression.Results Four of seven cases of CML-T had marked thrombocytosis (&gt;1000×109/L). Eleven of 12 cases had megakaryocyte morphology typical for CML. All cases were BCR-ABL1 positive. Eleven of 12 cases were negative for JAK2 V617F, while STAT5 was activated in six of seven CML-T and in four of five CML cases. No case had a detectable CALR exon 9 mutation. One case of CML developed ET-like morphology and had JAK2 V617F detected while in molecular remission for CML.Conclusions Detection of BCR-ABL1 is critical in the distinction of ET from CML. Thrombocytosis and STAT5 activation in CML-T are not consistently associated with CALR exon 9 or JAK2 V617F mutation. ER -