ArticleBMC cancer2014
ADAMTS2 gene dysregulation in T/myeloid mixed phenotype acute leukemia.
Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- ADAMTS2: More than a procollagen N-proteinase.Genes & diseases · 2025Review
- Emerging roles of ADAM6 and PRSS1 as novel diagnostic/prognostic biomarkers for acute lymphoblastic and myeloid leukemia in adults.BMC cancer · 2025Article
- Diagnosis of acute myeloid leukaemia on microarray gene expression data using categorical gradient boosted trees.Heliyon · 2023Article
- Genomic characterization of chromosome translocations in patients with T/myeloid mixed-phenotype acute leukemia.Leukemia & lymphoma · 2018Article
- Aleukemic extramedullary T lymphoid/myeloid bilineage hematopoietic and lymphoid malignancy with progression to bilineage leukemia at relapse: A case report.Oncology letters · 2017Article
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMixed phenotype acute leukemias (MPAL) include acute leukemias with blasts that express antigens of more than one lineage, with no clear evidence of myeloid or lymphoid lineage differentiation. T/myeloid (T/My) MPAL not otherwise specified (NOS) is a rare leukemia that expresses both T and myeloid antigens, accounting for less than 1% of all leukemias but 89% of T/My MPAL. From a molecular point of view, very limited data are available on T/My MPAL NOS. CASE PRESENTATION: In this report we describe a T/My MPAL NOS case with a complex rearrangement involving chromosomes 5 and 14, resulting in overexpression of the ADAM metallopeptidase with thrombospondin type 1 motif, 2 (ADAMTS2) gene due to its juxtaposition to the T cell receptor delta (TRD) gene segment.
conclusionDetailed molecular cytogenetic characterization of the complex rearrangement in the reported T/My MPAL case allowed us to observe ADAMTS2 gene overexpression, identifying a molecular marker that may be useful for monitoring minimal residual disease. To our knowledge, this is the first evidence of gene dysregulation due to a chromosomal rearrangement in T/My MPAL NOS.
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