Abstract
The rapid progress of diagnostic tools contributes to better understanding of biology and management of acute myelogenous leukemia. Some reports described a high incidence of extramedullary manifestation and a significant shorter survival in patients (pts.) with CD7+ and CD56+ co-expression of AML-blasts. Thus, retrospectively 12 cases of myeloid/natural killer cell precursor phenotype AML diagnosed between 7/95-3/98 were analysed (5 men and 7 women varying from 30 to 85 years of age, median 57,9 years). Extramedullary involvement was evident at initial presenting in 4 cases (one pts. sulcus coronaris penis, three involvement of CNS). Six of the pts. had a high leukocytes concentration (> 30 Gpt/1). At time of presentation the majority (11 pts.) of pts. had circulating blasts. According to the FAB classification 5 cases were classified as FAB M0 or Ml. Expression of CD13/CD33/ CD38/CD56/CD7 and HLA-DR without other NK-, T-cell and B-cell marker as well as MPO+/LF- was observed. Five out of the 12 pts. presented a germline configuration of the T-cell receptor β, γ, δ, and Ig heavy chain and Ig k gene by Southern blotting. Only five pts. were successfully treated with aggressive induction chemotherapy (cytarabine and anthracycline) and achieved complete or partial remission, whereas 7 pts. were refractory to induction chemotherapy. Median overall survival for the group was 4,5 month. The data presented suggest that the myeloid/natural killer cell precursor phenotype AML constitute a distinct biologic and clinical disease entity with worse clinical prognosis. It seems to be important to distinguish CD7/CD56 positive AML from other subtypes for the development of novel therapeutic approaches for this entity.
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Kahl, C. et al. (2001). CD7+ and CD56+ Acute Myelogenous Leukemia is a Distinct Biologic and Clinical Disease Entity. In: Büchner, T., Hiddemann, W., Wörmann, B., Schellong, G., Ritter, J., Creutzig, U. (eds) Acute Leukemias VIII. Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, vol 40. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18156-6_20
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DOI: https://doi.org/10.1007/978-3-642-18156-6_20
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