HEMATOLOGIC MALIGNANCIES WITH THE T(10-11)(P13-Q21) HAVE THE SAME MOLECULAR EVENT AND A VARIETY OF MORPHOLOGIC OR IMMUNOLOGICAL PHENOTYPES

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 cytogene tically similar translocations involve the same molecular breakpoint i s unknown. Using fluorescence in situ hybridization (FISH) with a seri es of probes on 11q, we mapped the 11q breakpoint of the U937 cell lin e, 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). Subsequentl y, we identified a yeast artificial chromosome (YAC) clone, y960g8, th at included the breakpoint on 11q. From this YAC, we isolated a PI clo ne, 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 (AM oL), 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 P9IBI were split by the translocation in each patient. We showed that P9IBI included a recently identified gene , CALM (Clathrin Assembly Lymphoid Myeloid leukemia gene), and that AF 10 was also rearranged in each patient by FISH when we used y807b3, wh ich contains the AF10 gene. These findings indicate that hematologic m alignant diseases with fusion of AF10 and CALM show various morphologi c and immunologic phenotypes, suggesting that this fusion occurs in mu ltipotential or very early precursor cells. (C) 1997 Wiley-Liss, Inc.