TEL-AML1 translocations with TEL and CDKN2 inactivation in acute lymphoblastic leukemia cell lines
| Autor: | D H, Kim, R L, Moldwin, C, Vignon, S K, Bohlander, Y, Suto, L, Giordano, R, Gupta, S, Fears, G, Nucifora, J D, Rowley |
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| Rok vydání: | 1996 |
| Předmět: |
Chromosomes
Human Pair 12 Base Sequence Proto-Oncogene Proteins c-ets Chromosomes Human Pair 21 Gene Expression Regulation Leukemic Molecular Sequence Data DNA Neoplasm Precursor Cell Lymphoblastic Leukemia-Lymphoma Burkitt Lymphoma Polymerase Chain Reaction Translocation Genetic Neoplasm Proteins DNA-Binding Proteins Repressor Proteins Proto-Oncogene Proteins Core Binding Factor Alpha 2 Subunit Disease Progression Tumor Cells Cultured Humans Genes Tumor Suppressor Carrier Proteins Child Cyclin-Dependent Kinase Inhibitor p16 In Situ Hybridization Fluorescence Transcription Factors |
| Zdroj: | Blood. 88(3) |
| ISSN: | 0006-4971 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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