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Acute Myelomonocytic Leukemia (AMML)

Acute Myelomonocytic Leukemia (AMML) - AML-M4  is defined as an acute leukemia with differentiation along both myeloid and monocytic lines. Monocytes and promonocytes represent > 20%, but < 80% of the marrow differential. Both myeloblasts and monoblasts are present. A high number of circulating monocytes may be present. Acute myelomonocytic leukemia (AML-M4) is a common type of pediatric AML. A characteristic chromosomal abnormality observed in AML-M4 is inv(16).  outcome of AML remains poor with an overall survival of 35-60%. Children with AML-M4 carrying the inv(16) abnormality have a better prognosis (61% 5-year overall survival).


Positivity May vary between monocyte and myeloid populations and positive for CD4, CD11b, CD11c, CD13, CD14 (possibly), CD15, CD33, CD36, CD64, CD65, CD68, CD71 (variable), CD163, HLA-DR, lysozyme and myeloperoxidase, Variable CD56, CD34 and CD117 and Negative for CD41, CD61, glycophorin A and keratin



































Above case shows (myeloblasts- red, lymp-green, grans-blue, monoblast-pink) positivity for myeloblast- CD34, MPO, CD33, CD13, CD117, CD15, CD65, CD11b, CD15, CD64, CD9, CD4 andfor monoblast-CD33, CD13, CD15, CD65, CD11b, CD15, CD64, CD14, CD4, CD36 and negativity for CD7, CD19, HLA-DR, CD56, CD38, cCD79a, cCD3, CD2


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  4. Monahan BP, Rector JT, Liu PP,Cotelingam JD, Dahut W. Clinicalaspects of expression of inversion16 chromosomal fusion transcriptCBFB/MYH11 in acute myelogenous leukemia subtype M1 with abnormal bone marrow eosinophilia. Leukemia 1996;10:1653-75.

  5. Haferlach T, Winkemann M,Loffler H, Schoch R, Gassmann W,Fonatsch C, et al. The abnormal eosinophils arepart of theleukemic cell population in acute myelomonocytic leukemia with abnormal eosinophils (AML M4Eo)and carry the pericentric inversion16: a combination of May-Grünwald-Giemsa staining and fluorescence in situ hybridization.Blood 1996;87:2459-63.

  6. Hernandez JM, Gonzàlez BN,Granata I, Gutiérrez N, Chillón C,Ramos F, et al. Detection of inv(16)and t(16;16) by fluorescence in situ hybridization in acute myeloid leukemia M4Eo. Haematologica2000;85:481-5.

  7. Helbling D, Mueller BU,Timchenko NA, Schardt J, Eyer M,Betts DR, et al. CBFB-SMMHC is correlated with increased calreticulin expression and suppresses thegranulocytic differentiation factor CEBPA in AML with inv(16). Blood2005;106:1369-75.

  8. Egan N, O’Reilly J, Clipper L,Higgins M, Herrmann R, Cannell P.Detection of CBFB in a patient with acute myelomonocytic leukemia (AML M4Eo) and inversion 16. Cancer Genet Cytogenet 2004;154:60-2.

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  11. Merchant SH, Haines S, Hall B,Hozier J, Viswanatha DS. Fluorescence in situ hybridization identifies cryptic t(16;16)(p13;q22) masked by del(16)(q22) in a case of AML-M4 Eo. J Mol Diagn 2004;6:271-4.

  12. Sun X, Medeiros J, Rassidakis GZ,Bueso-Ramos C. Dysplasia andhigh proliferation rate are common in acute myeloid leukemia with inv(16)(p13q22). Am J Clin Pathol2003;120:236-45.

  13. Aventìn A, Espadadel M, Casa S,Duarte J, Nomdedéu J, Sierra J.Chromosome 16 inversion-associated translocations in acute myeloid leukemia elucidated using a dual-color CBFB DNA probe.Cancer Genet Cytogenet 2002;134:142-4.

  14. Bloomfiel CD, Lawrence D, ByrdJC, Carroll A, Pettenati MJ, Tantravahi R, et al. Frequency of pro-longed remission duration afterhigh-dose cytarabine intensification in acute myeloid leukemia varies by cytogenetic subtype.Cancer Res 1998;58:4173-9.

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