ReviewActa pharmacologica Sinica2017
Human T-cell lymphotropic virus type 1 and its oncogenesis.
Review in Acta pharmacologica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- SARS-CoV-2 cell entry beyond the ACE2 receptor.Molecular biology reports · 2022Pooled it
- Remodeling of Metabolic and Secretory Organelles During Oncogenic and Oncomodulatory Viral Infections.Viruses · 2026Review
- Insights into oncovirus-driven tumor dynamics: a perspective from intravital imaging.Frontiers in cell and developmental biology · 2026Review
- Article
- Reactive Oxygen Species: A Double-Edged Sword in the Modulation of Cancer Signaling Pathway Dynamics.Cells · 2025Review
- Machine learning based characterization of high risk carriers of HTLV-1-associated myelopathy (HAM).Scientific reports · 2025Article
- HTLV-1 infection and microRNAs: unraveling the complex crosstalk.Infectious agents and cancer · 2025Review
- An open-source multi-semantic annotation dataset and automated recognition tool for viral carcinogenesis factors.Database : the journal of biological databases and curation · 2025Article
- The glioblastoma virome across tumor and extracellular compartments.Frontiers in oncology · 2025Article
- EZH2-Myc Hallmark in Oncovirus/Cytomegalovirus Infections and Cytomegalovirus' Resemblance to Oncoviruses.Cells · 2024Review
- Sequential transcriptome profiling: comparative analysis of normal and canine lymphoma preceding detailed T-cell and B-cell subtype comparison.Frontiers in veterinary science · 2024Article
- Introduction to Nutrition and Cancer.Cancer treatment and research · 2024Review
- Role and mechanism ofFrontiers in pharmacology · 2024Article
- Therapeutic approaches for HTLV-1-associated adult T-cell leukemia/lymphoma: a comprehensive review.Medical oncology (Northwood, London, England) · 2023Review
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Onco-Pathogen Mediated Cancer Progression and Associated Signaling Pathways in Cancer Development.Pathogens (Basel, Switzerland) · 2023Review
- Gut microbiota, an emergent target to shape the efficiency of cancer therapy.Exploration of targeted anti-tumor therapy · 2023Review
- The cGAS/STING signaling pathway: a cross-talk of infection, senescence and tumors.Cell cycle (Georgetown, Tex.) · 2023Article
- Multi-omics peripheral and core regions of cancer.NPJ systems biology and applications · 2022Article
- Small extracellular vesicles as key players in cancer development caused by human oncogenic viruses.Infectious agents and cancer · 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
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia/lymphoma (ATL), a rapidly progressing clonal malignancy of CD4+ T lymphocytes. Exploring the host-HTLV-1 interactions and the molecular mechanisms underlying HTLV-1-mediated tumorigenesis is critical for developing efficient therapies against the viral infection and associated leukemia/lymphoma. It has been demonstrated to date that several HTLV-1 proteins play key roles in the cellular transformation and immortalization of infected T lymphocytes. Of note, the HTLV-1 oncoprotein Tax inhibits the innate IFN response through interaction with MAVS, STING and RIP1, causing the suppression of TBK1-mediated phosphorylation of IRF3/IRF7. The HTLV-1 protein HBZ disrupts genomic integrity and inhibits apoptosis and autophagy of the target cells. Furthermore, it is revealed that HBZ enhances the proliferation of ATL cells and facilitates evasion of the infected cells from immunosurveillance. These studies provide insights into the molecular mechanisms by which HTLV-1 mediates the formation of cancer as well as useful strategies for the development of new therapeutic interventions against ATL. In this article, we review the recent advances in the understanding of the pathogenesis, the underlying mechanisms, clinical diagnosis and treatment of the disease caused by HTLV-1 infection. In addition, we discuss the future direction for targeting HTLV-1-associated cancers and strategies against HTLV-1.
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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.