|
SK Bohlander1, V Muschinsky1, K Schrader2, R Siebert3, B Schlegelberger3, L Harder3, V Schemmel4, C Fonatsch5, W-D Ludwig6, W Hiddemann7 & MH Dreyling7
1Institute of Human Genetics, Georg-August University, Göttingen, Germany
2Department of Internal Medicine, Georg-August University, Göttingen, Germany
3Institute of Human Genetics, University of Kiel, Kiel, Germany
4NHL-BFM-Studienzentrale, Department of Pediatrics, Medizinische Hochschule Hannover, Hannover, Germany
5Institute of Medical Biology, University of Vienna, Vienna, Austria
6Department of Hematology/Oncology and Tumor Immunology, Robert-Rössle-Hospital, Humboldt University, Berlin, Germany
7Department of Internal Medicine, Ludwigs-Maximilian University, Munich, Germany
Correspondence to: SK Bohlander, Institute of Human Genetics, Heinrich-Düker-Weg 12, 37073 Göttingen, Germany; Fax: +49 (0)551 39 9303
|
The recurring translocation t(10;11)(p13;q14) which is found in acute myeloid leukemia (AML) and in acute lymphoblastic leukemia (ALL) results in the fusion of the putative transcription factor AF10 to CALM encoding a clathrin assembly protein. Previous studies using mainly fluorescence in situ hybridization (FISH) analysis have shown that the CALM/AF10 rearrangement is found in immature acute myeloid leukemia (AML) of subtype M0 and M1 and in T cell ALL. In this study we analyzed the CALM/AF10 and AF10/CALM fusion mRNAs in a series of three patients with AML, one patient with T-ALL and two patients with precusor T lymphoblastic lymphoma. In all six patients the breakpoint in CALM is at the 3' end of the coding region (nt1926/1927 or nt 2091/2092). Three breakpoints could be identified in AF10 (nt 588/589, nt 882/883 and nt 978/979). These data demonstrate that the CALM/AF10 fusions found in patients differ only slightly with respect to the portion of AF10 present and that there is no obvious difference between the fusions found in AML patients compared to those found in patients with lymphoid malignancies. Leukemia (2000) 14, 93–99.
|
