We have had experience with many pediatric cases regarding the distinction of ALL from hematogones, and we continue to struggle with these interesting and difficult cases. We have not found any one particular marker that can identify a cell as a lymphoid as opposed to a hematogone. We find CD22 expression on normal immature and maturing B-cells as well, and use an entire panel of B-cell markers in an attempt to assess maturation. Maturational patterns of expression with CD10, CD20, CD22, CD24, TdT and immunoglobulin light chains as well as CD45 can be useful. Histograms of ALL will usually exhibit fairly discreet, well-circumscribed populations without evidence of maturation. This guideline is not hard and fast, however, and morphologic and clinical correlation is exceedingly important. ALL patients usually have some symptomatology, such as malaise, fevers and bone pain. Acute lymphoblastic leukemia almost always presents with a rapid expansion of lymphoid blasts and it would be very unusual for a patient to "smolder" along with 12% blasts for 6 months, so if this patient has not been diagnosed and treated for ALL, I strongly doubt that this presentation represents that entity. However, if the patient had a definitive diagnosis and was treated, the situation gets very sticky. We communicate closely with the clinician, and err on the conservative side, as waiting another week for the disease to declare itself is better than intensifying therapy. Additionally, I'm not sure that the description of a "clonal" population is accurate, as light chains restriction could not be demonstrated. I have been trained to limit the distinction of clonality to populations demonstrate heavy or light chain restriction by flow cytometry or molecular studies as well as T-cell gene receptor rearrangement by molecular studies. I would appreciate comments from the community regarding this. Michael S. Brown, MD Hematopathology Fellow Instructor University of Utah ARUP Laboratories, Inc.
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