Hi, I agree with you that the expression of individual markers is not relevant and one has to look at patterns of B-cell maturation. The results from the work of Concerted Action on Minimal Residual Disease has been published in Leukemia, 1999,13,419-427 and I find these antibody combinations very useful in clinical practice. In B-precursor ALL we find aberrant patterns in at least one of combinations in approx. 90% of cases. In majority of cases two or more combinations show aberrant patterns. I also agree that in difficult cases the Ig and TCR rearrangement study should be performed. Best wishes Anna At 11:45 2000-01-12 -0700, you wrote: > >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. > > Anna Porwit Haematopathology Lab. Department of Pathology Karolinska Hospital, Stockholm anpo@mb.ks.se tel.:+46-851774518 fax.:+46-851775843
This archive was generated by hypermail 2b29 : Sat Mar 10 2001 - 19:31:03 EST