Megakaryoblastic lineage of peripheral blood blasts of CML blast ...

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Megakaryoblastic Lineage of Peripheral Blood Blasts of CML Blast Crisis Identified by Budding. Dysplastic ... E-mail: [email protected] Received for ...

American Journal of Hematology 75:239–240 (2004)

Images in Hematology

Megakaryoblastic Lineage of Peripheral Blood Blasts of CML Blast Crisis Identified by Budding Dysplastic Platelets Mona Anand, Rajive Kumar,* and Sarika Singh Unit of Laboratory Oncology, Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India

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Chronic myeloid leukemia (CML) is a disorder of the hematopoietic stem cell, its hallmark being the presence of the Philadelphia chromosome (Ph). The Ph chromosome represents a reciprocal translocation between chromosomes 9 and 22, and the resulting fusion protein represents a combination of the bcr region that comes from chromosome 22 and the c-abl tyrosine kinase region from chromosome 9. Because it is a stem cell disorder, CML affects all of the formed elements found in the blood and bone marrow. The peripheral blood film typically shows a leukocytosis with many mature neutrophils along with some earlier myeloid forms and even an occasional blast. In addition, most CML patients exhibit an absolute basophilia, and eosinophilia is often present as well. The leukocytes from patients *Correspondence to: Dr. Rajive Kumar, E-99, AIIMS Campus, Ansari Nagar, New Delhi-110029, India. E-mail: [email protected] Received for publication 17 December 2003; Accepted 17 December 2003

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ª 2004 Wiley-Liss, Inc.

Published online in Wiley InterScience ( DOI: 10.1002/ajh.20041


Images in Hematology: Anand et al.

with CML generally do not reveal dysplastic features, although the basophils occasionally exhibit hypogranulation. The platelet count is frequently elevated and the platelets on the blood film are often large and dysmorphic. Patients with CML typically progress through an accelerated phase characterized by progressive splenomegaly, a further elevation of the white blood count with increasing basophilia, and an increasing percentage of blasts. As such, the accelerated phase of CML is a harbinger of blast crisis. Blast crisis is defined by the presence of more than 30% blasts in the bone marrow, which in most instances, are of myeloid or lymphoid lineage. However, some cases of blast crisis exhibit a ‘‘mixed pattern,’’ where, in addition to immature cells with a typical myeloid appearance, many of the cells demonstrate features of megakaryoblasts, erythroblasts, and/or primitive basophils/mast cells. In this report, we describe a case in which a large proportion of the blasts are clearly of megakaryocytic lineage. The megakaryocytic lineage of these blasts was based on the finding in the peripheral blood of both highly dysplastic platelets

and megakaryocytic cytoplasmic masses budding from the blasts. This megakaryoblastic component is particularly well depicted in this report. The presence on the peripheral blood smear of a highly dysplastic platelet combined with a large megakaryocytic cytoplasmic mass is shown in Image #1. Three large blasts with prominent nucleoli are shown in Image #2. While two of the blasts are of morphologically indeterminate lineage, one blast is seen to be producing a highly dysplastic, megakaryocytic cytoplasmic/platelet mass. Final confirmation of the megakaryocytic lineage of these blasts is shown by the presence of CD41 (i.e., GPIIb/IIIa), a glycoprotein that is expressed on the surface of platelets and platelet precursors. Convincing evidence for the CD41 positivity of these cells is provided by their immunological staining using a monoclonal mouse anti-human glycoprotein IIb/IIIa (CD41 clone-5B12, Dako) (see Image #3). In summary, this set of images fulfills all of the criteria necessary to establish the megakaryocytic lineage of the immature cells found in this patient with CML in blast crisis.

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