ArticleFrontiers in genetics2019
New Recurrent Structural Aberrations in the Genome of Chronic Lymphocytic Leukemia Based on Exome-Sequencing Data.
Article in Frontiers in genetics, 2019. 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, 10 citations in OpenAlex.
- The landscape of somatic mutations in lymphoblastoid cell lines.Cell genomics · 2023Article
- Cell-type specificity of the human mutation landscape with respect to DNA replication dynamics.Cell genomics · 2023Article
- Review
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- Differential DNA Methylation by Hispanic Ethnicity Among Firefighters in the United States.Epigenetics insights · 2021Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic lymphocytic leukemia (CLL) is the most frequent lymphoproliferative syndrome in Western countries, and it is characterized by recurrent large genomic rearrangements. During the last decades, array techniques have expanded our knowledge about CLL's karyotypic aberrations. The advent of large sequencing databases expanded our knowledge cancer genomics to an unprecedented resolution and enabled the detection of small-scale structural aberrations in the cancer genome. In this study, we have performed exome-sequencing-based copy number aberration (CNA) and loss of heterozygosity (LOH) analysis in order to detect new recurrent structural aberrations. We describe 54 recurrent focal CNAs enriched in cancer-related pathways, and their association with gene expression and clinical evolution. Furthermore, we discovered recurrent large copy number neutral LOH events affecting key driver genes, and we recapitulate most of the large CNAs that characterize the CLL genome. These results provide "proof-of-concept" evidence supporting the existence of new genes involved in the pathogenesis of CLL.
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