t(9;11)-Induced leukemia is present both in children and adults, and depending on age, can cause predominantly acute lymphoblastic (ALL) or acute myeloid leukemia (AML), respectively. In general, in infants, it is characterized by poor (ALL) or intermediate (AML) prognosis, whereas in adults, it is classified as being of intermediate-high risk [15,24,31]. Its hallmark is the chromosomal translocation between chromosomes 9 and 11, leading to the formation of the MLL-AF9 fusion gene. The expressed ...
t(9;11)-Induced leukemia is present both in children and adults, and depending on age, can cause predominantly acute lymphoblastic (ALL) or acute myeloid leukemia (AML), respectively. In general, in infants, it is characterized by poor (ALL) or intermediate (AML) prognosis, whereas in adults, it is classified as being of intermediate-high risk [15,24,31]. Its hallmark is the chromosomal translocation between chromosomes 9 and 11, leading to the formation of the MLL-AF9 fusion gene. The expressed chimeric protein was shown to be crucial for leukemia progression. MLL-AF9 recruits - among other factors - the super elongation complex (SEC), leading to aberrant activation of target genes [4,5,9,17,24]. The Polycomb group of proteins plays crucial roles in many processes, such as embryogenesis, differentiation, and maintaining cell homeostasis, and recently reports linking it to MLL-AF9 have emerged. This review will focus on its role in t(9;11)-related leukemia, highlighting the possible therapeutic-targeting strategies.
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