Evidence map›Paper›PMID 38468282›Full record

ReviewInflammation and regeneration2024

Gene editing technology to improve antitumor T-cell functions in adoptive immunotherapy.

Yusuke Ito, Satoshi Inoue, Yuki Kagoya

Abstract readReview
In one paragraph

Review in Inflammation and regeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Yusuke ItoDivision of Tumor Immunology, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, 160-8582, Japan.
Satoshi InoueDivision of Tumor Immunology, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, 160-8582, Japan.
Yuki KagoyaDivision of Tumor Immunology, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, 160-8582, Japan. ykagoya@keio.jp.ORCID http://orcid.org/0000-0002-6216-6730

Funding

Fusion Oriented REsearch for disruptive Science and Technology JPMJFR2060Japan Agency for Medical Research and Development JP23ama221303Japan Agency for Medical Research and Development JP23bm0704066Japan Agency for Medical Research and Development JP23ym0126072Japan Society for the Promotion of Science 23H02779
6 · The paper itself

Abstract

Adoptive immunotherapy, in which tumor-reactive T cells are prepared in vitro for adoptive transfer to the patient, can induce an objective clinical response in specific types of cancer. In particular, chimeric antigen receptor (CAR)-redirected T-cell therapy has shown robust responses in hematologic malignancies. However, its efficacy against most of the other tumors is still insufficient, which remains an unmet medical need. Accumulating evidence suggests that modifying specific genes can enhance antitumor T-cell properties. Epigenetic factors have been particularly implicated in the remodeling of T-cell functions, including changes to dysfunctional states such as terminal differentiation and exhaustion. Genetic ablation of key epigenetic molecules prevents the dysfunctional reprogramming of T cells and preserves their functional properties.Clustered, regularly interspaced, short palindromic repeats (CRISPR)/CRISPR-associated protein (Cas)-based gene editing is a valuable tool to enable efficient and specific gene editing in cultured T cells. A number of studies have already identified promising targets to improve the therapeutic efficacy of CAR-T cells using genome-wide or focused CRISPR screening. In this review, we will present recent representative findings on molecular insights into T-cell dysfunction and how genetic modification contributes to overcoming it. We will also discuss several technical advances to achieve efficient gene modification using the CRISPR and other novel platforms.

Indexed as

Adoptive immunotherapyChimeric antigen receptorCRISPR/Cas9DNA methylationEpigeneticsMemory T cellPRDM1T-cell exhaustion

Identifiers

PMID38468282
PMCPMC10926667

What OpenQuestion holds

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Registered trials

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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.