ArticleLeukemia & lymphoma2018
Genomic characterization of chromosome translocations in patients with T/myeloid mixed-phenotype acute leukemia.
Article in Leukemia & lymphoma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- FAT1 Gene Expression in Iranian Acute Lymphoid and Myeloid Leukemia Patients.International journal of hematology-oncology and stem cell research · 2023Article
- Redefining the biological basis of lineage-ambiguous leukemia through genomics: BCL11B deregulation in acute leukemias of ambiguous lineage.Best practice & research. Clinical haematology · 2021Review
- Enhancer Hijacking Drives OncogenicCancer discovery · 2021Article
- T(6;14)(q25;q32) involves BCL11B and is highly associated with mixed-phenotype acute leukemia, T/myeloid.Leukemia · 2020Article
- Clinical Characteristics And Outcome Of Biphenotypic Acute Leukemia: 10 Case Reports And Literature Review.Cancer management and research · 2019Article
- Not Only Mutations Matter: Molecular Picture of Acute Myeloid Leukemia Emerging from Transcriptome Studies.Journal of oncology · 2019Review
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Mixed-phenotype acute leukemia (MPAL) is a progenitor type of leukemia with ambiguous expression of lineage markers. The diagnosis of MPAL is based on flow cytometric analysis of immunophenotype, which commonly identifies myeloid lineage markers as well as B- or T- lymphoid lineage markers on leukemic blasts. Due to the rare occurrence of this disease, few studies have delineated the molecular bases of MPAL. Combining conventional karyotyping with whole genomic sequencing (WGS) and RNA sequencing (RNA-seq), we report here our identification and characterization of chromosome translocations, gene mutations and gene expression profile in four patients with T/Myeloid MPAL, including two t(6;14)(q25;q32) one t(8;14)(q24.2;q32) and one t(7;8)(p14;q24.2). Notably, seven of the eight translocation breakpoints reside in the non-coding regions and their locations appear to be shared by two or more patients. Gene expression analysis of matched diagnostic vs. remission samples provided evidence of transcriptomes alteration involving nucleosome organization and chromatin assembly.
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