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© 2003 American Society for Clinical Oncology
In Reply:
1 Ludwig-Maximilians University, München, Germany We would like to thank Dr Bennett for his comments on our report1, and we appreciate his outstanding contributions in this field. With regard to the frequency of granulocytic dysplasia (dysG), we confirm that the cited criteria2 were strictly applied. However, the true frequency of dysG is the sum of column 5 (16.6%) and column 8 (trilineage dysplasia, 14.9%), or 31.5%1, which is in agreement with published data. Furthermore, an inferior staining of the smears, as suggested by Bennett, would have resulted in rather higher frequencies of dysG because of the criterion of hypogranularity and therefore may not explain the observed differences. We agree with Bennett that the optimization of logistics and procedures to maximize the percentage of patients with adequate cytogenetics is essential for modern clinical trials. This may result in high rates of successful cytogenetic studies (ie, up to 98.2%; 1,310 of 1,334 within the last 2 years), which is achieved in our laboratory providing reference diagnostics for the German Acute Myeloid Leukemia Cooperative Group studies.
As suggested by Bennett, additional analyses were performed to further clarify whether there is a prognostic impact of dysG alone. Thus the complete response rates for patients with no dysplasia, dysG alone, and dysG in combination with dyserythropoiesis or dysmegakaryopoiesis were 71.5%, 56.7%, and 65.9%, respectively (
In conclusion, we agree with Bennett that a comprehensive characterization of the individual leukemia by cytomorphologic, immunophenotypic, cytogenetic, and molecular genetic profiling will provide the best basis for the accurate management of a patient with acute myeloid leukemia.3–7
REFERENCES
1. Haferlach T, Schoch C, Loffler H, et al: Morphologic dysplasia in de novo acute myeloid leukemia (AML) is related to unfavorable cytogenetics but has no independent prognostic relevance under the conditions of intensive induction therapy: Results of a multiparameter analysis from the German AML Cooperative Group studies. J Clin Oncol 21:256–265, 2003 2. Goasguen JE, Matsuo T, Cox C, et al: Evaluation of the dysmyelopoiesis in 336 patients with de novo acute myeloid leukemia: Major importance of dysgranulopoiesis for remission and survival. Leukemia 6:520–525, 1992[Medline] 3. Haferlach T, Schoch C, Schnittger S, et al: Distinct genetic patterns can be identified in acute monoblastic and acute monocytic leukaemia (FAB AML M5a and M5b): A study of 124 patients. Br J Haematol 118:426–431, 2002[CrossRef][Medline] 4. Kern W, Kohlmann A, Wuchter C, et al: Correlation of protein expression and gene expression in acute myeloid leukemia. Cytometry (in press)
5. Schoch C, Kohlmann A, Schnittger S, et al: Acute myeloid leukemias with reciprocal rearrangements can be distinguished by specific gene expression profiles. Proc Natl Acad Sci 99:10008–10013, 2002
6. Schnittger S, Schoch C, Dugas M, et al: Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia (AML): Correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study, and usefulness as a marker for detection of minimal residual disease. Blood 100:59–66, 2002 7. Kohlmann A, Schoch S, Schnittger S, et al: Molecular characterization of acute leukemias using microarray technology. Genes Chromosomes Cancer 37:396–405, 2003[CrossRef][Medline]
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Copyright © 2003 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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2 test; P = .069). There were also no significant differences between these three groups with regard to overall survival, event-free survival, and relapse-free survival (Figs 1
