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• W2901565588 abstract "Chronic myeloid leukaemia (CML) is a myeloproliferative neoplasm that originates in an abnormal pluripotent bone marrow stem cell, usually presenting with leukocytosis with increased number of granulocytes (neutrophils, eosinophils and basophils) and their progenitors. CML is consistently associated with the reciprocal translocation of breakpoint cluster region protein (BCR) gene on chromosome 9 to Abelson murine leukaemia viral oncogene homolog 1 (ABL) gene on chromosome 22, resulting in a BCR-ABL fusion gene, which encodes an unregulated tyrosine kinase that allows the cells to proliferate without being regulated by cytokines.1Rowley J.D. Letter: a new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining.Nature. 1973; 243: 290-293Crossref PubMed Scopus (3369) Google Scholar CML can rarely present as isolated thrombocytosis. Historically, atypical presentations of CML with marked thrombocytosis unaccompanied by significantly elevated granulocytes are usually associated with blast crisis or lymphoblastic transformation.2Peterson L.C. Bloomfield C.D. Brunning R.D. Blast crisis as an initial or terminal manifestation of chronic myeloid leukemia. A study of 28 patients.Am J Med. 1976; 60: 209-220Abstract Full Text PDF PubMed Scopus (104) Google Scholar, 3Anastasi J. Feng J. Dickstein J.I. et al.Lineage involvement by BCR/ABL in Ph+ lymphoblastic leukemias: chronic myelogenous leukemia presenting in lymphoid blast vs Ph+ acute lymphoblastic leukemia.Leukemia. 1996; 10: 795-802PubMed Google Scholar Since 2000, few case reports have described patients who presented initially with thrombocytosis without leukocytosis.4Rice L. Popat U. Every case of essential thrombocythemia should be tested for the Philadelphia chromosome.Am J Hematol. 2005; 78: 71-73Crossref PubMed Scopus (26) Google Scholar, 5Cesar J.M. Cabello P. Ferro T. et al.Emergence of chronic myelogenous leukemia in a patient with primary thrombocythemia and absence of BCR/ABL rearrangement.Cancer Genet Cytogenet. 2006; 167: 74-77Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar, 6Weng W.H. Shih L.Y. Occurrence of BCR-ABL1-positive chronic myeloid leukemia following essential thrombocythemia.Acta Haematol. 2011; 126: 220-223Crossref PubMed Scopus (4) Google Scholar In two of these case reports, the cytogenetic studies were initially negative for the fusion gene in one case5Cesar J.M. Cabello P. Ferro T. et al.Emergence of chronic myelogenous leukemia in a patient with primary thrombocythemia and absence of BCR/ABL rearrangement.Cancer Genet Cytogenet. 2006; 167: 74-77Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar while the molecular studies for BCR-ABL transcript were initially negative in the other.6Weng W.H. Shih L.Y. Occurrence of BCR-ABL1-positive chronic myeloid leukemia following essential thrombocythemia.Acta Haematol. 2011; 126: 220-223Crossref PubMed Scopus (4) Google Scholar At the molecular level, co-expression of p190 and p210 is associated with high platelet counts, marked splenomegaly and additional chromosomal abnormalities.7Arana-Trejo R.M. Ruíz Sánchez E. Ignacio-Ibarra G. et al.BCR/ABL p210, p190 and p230 fusion genes in 250 Mexican patients with chronic myeloid leukaemia (CML).Clin Lab Haematol. 2002; 24: 145-150Crossref PubMed Scopus (40) Google Scholar The μ-BCR breakpoint associated with p230 BCR-ABL protein can also present with thrombocytosis.8Melo J.V. BCR-ABL gene variants.Baillieres Clin Haematol. 1997; 10: 203-222Abstract Full Text PDF PubMed Scopus (122) Google Scholar We undertook a retrospective review of 345 cases diagnosed in Western Australia from 2005 to 2016, with cytogenetic and molecular data available. Of these, we found 130 cases (38%) presented with thrombocytosis with a platelet count >450 × 109/L, accompanied with elevated white cell count >11 × 109/L. Only three cases (0.9%) presented with thrombocytosis and normal white cell counts (Table 1). All cases had abnormal blood films: left shift, red cell and platelet anisocytosis, and presence of occasional blasts are features described in the blood film morphology review. However, basophilia, typical of CML, was not observed.Table 1Characteristics of CML cases presenting with isolated thrombocytosisAge(years)GenderHb(g/L)WCC(×109/L)Plt(×109/L)MorphologyBreak-pointAdditional cytogenetic abnormalities66M15010539Left shiftB2A2Nil35F1075637Large platelet; occasional blasts seenB2A2Variant translocation80M1046499Myelocytes and rare dysplastic myeloid precursors; occasional blasts seenB3A2-YHb, haemoglobin; WCC, white cell count; Plt, platelets. Open table in a new tab Hb, haemoglobin; WCC, white cell count; Plt, platelets. At the genetic level, all three cases had major breakpoints, and no major route abnormalities were observed on conventional karyotype. In all three cases, we were able to detect the Ph chromosome by conventional fluorescence in situ hybridisation (FISH) either on the bone marrow or peripheral blood specimens. Thrombocytosis resolved in all three cases when BCR-ABL transcript levels declined with the commencement of tyrosine kinase inhibitors. While CML should be considered in the majority of unexplained leukocytosis with accompanying thrombocytosis, CML presenting with isolated thrombocytosis is rare. The approach recommended by some authors of screening all patients with unexplained persistent thrombocytosis9Passamonti F. Maffioli M. Update from the latest WHO classification of MPNs: a user's manual.Hematol Am Soc Hematol Educ Program. 2016; 2016: 534-542Crossref PubMed Scopus (35) Google Scholar may not be economically justifiable, given the cost of molecular or FISH testing. Rather, our data support the approach of reserving CML screening for cases where other myeloproliferative neoplams have been excluded, unless leukocytosis or atypical morphology is noted on the blood film. We recommend bone marrow examination with cytogenetic analysis to further investigate unexplained isolated thrombocytosis that is negative for JAK2, CALR and MPL mutations, in order to exclude CML and other rare causes such as 5q-syndrome. This approach will avoid missing atypical presentation of CML in the current era where targeted therapy significantly reduces transformation risks and improves survival. This approach is also in line with the British recommended diagnostic approach of unexplained thrombocytosis.10Harrison C.N. Butt N. Campbell P. et al.Modification of British Committee for Standards in Haematology diagnostic criteria for essential thrombocythaemia.Br J Haematol. 2014; 167: 421-423Crossref PubMed Scopus (36) Google Scholar The authors state that there are no conflicts of interest to disclose." @default.
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• W2901565588 title "Approximately 1% of chronic myeloid leukaemia cases present with isolated thrombocytosis and express common major breakpoints: a finding from a laboratory audit" @default.
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• W2901565588 doi "https://doi.org/10.1016/j.pathol.2018.09.059" @default.
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