ReviewFrontiers in microbiology2018
HTLV-1-Mediated Epigenetic Pathway to Adult T-Cell Leukemia-Lymphoma.
Review in Frontiers in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- Host genetic determinants of HTLV-1 infection outcomes.Immunologic research · 2026Review
- Article
- From Genomic and Epigenomic Maps to Medicines in Adult T-Cell Leukemia/Lymphoma.Cancer science · 2026Review
- Pathobiological link between CD30 and abnormal lymphocytes in adult T-cell leukemia/lymphoma.Journal of clinical and experimental hematopathology : JCEH · 2025Review
- Chromatin remodeling enhances MAP3K8 expression in HAM: a key pathogenesis for therapeutic intervention.Nature communications · 2025Article
- Review
- Bidirectional anti-tumor and immunological strategies by targeting GARP-TGF-β axis in adult T-cell leukemia/lymphoma.Leukemia · 2025Article
- Rewired chromatin structure and epigenetic gene dysregulation during HTLV-1 infection to leukemogenesis.Cancer science · 2025Article
- The role of pioneering transcription factors, chromatin accessibility and epigenetic reprogramming in oncogenic viruses.Frontiers in microbiology · 2025Review
- Integrative analysis of ATAC-seq and RNA-seq for cells infected by human T-cell leukemia virus type 1.PLoS computational biology · 2025Article
- Article
- Development of Innate-Immune-Cell-Based Immunotherapy for Adult T-Cell Leukemia-Lymphoma.Cells · 2024Article
- Article
- HTLV-1 bZIP Factor-Induced Reprogramming of Lactate Metabolism and Epigenetic Status Promote Leukemic Cell Expansion.Blood cancer discovery · 2023Article
- IMiD/CELMoD-induced growth suppression of adult T-cell leukemia/lymphoma cellsFrontiers in oncology · 2023Article
- Human tumor viruses: induction of three-dimensional alterations in the host genome structure.Frontiers in microbiology · 2023Review
- The role of epigenetics in T-cell lymphoma.International journal of hematology · 2022Review
- Review
- Clonal Selection and Evolution of HTLV-1-Infected Cells Driven by Genetic and Epigenetic Alteration.Viruses · 2022Review
- Tuning Rex rules HTLV-1 pathogenesis.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell leukemia virus type 1 (HTLV-1), the first reported human oncogenic retrovirus, is the etiologic agent of highly aggressive, currently incurable diseases such as adult T-cell leukemia-lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 proteins, including Tax and HBZ, have been shown to have critical roles in HTLV-1 pathogenicity, yet the underlying mechanisms of HTLV-1-driven leukemogenesis are unclear. The frequent disruption of genetic and epigenetic gene regulation in various types of malignancy, including ATL, is evident. In this review, we illustrate a focused range of topics about the establishment of HTLV-1 memory: (1) genetic lesion in the Tax interactome pathway, (2) gene regulatory loop/switch, (3) disordered chromatin regulation, (4) epigenetic lock by the modulation of epigenetic factors, (5) the loss of gene fine-tuner microRNA, and (6) the alteration of chromatin regulation by HTLV-1 integration. We discuss the persistent influence of Tax-dependent epigenetic changes even after the disappearance of HTLV-1 gene expression due to the viral escape from the immune system, which is a remaining challenge in HTLV-1 research. The summarized evidence and conceptualized description may provide a better understanding of HTLV-1-mediated cellular transformation and the potential therapeutic strategies to combat HTLV-1-associated diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.