Characterization of t(11;19)(q23;p13.3) by fluorescence in situ hybridization analysis in a pediatric patient with therapy-related acute myelogenous leukemia
| Autor: | Linda A. Cannizzaro, Lirong Cheng, K. H. Ramesh, Damin Wei, Eva Radel, Howard Ratech |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Cancer Research
medicine.medical_treatment Biology Translocation Genetic Myelogenous hemic and lymphatic diseases Acute lymphocytic leukemia Proto-Oncogenes Genetics medicine Humans Molecular Biology In Situ Hybridization Fluorescence Etoposide Chemotherapy medicine.diagnostic_test Chromosomes Human Pair 11 Myeloid leukemia Neoplasms Second Primary Histone-Lysine N-Methyltransferase medicine.disease DNA-Binding Proteins Leukemia Myeloid Acute Leukemia medicine.anatomical_structure Child Preschool Immunology Cancer research Female Bone marrow Chromosomes Human Pair 19 Myeloid-Lymphoid Leukemia Protein Transcription Factors Fluorescence in situ hybridization medicine.drug |
| Zdroj: | Cancer Genetics and Cytogenetics. 129:17-22 |
| ISSN: | 0165-4608 |
| DOI: | 10.1016/s0165-4608(01)00429-0 |
| Popis: | This case presents a Caucasian girl diagnosed with early pre-B cell acute lymphoblastic leukemia at age 2 years. The only chromosomal anomaly detected in her bone marrow cells at this time was an add(12p). By age 4 years, she had a bone marrow and central nervous system (CNS) relapse of ALL and was treated with chemotherapy that included etoposide. She was in complete remission for 2 years following chemotherapy with etoposide, but later developed therapy-related acute myeloid leukemia (t-AML). At this time, a t(11;19)(q23;p13.3) rearrangement was detected in her bone marrow cells. The AML relapsed again 1 year after allogeneic bone marrow transplant (BMT). The presence of a chromosome 11 abnormality involving band 11q23 in this patient suggests that the transformation from ALL to t-AML was a consequence of etoposide included in her chemotherapy. Studies have shown that the 11q23 breakpoint in the t(11;19) rearrangement is consistent, and involves the MLL gene in t-AML patients. However, the breakpoint in 19p is variable in that it could be located either at 19p13.1 or 19p13.3 and thus could involve either of two genes: ELL (11–19 lysine-rich leukemia gene) on 19p13.1 or ENL (11–19 leukemia gene) on 19p13.3. In this study, the t(11;19)(q23;p13.3) was further characterized and the breakpoint regions were defined by fluorescence in situ hybridization (FISH) analysis. |
| Databáze: | OpenAIRE |
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