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Journal of Clinical Oncology, Vol 21, Issue 15 (August), 2003: 3004
© 2003 American Society for Clinical Oncology


CORRESPONDENCE

Morphologic Dysplasia in Acute Myeloid Leukemia: Importance of Granulocytic Dysplasia

John M. Bennett

James P. Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY

To the Editor:

The article by Haferlach et al1 represents an important contribution to our understanding of the identifiable prognostic factors that determine outcome in adults with acute myeloid leukemia (AML). Because the first-named author and two of the referenced authors (Goasguen and Gahn) received morphology training in my laboratory, I feel quite comfortable with and confident in their ability to recognize morphologic dysplasia.

Nonetheless, I am somewhat puzzled by the discrepancy in the recognition of granulocytic dysplasia (dysG), as revealed in Table 2 on page 258. The current study has the lowest rate of all reported, with a range of 16.6% to 54.8%. The definition requires the presence of nuclear dysplasia (pseudo Pelger changes) or hypogranularity. The recognition of the latter requires an excellent Romanowsky stain. In the article by Goasguen et al2 (reference 22 in the article by Haferlach et al1) dysG had a low complete response rate.

Because some 20% of cases will not have karyotyping available, even with fluorescent in situ hybridization as a complement to standard cytogenetics, the absence of dysplasia will continue to be of some prognostic importance.

Did the authors examine the role of dysG alone for prognostic impact, and is there an explanation for the discrepancy regarding the low rate of dysG in their series? The use of flow cytometry and light scattering may remove some of the subjectivity in judging hypogranularity.3

I agree that molecular genetics will provide significant insight into the biology and management of patients with AML. It is, however, costly and time consuming, and insurance carriers will need to be educated regarding the value for adequate reimbursement.

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[Abstract/Free Full Text]

2. Goasguen JE, Matsuo T, Cox C, et al: Evaluation of the dysmyelopoeiesis in 336 patients with de novo acute myeloid leukemia: Major importance of dysgranulopoiesis for remission and survival. Leukemia 6:520–525, 1992[Medline]

3. Terstappen LW, Konemann S, Safford M, et al: Flow cytometric characterization of acute myeloid leukemia: Part 1. Significance of light scattering properties. Leukemia 5:315–321, 1991[Medline]


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  • In Reply:
    Torsten Haferlach, Wolfgang Kern, Claudia Schoch, Wolfgang Hiddemann, and Maria Cristina Sauerland
    JCO 2003 21: 3004-3005 [Full Text]


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U. Bacher, T. Haferlach, C. Schoch, W. Kern, and S. Schnittger
Implications of NRAS mutations in AML: a study of 2502 patients
Blood, May 15, 2006; 107(10): 3847 - 3853.
[Abstract] [Full Text] [PDF]


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