Analysis of the t(6;11)(q27;q23) in leukemia shows a consistent breakpoint in AF6 in three patients and in the ML-2 cell line

✍ Scribed by Satoru Tanabe; Nancy J. Zeleznik-Le; Hirofumi Kobayashi; Christine Vignon; Rafael Espinosa III; Michelle M. LeBeau; Michael J. Thirman; Janet D. Rowley

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 997 KB
• Volume: 15
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/(sici)1098-2264(199604)15:4<206::aid-gcc2>3.0.co;2-5

✦ Synopsis

The t(6; I l)(q27;q23) is one of the most common translocations observed in patients with acute myeloid leukemia (AML). The translocation breakpoint involves the MLL gene, which is the human homolog of the Drosophik trithorax gene, at I I q23 and the AF6 gene at 6q27. Reverse transcriptase-polymerase chain reaction (RT-PCR) using an M U sense primer and an AF6 antisense primer detected the MLUAF6 fusion cDNA from three leukemia patients with the t(6;l I) [two AML and one T-acute lymphoblastic leukemia (ALL)] and one cell line. The fusion point in the AF6 cDNA from these cases is identical, regardless of the leukemia phenotype. The ML-2 cell line, which was established from a patient with AML that developed after complete remission of T-cell lymphoma, has retained an I I q23-24 deletion from the lymphoma stage and has acquired the t(6; I I) with development of AML. The ML-2 cells have no normal MLL gene on Southern blot analysis, which indicates that an intact MLL gene is not necessary for survival of leukemic cells.