Hematologic Malignancies With the t(10;11)(p13;q21) Have the Same Molecular Event and a Variety of Morphologic or Immunologic Phenotypes

Hematologic Malignancies With the t(10;11)(p13;q21) Have the Same Molecular Event and a Variety of Morphologic or Immunologic Phenotypes

Hematologic Malignancies With the t(10;11)(p13;q21) Have the Same Molecular Event and a Variety of Morphologic or Immunologic Phenotypes

Abstract

Previous studies described the t(10;11)(p13-14;q14-21) as a recurring translocation associated with T-cell acute lymphoblastic
leukemia (ALL). This translocation has also been reported in monocytic leukemia or ALL with a very early pre-B phenotype.
However, whether these cytogenetically similar translocations involve the same molecular breakpoint is unknown. Using
fluorescence in situ hybridization (FISH) with a series of probes on 11q, we mapped the 11q breakpoint of the U937 cell line,
which was derived from a patient with diffuse histiocytic lymphoma and was shown by FISH to have the t(10;11)(p13-14;q14-
21). Subsequently, we identified a yeast artificial chromosome (YAC) clone, y960g8, that included the breakpoint on 11q. From
this YAC, we isolated a P1 clone, P91B1, that was split by the 10;11 translocation. We studied four patients with a t(10;11), one
of whom had acute monocytic leukemia (AMoL), one had acute lymphoblastic leukemia (ALL), one had lymphoblastic
lymphoma (LBL), and one had granulocytic sarcoma, by using FISH with y960g8 and P91B1. Y960g8 and P91B1 were split by the
translocation in each patient. We showed that P91B1 included a recently identified gene, CALM (Clathrin Assembly Lymphoid
Myeloid leukemia gene), and that AF10 was also rearranged in each patient by FISH when we used y807b3, which contains the
AF10 gene. These findings indicate that hematologic malignant diseases with fusion of AF10 andCALM show various morphologic
and immunologic phenotypes, suggesting that this fusion occurs in multipotential or very early precursor cells

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