Rhom-2 expression does not always correlate with abnormalities on chromosome 11 at band p13 in T-cell acute lymphoblastic leukemia
Autor: | TJ Fitzgerald, GA Neale, SC Raimondi, RM Goorha |
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Rok vydání: | 1992 |
Předmět: |
Male
Receptors Antigen T-Cell alpha-beta T-Lymphocytes Immunology Molecular Sequence Data Restriction Mapping Chromosome Disorders Biochemistry Polymerase Chain Reaction Proto-Oncogene Mas Translocation Genetic Immunophenotyping Proto-Oncogenes Humans Leukemia-Lymphoma Adult T-Cell Cloning Molecular Chromosome Aberrations Base Sequence Chromosomes Human Pair 11 RNA-Directed DNA Polymerase Cell Biology Hematology DNA Neoplasm Chromosome Banding Blotting Southern Oligodeoxyribonucleotides Child Preschool Chromosomes Human Pair 7 |
Zdroj: | Blood. 80(12) |
ISSN: | 0006-4971 |
Popis: | A frequent site for nonrandom recombination in T-cell acute lymphoblastic leukemia (T-ALL) is chromosome 11 at p13. The molecular characterization of a (7;11)(q35;p13) translocation showed that the translocation breakpoint was 2 kb 5′ to the T-ALLbcr locus resulting in the juxtaposition of the T-cell receptor (TCR) beta gene to the rhom-2 gene locus. Northern blot analysis did not detect expression of the rhom-2 gene in the leukemic blasts of the (7;11) translocation. However, using a sensitive polymerase chain reaction (PCR)-based assay, the (7;11) translocation showed a trace expression of rhom-2 at a level of 0.01% of TCR-beta message. Because rhom-2 is considered a proto- oncogene, the significance of the trace expression of rhom-2 in the (7;11) translocation was investigated by comparing the level of rhom-2 expression in 7 additional T-ALLs, normal thymocytes, and CEM (pre-T) and HPB (mature-T) cell lines using the PCR assay. The CEM cells, normal thymocytes, and one patient, whose blasts had no cytogenetic abnormality of chromosome 11, did not express rhom-2 indicating that rhom-2 is not normally expressed in T cells. The other six T-ALLs fell into three categories: (1) two T-ALLs overexpressed rhom-2 in the presence of a translocation; (2) two T-ALLs had trace expression in the presence of a translocation; and (3) two T-ALLs had trace expression with no observable abnormalities on chromosome 11 at p13. Therefore, the data indicate that not all translocations at the T-ALLbcr locus result in overexpression of rhom-2. To account for the sharp contrast in rhom-2 expression seen in these T-ALLs, a model is proposed with a negative regulatory element in the T-ALLbcr locus that is disrupted in some of the cases leading to overexpression of rhom-2. |
Databáze: | OpenAIRE |
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