ArticleThe Journal of clinical investigation2011
TCR-dependent transformation of mature memory phenotype T cells in mice.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 75 citations in OpenAlex.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Unveiling cellular communications through rapid pan-membrane-protein labeling.Nature communications · 2025Article
- SMARCB1-deficient malignant melanocytic uveal tumours: a new neural crest-derived tumour entity with SMARCB1-related germline predisposition.The Journal of pathology · 2025Article
- Lack of SMARCB1 expression characterizes a subset of human and murine peripheral T-cell lymphomas.Nature communications · 2024Article
- PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression.Nature communications · 2024Article
- Epigenetic modulators provide a path to understanding disease and therapeutic opportunity.Genes & development · 2024Review
- CD47 promotes peripheral T cell survival by preventing dendritic cell-mediated T cell necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Targeting Lymphoma-associated Macrophage Expansion via CSF1R/JAK Inhibition is a Therapeutic Vulnerability in Peripheral T-cell Lymphomas.Cancer research communications · 2022Article
- GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.Blood cancer journal · 2022Article
- Notch Signaling Promotes Mature T-Cell Lymphomagenesis.Cancer research · 2022Article
- Review
- A preclinical model of peripheral T-cell lymphoma GATA3 reveals DNA damage response pathway vulnerability.EMBO molecular medicine · 2022Article
- The SWI/SNF ATPase BRG1 facilitates multiple pro-tumorigenic gene expression programs in SMARCB1-deficient cancer cells.Oncogenesis · 2022Article
- Article
- Emerging Themes in Mechanisms of Tumorigenesis by SWI/SNF Subunit Mutation.Epigenetics insights · 2022Review
- Generation of a uniform thymic malignant lymphoma model with C57BL/6JJournal of toxicologic pathology · 2022Article
- Chronic T cell receptor stimulation unmasks NK receptor signaling in peripheral T cell lymphomas via epigenetic reprogramming.The Journal of clinical investigation · 2021Article
- Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler.Oncogene · 2021Article
- Engagement of lymphoma T cell receptors causes accelerated growth and the secretion of an NK cell-inhibitory factor.Cellular immunology · 2020Article
- Frequent mutations in the amino-terminal domain of BCL7A impair its tumor suppressor role in DLBCL.Leukemia · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
A fundamental goal in cancer research is the identification of the cell types and signaling pathways capable of initiating and sustaining tumor growth, as this has the potential to reveal therapeutic targets. Stem and progenitor cells have been implicated in the genesis of select lymphoid malignancies. However, the identity of the cells in which mature lymphoid neoplasms are initiated remains unclear. Here, we investigate the origin of peripheral T cell lymphomas using mice in which Snf5, a chromatin remodelling-complex subunit with tumor suppressor activity, could be conditionally inactivated in developing T cells. In this model of mature peripheral T cell lymphomas, the cell of origin was a mature CD44hiCD122loCD8⁺ T cell that resembled a subset of memory cells that has capacity for self-renewal and robust expansion, features shared with stem cells. Further analysis showed that Snf5 loss led to activation of a Myc-driven signaling network and stem cell transcriptional program. Finally, lymphomagenesis and lymphoma proliferation depended upon TCR signaling, establishing what we believe to be a new paradigm for lymphoid malignancy growth. These findings suggest that the self-renewal and robust proliferative capacities of memory T cells are associated with vulnerability to oncogenic transformation. Our findings further suggest that agents that impinge upon TCR signaling may represent an effective therapeutic modality for this class of lethal human cancers.
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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.