Evidence map›Paper›PMID 35440418›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022

Development of a TNF-α-mediated Trojan Horse for bacteria-based cancer therapy.

Che-Wei Hu, You-Chiun Chang, Cheng-Hao Liu, Yao-An Yu, Kurt Yun Mou

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% of its field
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Attenuated mutants ofExperimental biology and medicine (Maywood, N.J.) · 2024
    Article
  11. Bacterial-Mediated Tumor Therapy: Old Treatment in a New Context.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  12. Refined control of CRISPR-Cas9 gene editing inFrontiers in immunology · 2023
    Article
  13. Tumor Necrosis Factor-Mediators of inflammation · 2023
    Article
  14. Article
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

5 authors at 3 institutions in 1 country.

Che-Wei HuInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
You-Chiun ChangInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Taiwan International Graduate Program in Chemical Biology and Molecular Biophysics, National Taiwan University and Academia Sinica, Taipei 11529, Taiwan.
Cheng-Hao LiuInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Taiwan International Graduate Program in Molecular Medicine, National Yang Ming Chiao Tung University and Academia Sinica, Taipei 11529, Taiwan.
Yao-An YuInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Doctoral Degree Program of Translational Medicine, National Yang Ming Chiao Tung University and Academia Sinica, Taipei 112, Taiwan.
Kurt Yun MouInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan. Electronic address: ymou@ibms.sinica.edu.tw.
Institute of Biomedical Sciences, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor α (TNF-α) is upregulated in a chronic inflammatory environment, including tumors, and has been recognized as a pro-tumor factor in many cancers. Applying the traditional TNF-α antibodies that neutralize TNF-α activity, however, only exerts modest anti-tumor efficacy in clinical studies. Here, we develop an innovative approach to target TNF-α that is distinct from the neutralization mechanism. We employed phage display and yeast display to select non-neutralizing antibodies that can piggyback on TNF-α and co-internalize into cells through receptor ligation. When conjugating with toxins, the antibody exhibited cytotoxicity to cancer cells in a TNF-α-dependent manner. We further implemented the immunotoxin to an E. coli vehicle specially engineered for a high secretion level. In a syngeneic murine melanoma model, the bacteria stimulated TNF-α expression that synergized with the secreted immunotoxin and greatly inhibited tumor growth. The treatment also dramatically remodeled the tumor microenvironment in favor of several anti-tumor immune cells, including N1 neutrophils, M1 macrophages, and activated CD4

Indexed as

ImmunotoxinsMelanomaAnimalsEscherichia coliMiceTumor MicroenvironmentTumor Necrosis Factor-alphaImmunotoxinsTumor Necrosis Factor-alphaantibodybacterial therapyimmunotherapyimmunotoxinmelanomaphage displayTNF-αtumor-infiltrating immune cellsyeast surface display

Identifiers

PMID35440418
PMCPMC9263318
OpenAlexW4223898939

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.