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TEL-AML1 translocations with TEL and CDKN2 inactivation in acute
lymphoblastic leukemia cell lines
DH Kim, RL Moldwin, C Vignon, SK Bohlander, Y Suto, L Giordano, R Gupta, S Fears, G Nucifora and JD Rowley
Department of Pediatrics, University of Chicago IL, USA.
The t(12;21) (p 13; q22) results in the fusion of the TEL gene located on
chromosome 12 with the AML1 gene located on the derivative chromosome 21.
Because this translocation is difficult to detect using standard
cytogenetic techniques, 27 previously karyotyped B-lineage acute
lymphoblastic leukemia (ALL) cell lines were evaluated for the presence of
the TEL-AML1 fusion using the reverse transcriptase- polymerase chain
reaction (RT-PCR), fluorescence in situ hybridization (FISH), and cDNA
sequencing. Six cell lines expressed the TEL-AML1 chimeric transcript by
RT-PCR and the t(12;21) was confirmed by FISH analysis with probes for TEL,
AML1, and chromosome 12. While only one of the 6 cell lines with the
t(12;21) lost the der(12)t(12;21)-encoded AML1-TEL fusion transcript, 4
cell lines lacked expression of the nontranslocated allele of TEL and 5
cell lines lacked expression of CDKN2. Moreover, in 2 patients (1 with the
TEL-AML1 transcript and 1 without), TEL expression was lost with disease
progression; le, TEL was expressed in the initial cell lines (established
at diagnosis or first relapse) whereas TEL was not expressed in the cell
lines established from these patients in late-stage disease. These data
show the coexistence of multiple genetic defects in childhood B-lineage ALL
Cell lines with t(12;21) will facilitate the study of TEL-AML1 and AML1-TEL
fusion proteins as well as TEL and CDKN2 gene inactivation in leukemia
transformation and progression.
Volume 88,
Issue 3,
pp. 785-794,
08/01/1996
Copyright © 1996 by The American Society of Hematology
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