ArticleImmunity2016
Targeting of Tumor-Associated Glycoforms of MUC1 with CAR T Cells.
Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed.
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Revolutionising cancer intervention: the repercussions of CAR-T cell therapy on modern oncology practices.Medical oncology (Northwood, London, England) · 2025Review
- Research progress of MUC1 in genitourinary cancers.Cellular & molecular biology letters · 2024Review
- Multi-armored allogeneic MUC1 CAR T cells enhance efficacy and safety in triple-negative breast cancer.Science advances · 2024Article
- Review
- CAR-T treatment for cancer: prospects and challenges.Frontiers in oncology · 2023Review
- Review
- Chimeric antigen receptor clustering via cysteines enhances T-cell efficacy against tumor.Cancer immunology, immunotherapy : CII · 2022Article
- CAR T cells redirected against tumor-specific antigen glycoforms: can low-sugar antigens guarantee a sweet success?Frontiers of medicine · 2022Review
- Review
- From Anti-HER-2 to Anti-HER-2-CAR-T Cells: An Evolutionary Immunotherapy Approach for Gastric Cancer.Journal of inflammation research · 2022Review
- Remote controlling of CAR-T cells and toxicity management: Molecular switches and next generation CARs.Translational oncology · 2021Review
- CAR-T cells: Early successes in blood cancer and challenges in solid tumors.Acta pharmaceutica Sinica. B · 2021Review
- Reprogramming Immune Cells for Enhanced Cancer Immunotherapy: Targets and Strategies.Frontiers in immunology · 2021Review
- Mass Spectrometric Mapping of Glycoproteins Modified by Tn-Antigen Using Solid-Phase Capture and Enzymatic Release.Analytical chemistry · 2020Article
- Article
- Mass spectrometry for the identification and analysis of highly complex glycosylation of therapeutic or pathogenic proteins.Expert review of proteomics · 2020Review
- MUC1 as a target for CAR-T therapy in head and neck squamous cell carinoma.Cancer medicine · 2020Article
- Next generation chimeric antigen receptor T cells: safety strategies to overcome toxicity.Molecular cancer · 2019Review
- Strategies to Address Chimeric Antigen Receptor Tonic Signaling.Molecular cancer therapeutics · 2018Review
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Authors and funding
9 authors.
Funding
Abstract
We read with interest the manuscript by June and colleagues published recently in Immunity in which they describe targeting of aberrantly glycosylated tumor-associated cell membrane mucin MUC1 using chimeric antigen receptor-engineered human T cells (Posey et al., 2016). In that study, the authors used a second generation 4-1BB costimulatory-molecule-based chimeric antigen receptor (CAR) (Imai et al., 2004) in which targeting was achieved using a single-chain variable fragment (scFv) derived from the 5E5 antibody. This CAR selectively binds MUC1 that carries the Tn or sialyl (S)Tn glycan. Both of these truncated glycans are aberrantly expressed on the MUC1 glycoprotein in a spectrum of malignancies and consequently represent attractive targets for immunotherapeutic exploitation.
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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.