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Acute myelomonocytic leukemia with t(10;11)(p13;q23): Heterogeneity of breakpoints at 11q23 and association with recombinase activation

✍ Scribed by Susan E. Height; Melissa G. Dainton; Lyndal Kearney; G. John Swansbury; Estella Matutes; Dr. Martin J. S. Dyer; Jennie G. Treleaven; Ray L. Powles; Daniel Catovsky

Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
673 KB
Volume
11
Category
Article
ISSN
1045-2257

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✦ Synopsis

The human trithorax homolog gene (MLL) is directly involved in over 90% of cases of acute leukemia with abnormalities of I I q23. However, involvement of other genes at I I q23 both centromeric and telomeric of MLL has been identified in different subtypes of leukemia and lymphoma. We describe a case of acute myelomonocytic leukemia (AMML; FAB type M4) with t( 10; I I)(p I 3;q23) in which the breakpoint at I I q23 was centromeric to the MLL gene and distinct from the breakpoint seen in promyelocytic leukemias with t( I I ; I7)(q23;q22), thus providing further evidence of heterogeneity of breakpoints in I I q23 in acute leukemia. Rearrangements of immunoglobulin (IG) and T-cell receptor (JCR) genes were also observed, with no immunophenotypic evidence for commitment to the lymphoid lineages, indicating that inappropriate activation of the recombinases may be a feature of this particular variant translocation. Genes Chromosom Cancer 11:136-139 (1994).

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