Felix C A, Winick N J, Negrini M, Bowman W P, Croce C M, Lange B J
Department of Pediatrics, Children's Hospital of Philadelphia, Pennsylvania 19104.
Cancer Res. 1993 Jul 1;53(13):2954-6.
Translocations at chromosomal band 11q23 characterize most de novo acute lymphoblastic leukemias (ALL) of infants, acute myeloid leukemias (AML) of infants and young children, and secondary AMLs following epipodophyllotoxin exposure. The chromosomal breakpoints at 11q23 have been cloned from isolated cases of de novo ALL and AML. Using an 859-base pair BamHI fragment of human ALL-1 complementary DNA that recognizes the genomic breakpoint region for de novo ALL and AML, we investigated two cases of secondary AML that followed etoposide-treated primary B-lineage ALL. In the first case, the translocation occurred between chromosomes 9 and 11 and the breakpoint at 11q23 localized to the same 9-kilobase region of the ALL-1 gene that is disrupted in most of the de novo leukemias. In the second case the translocation was between chromosomes 11 and 19. The breakpoint occurred outside of the ALL-1 breakpoint cluster region.
位于染色体带11q23的易位是大多数婴儿新发急性淋巴细胞白血病（ALL）、婴幼儿急性髓细胞白血病（AML）以及接触表鬼臼毒素后继发性AML的特征。已从新发ALL和AML的个别病例中克隆出11q23处的染色体断点。利用人ALL-1互补DNA的一个859碱基对的BamHI片段（该片段可识别新发ALL和AML的基因组断点区域），我们研究了两例继发于依托泊苷治疗的原发性B系ALL后的继发性AML病例。在第一例中，易位发生在9号和11号染色体之间，11q23处的断点定位于ALL-1基因的同一个9千碱基区域，该区域在大多数新发白血病中被破坏。在第二例中，易位发生在11号和19号染色体之间。断点出现在ALL-1断点簇区域之外。
