ArticleBMC medical genomics2017
Multidisciplinary insight into clonal expansion of HTLV-1-infected cells in adult T-cell leukemia via modeling by deterministic finite automata coupled with high-throughput sequencing.
Article in BMC medical genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Host genetic determinants of HTLV-1 infection outcomes.Immunologic research · 2026Review
- Integrated TCRγ Clonality Workflow for Molecular Diagnosis in HTLV-1 Carriers and Adult T-Cell Leukemia/Lymphoma.Diagnostics (Basel, Switzerland) · 2026Article
- A novel hybrid method with convergence analysis for approximation of HTLV-I dynamics model.Scientific reports · 2024Article
- An Improved Sequencing-Based Bioinformatics Pipeline to Track the Distribution and Clonal Architecture of Proviral Integration Sites.Frontiers in microbiology · 2020Article
- RNA sequencing identifies clonal structure of T-cell repertoires in patients with adult T-cell leukemia/lymphoma.NPJ genomic medicine · 2019Article
- Mutational Intratumor Heterogeneity is a Complex and Early Event in the Development of Adult T-cell Leukemia/Lymphoma.Neoplasia (New York, N.Y.) · 2018Article
- Inferring clonal structure in HTLV-1-infected individuals: towards bridging the gap between analysis and visualization.Human genomics · 2017Article
- Clonality of HTLV-1-infected T cells as a risk indicator for development and progression of adult T-cell leukemia.Blood advances · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundClonal expansion of leukemic cells leads to onset of adult T-cell leukemia (ATL), an aggressive lymphoid malignancy with a very poor prognosis. Infection with human T-cell leukemia virus type-1 (HTLV-1) is the direct cause of ATL onset, and integration of HTLV-1 into the human genome is essential for clonal expansion of leukemic cells. Therefore, monitoring clonal expansion of HTLV-1-infected cells via isolation of integration sites assists in analyzing infected individuals from early infection to the final stage of ATL development. However, because of the complex nature of clonal expansion, the underlying mechanisms have yet to be clarified. Combining computational/mathematical modeling with experimental and clinical data of integration site-based clonality analysis derived from next generation sequencing technologies provides an appropriate strategy to achieve a better understanding of ATL development.
methodsAs a comprehensively interdisciplinary project, this study combined three main aspects: wet laboratory experiments, in silico analysis and empirical modeling.
resultsWe analyzed clinical samples from HTLV-1-infected individuals with a broad range of proviral loads using a high-throughput methodology that enables isolation of HTLV-1 integration sites and accurate measurement of the size of infected clones. We categorized clones into four size groups, "very small", "small", "big", and "very big", based on the patterns of clonal growth and observed clone sizes. We propose an empirical formal model based on deterministic finite state automata (DFA) analysis of real clinical samples to illustrate patterns of clonal expansion.
conclusionsThrough the developed model, we have translated biological data of clonal expansion into the formal language of mathematics and represented the observed clonality data with DFA. Our data suggest that combining experimental data (absolute size of clones) with DFA can describe the clonality status of patients. This kind of modeling provides a basic understanding as well as a unique perspective for clarifying the mechanisms of clonal expansion in ATL.
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