European Journal of Molecular & Clinical Medicine

Abstract

Background:Acute myeloid leukemia (AML) is a clonal malignant disease of hematopoietic
tissues that is defined by the accumulation of leukemic blast cells in the marrow resulting in
hematopoietic failure.Among human peripheral blood cells,Cluster of Differentiation 96
(CD96) expression was observed on T and Natural Killer (NK) cells but not on the majority of B
cells, monocytes, and granulocytes. In contrast to the role of CD96 participating in immune
surveillance of tumors, CD96 itself was identified as a tumor marker. Indeed, well before first
studies deciphered its functions, CD96 was reported to be upregulated in subpopulations of TAcute
lymphoblastic leukemia (ALL) and AML. Increased expression of CD96 was shown in
several subsequent studies to correlate with poor prognosis and enhanced resistance to
chemotherapy. A promising treatment strategywould therefore be to sort out CD96-expressing
stem cells before autologous transplantation of AML patients.