A 4-year-old male with the diagnosis of T-cell acute lymphoblastic leukemia (T-ALL) relapsed after 19 months with an acute myeloid leukemia (AML). Immunoglobulin and T-cell receptor gene rearrangements analyses reveal that both leukemias were rearranged with a clonal relationship between them. Comparative genomic hybridization (Array-CGH) and whole-exome sequencing analyses of both samples suggest that this leukemia may have originated from a common T/myeloid progenitor. The presence of homozygous deletion of p16/INK4A, p14/ARF, p15/INK4B, and heterozygous deletion of WT1 locus remained stable in the leukemia throughout phenotypic switch, revealing that this AML can be genetically associated to T-ALL.
Paganin, M., Buldini, B., Germano, G., Seganfreddo, E., Meglio, A., Magrin, E., et al. (2016). A Case of T-cell Acute Lymphoblastic Leukemia Relapsed As Myeloid Acute Leukemia. PEDIATRIC BLOOD & CANCER, 63(9), 1660-1663 [10.1002/pbc.26054].
A Case of T-cell Acute Lymphoblastic Leukemia Relapsed As Myeloid Acute Leukemia
Rizzari, Carmelo;Cazzaniga, Giovanni;
2016
Abstract
A 4-year-old male with the diagnosis of T-cell acute lymphoblastic leukemia (T-ALL) relapsed after 19 months with an acute myeloid leukemia (AML). Immunoglobulin and T-cell receptor gene rearrangements analyses reveal that both leukemias were rearranged with a clonal relationship between them. Comparative genomic hybridization (Array-CGH) and whole-exome sequencing analyses of both samples suggest that this leukemia may have originated from a common T/myeloid progenitor. The presence of homozygous deletion of p16/INK4A, p14/ARF, p15/INK4B, and heterozygous deletion of WT1 locus remained stable in the leukemia throughout phenotypic switch, revealing that this AML can be genetically associated to T-ALL.File | Dimensione | Formato | |
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