Identification of t(9;14)(q34;q32) and detection of EML1-ABL1 and TLX1 expression. (A) FISH with 5′ ABL1 (green signal) and 3′ ABL1 (red signal) probes on metaphase cells of the T-ALL patient with the cryptic t(9;14)(q34;q32). The translocation causes separation of the 2 probes with the 5′ ABL1 probe hybridizing to der(9) and the 3′ ABL1 probe hybridizing to der(14). (B) FISH with CDKN2A probe (red signal) and chromosome 9 centromere probe (green signal) on interphase cells of the patient with t(9;14)(q34;q32). The absence of a second red signal in each cell is caused by hemizygous CDKN2A deletion. FISH data were collected on a Leica DMRB (Wetzlar, Germany) fluorescence microscope equipped with a triple band-pass filter and a cooled black and white charged couple device camera (Photometrics, Tuscon, AZ) run by Quips SmartCapture FISH Imaging Software (Vysis, Downers Grove, IL). (C) Detection of TLX1 transcripts in the patient with t(9;14) by RT-PCR. TLX2, TLX3, or NKX2-5 transcripts were not detected in this patient. (D; Left) RT-PCR detection of the EML1-ABL1 fusion transcript in the patient with t(9;14) (patient 1) and absence of these fusion transcripts in 3 other T-ALL patients (patients 2-4). (Right) RT-PCR analysis of EML1 expression in the 4 patient samples analyzed in the left part of the figure and in 4 T-ALL cell lines. ZNF384 was amplified as a control of RNA quality. (E) Schematic representation of the EML1, ABL1, and EML1-ABL1 fusion proteins. The sequence of the in-frame fusion between exon 17 of EML1 and exon 2 of ABL1 is indicated at the bottom. SH3 indicates Src homology 3.