ArticleJournal of virology2001
Analysis of p53 inactivation in a human T-cell leukemia virus type 1 Tax transgenic mouse model.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 33 citations in OpenAlex.
- Host genetic determinants of HTLV-1 infection outcomes.Immunologic research · 2026Review
- A multi-omics approach reveals specific oncogenic and inflammatory potential of viral oncoproteins Tax from neglected HTLV-1b and -1c genotypes.PLoS pathogens · 2026Article
- Mouse Models for HTLV-1 Infection and Adult T Cell Leukemia.International journal of molecular sciences · 2023Review
- Primary cells from patients with adult T cell leukemia/lymphoma depend on HTLV-1 Tax expression for NF-κB activation and survival.Blood cancer journal · 2023Article
- Interplay between innate immunity and the viral oncoproteins Tax and HBZ in the pathogenesis and therapeutic response of HTLV-1 associated adult T cell leukemia.Frontiers in immunology · 2022Review
- Peripheral T cell lymphomas: from the bench to the clinic.Nature reviews. Cancer · 2020Review
- Mouse Models That Enhanced Our Understanding of Adult T Cell Leukemia.Frontiers in microbiology · 2018Review
- Animal Models Utilized in HTLV-1 Research.Virology : research and treatment · 2013Review
- Wip1 and p53 contribute to HTLV-1 Tax-induced tumorigenesis.Retrovirology · 2012Article
- Animal models on HTLV-1 and related viruses: what did we learn?Frontiers in microbiology · 2012Article
- Review
- The ARF tumor suppressor regulates bone remodeling and osteosarcoma development in mice.PloS one · 2010Article
- Viral oncogenes, noncoding RNAs, and RNA splicing in human tumor viruses.International journal of biological sciences · 2010Review
- The role of NF-{kappa}B-1 and NF-{kappa}B-2-mediated resistance to apoptosis in lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Human T-cell leukemia virus type 1 Tax attenuates gamma-irradiation-induced apoptosis through physical interaction with Chk2.Oncogene · 2006Article
- Article
- Reduced cell turnover in lymphocytic monkeys infected by human T-lymphotropic virus type 1.Oncogene · 2005Article
- Animal models for human T-lymphotropic virus type 1 (HTLV-1) infection and transformation.Oncogene · 2005Review
- Clinicobiological, immunophenotypic, and molecular characteristics of monoclonal CD56-/+dim chronic natural killer cell large granular lymphocytosis.The American journal of pathology · 2004Article
- Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity.Retrovirology · 2004Review
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 2 institutions in 1 country.
Funding
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia/lymphoma (ATLL). The HTLV-1 Tax protein has been strongly linked to oncogenesis and is considered to be the transforming protein of this virus. A Tax transgenic mouse model was utilized to study the contribution of p53 inactivation to Tax-mediated tumorigenesis. These mice develop primary, peripheral tumors consisting of large granular lymphocytic (LGL) cells, which also infiltrate the lymph nodes, bone marrow, spleen, liver, and lungs. Primary Tax-induced tumors and tumor-derived cell lines exhibited functional inactivation of the p53 apoptotic pathway; such tumors and tumor cell lines were resistant to an apoptosis-inducing stimulus. In contrast, p53 mutations in tumors were found to be associated with secondary organ infiltration. Three of four identified mutations inhibited transactivation and apoptosis induction activities in vitro. Furthermore, experiments which involved mating Tax transgenic mice with p53-deficient mice demonstrated minimal acceleration in initial tumor formation, but significantly accelerated disease progression and death in mice heterozygous for p53. These studies suggest that functional inactivation of p53 by HTLV-1 Tax, whether by mutation or another mechanism, is not critical for initial tumor formation, but contributes to late-stage tumor progression.
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.