ReviewPathogens (Basel, Switzerland)2020
Mechanisms of Oncogenesis by HTLV-1 Tax.
Review in Pathogens (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 104 citations in OpenAlex.
- Replication Stress Tolerance in Adult T-Cell Leukemia.Biomolecules · 2026Review
- Rewiring of the Apoptotic Rheostat in HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma.Cancers · 2026Review
- HTLV-1 HBZ inhibits DHX9 to reprogram circRNA biogenesis in ATLL.Tumour virus research · 2026Article
- Molecular and Phylogenetic Characterization of HTLV-1 Infection in Patients With Hematological Malignancies in the State of Pará, Northern Brazil.Journal of medical virology · 2026Article
- Role of Oncoviruses in Cancer Progression and Emerging Phytochemical-Based Therapies from Medicinal Plants.Molecular biotechnology · 2026Review
- Exploiting the Notch pathway in HTLV-1-driven adult T-cell leukemia/lymphoma: a mini-review.Annals of hematology · 2026Review
- HTLV-1 subverts the innate immune effector gene IRF7 by viral HBZ protein for oncogenesis.Nature communications · 2026Article
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Article
- Pathobiological link between CD30 and abnormal lymphocytes in adult T-cell leukemia/lymphoma.Journal of clinical and experimental hematopathology : JCEH · 2025Review
- The critical role of ferroptosis in virus-associated hematologic malignancies and its potential value in antiviral-antitumor therapy.Virulence · 2025Review
- The Significance of the Microenvironment in T/Nk-Cell Neoplasms.International journal of molecular sciences · 2025Review
- Viral zoonosis and human cancer: a perspective.Infectious agents and cancer · 2025Review
- Review
- HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States.Viruses · 2025Review
- An HTLV-1-Infected Humanized Mouse Model Expressing HLA-A*02:01 Demonstrates Effective CTL-Mediated Suppression of HTLV-1.Viruses · 2025Article
- Melphalan improves toxicity of arsenic trioxide in adult T-cell leukemia/lymphoma cells.Biochemistry and biophysics reports · 2025Article
- Intron-oriented HTLV-1 integration in an adult T-cell leukemia/lymphoma cell line sustains expression of intact ift81 mRNA.FEBS letters · 2025Article
- Oncoviruses in the Oral Cavity: Recent Advances in Understanding Viral Infections and Tumorigenesis.International journal of molecular sciences · 2025Review
- Splicing-dependent restriction of the HBZ gene by Tax underlies biphasic HTLV-1 infection.PLoS pathogens · 2025Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The human T-cell lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL), a neoplasm of CD4+CD25+ T cells that occurs in 2-5% of infected individuals after decades of asymptomatic latent infection. Multiple HTLV-1-encoded regulatory proteins, including Tax and HTLV-1 basic leucine zipper factor (HBZ), play key roles in viral persistence and latency. The HTLV-1 Tax oncoprotein interacts with a plethora of host cellular proteins to regulate viral gene expression and also promote the aberrant activation of signaling pathways such as NF-κB to drive clonal proliferation and survival of T cells bearing the HTLV-1 provirus. Tax undergoes various post-translational modifications such as phosphorylation and ubiquitination that regulate its function and subcellular localization. Tax shuttles in different subcellular compartments for the activation of anti-apoptotic genes and deregulates the cell cycle with the induction of DNA damage for the accumulation of genomic instability that can result in cellular immortalization and malignant transformation. However, Tax is highly immunogenic and therefore HTLV-1 has evolved numerous strategies to tightly regulate Tax expression while maintaining the pool of anti-apoptotic genes through HBZ. In this review, we summarize the key findings on the oncogenic mechanisms used by Tax that set the stage for the development of ATLL, and the strategies used by HTLV-1 to tightly regulate Tax expression for immune evasion and viral persistence.
Indexed as
Identifiers
What Socratic 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 Socratic graph.