Premium
Proposal for the recognition of minimally differentiated acute myeloid leukaemia (AML‐MO)
Author(s) -
Bennett J. M.,
Catovsky D.,
Daniel MT.,
Flandrin G.,
Galton D. A. G.,
Gralnick H. R.,
Sultan C.
Publication year - 1991
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1991.tb04444.x
Subject(s) - cd33 , myeloid , lymphoblast , myeloperoxidase , immunocytochemistry , myeloid leukaemia , antigen , monoclonal antibody , precursor cell , immunology , lineage (genetic) , medicine , immunohistochemistry , lineage markers , biology , antibody , pathology , cell , cell culture , gene , cd34 , genetics , stem cell , inflammation , phenotype
Summary. We describe a form of acute myeloid leukaemia (AML), designated AML‐MO, with minimal myeloid differentiation, not included previously in the FAB classification. AML‐MO cannot be diagnosed on morphological grounds alone as the blast cells are large and agranular, sometimes resembling L2 or, rarely, L1 lymphoblasts, and should be identified by the following features: negative myeloperoxidase (MPO) and Sudan Black B reaction (or positive in less than 3% of blasts), negative B and T lineage markers and expression of myeloid antigens recognized by at least one monoclonal antibody, CD13 or CD33. Other myeloid markers are also often positive and these include CDllb and the enzyme MPO demonstrated by immunocytochemistry and or electron microscopy analysis. The findings in a group of 10 cases satisfying the criteria for AML‐MO are described. AML‐MO represents 2–3% of all cases of AML and 1–1·5% of all acute leukaemias. Its clinical and biological significance is not yet apparent but its identification in a larger number of cases may achieve this aim.