Evidence map›Paper›PMID 30078052›Full record

ArticleCancer immunology, immunotherapy : CII2018

Increased antitumor activities of glypican-3-specific chimeric antigen receptor-modified T cells by coexpression of a soluble PD1-CH3 fusion protein.

Zeyan Pan, Shengmeng Di, Bizhi Shi, Hua Jiang, Zhimin Shi, Ying Liu, Yi Wang, Hong Luo, Min Yu, Xiuqi Wu and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. A novel PD-L1-targeted shark VMolecular therapy oncolytics · 2022
    Article
  10. Article
  11. Mechanisms of CAR T cell exhaustion and current counteraction strategies.Frontiers in cell and developmental biology · 2022
    Review
  12. Article
  13. Review
  14. APL bioengineering · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. The Role of Glypicans in Cancer Progression and Therapy.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020
    Review
  20. 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

11 authors at 3 institutions in 1 country.

Zeyan PanState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Shengmeng DiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Bizhi ShiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Hua JiangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Zhimin ShiCARsgen Therapeutics, Shanghai, China.
Ying LiuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Yi WangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Hong LuoState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Min YuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Xiuqi WuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China.
Zonghai LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25/Ln. 2200, XieTu Road, Shanghai, 200032, China. zonghaili@shsmu.edu.cn.
State Key Laboratory of Oncogene and Related Genes · CNRenji Hospital · CNShanghai Cancer Institute · CN

Funding

Collaborative Innovation Center for Translational Medicine at Shanghai Jiao Tong University School of Medicine TM201601Research Fund of Shanghai Municipal Commission of Health and Family Planning NO. 20174Y0178Shanghai Science and Technology Innovation Action Plan No. 16DZ1910700the "13th Five-Year Plan" National Science and Technology Major Project of China 2017ZX10203206006the National Natural Science Foundation of China 81472569
6 · The paper itself

Abstract

Our recent clinical study demonstrated that glypican-3 (GPC3)-specific chimeric antigen receptor-modified T (CAR-T) cells are a promising treatment for hepatocellular carcinoma (HCC). However, the interaction of programmed cell death 1 (PD-1) and PD-L1-mediated T-cell inhibition is involved in immune evasion in a wide range of solid tumors, including HCC. To overcome this problem, we introduced a fusion protein composed of a PD-1 extracellular domain and CH3 from IgG4 into GPC3-specific CAR-T cells (GPC3-28Z) to block the PD-1/PD-L1 pathway. GPC3-specific CAR-T cells carrying the PD-1-CH3 fusion protein (sPD1) specifically recognized and lysed GPC3-positive HCC cells. The proliferation capacity of GPC3-28Z-sPD1 T cells after weekly stimulation with target cells was much higher than that of control GPC3-28Z T cells. Additionally, the coexpression of sPD1 could protect CAR-T cells from exhaustion when incubated with target cells, as phosphorylated AKT and Bcl-xL expression levels were higher in GPC3-28Z-sPD1 T cells than in GPC3-28Z cells. Importantly, in two HCC tumor xenograft models, GPC3-28Z-sPD1 T cells displayed a significantly higher tumor suppression capacity than GPC3-28Z T cells. In addition, an increased number of CD3

Indexed as

AnimalsCarcinoma, HepatocellularCells, CulturedGlypicansHumansImmunoglobulin GLiver NeoplasmsMiceMice, Inbred NODMice, SCIDProgrammed Cell Death 1 ReceptorProtein DomainsReceptors, Antigen, T-CellRecombinant Fusion ProteinsT-LymphocytesXenograft Model Antitumor AssaysGlypicansGPC3 protein, humanImmunoglobulin GPDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-CellRecombinant Fusion ProteinsChimeric antigen receptorGlypican-3Hepatocellular carcinomaPD-1/PD-L1sPD1

Identifiers

PMID30078052
PMCPMC11028056
OpenAlexW2887707004

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.