Evidence map›Paper›PMID 38231470›Full record

ReviewCancer research2024

Post-translational Modification of PD-1: Potential Targets for Cancer Immunotherapy.

Te-An Lee, En-Yun Tsai, Shou-Hou Liu, Shih-Duo Hsu Hung, Shing-Jyh Chang, Chi-Hong Chao, Yun-Ju Lai, Hirohito Yamaguchi, Chia-Wei Li

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
10.7field-weighted citation impact, top 1% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

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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

9 authors at 6 institutions in 2 countries.

Te-An LeeInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0000-0003-1987-2653
En-Yun TsaiInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0009-0003-8454-4442
Shou-Hou LiuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0009-0003-6605-2698
Shih-Duo Hsu HungInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0009-0001-4225-1583
Shing-Jyh ChangHsinchu MacKay Memorial Hospital, Hsinchu, Taiwan.ORCID 0009-0004-1793-2450
Chi-Hong ChaoDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan.ORCID 0000-0001-9890-4902
Yun-Ju LaiSolomont School of Nursing, Zuckerberg College of Health Sciences, University of Massachusetts Lowell, Lowell, Massachusetts.ORCID 0000-0003-0802-937X
Hirohito YamaguchiGraduate Institute of Biomedical Sciences, Research Center for Cancer Biology and Center for Molecular Medicine, China Medical University, Taichung, Taiwan.ORCID 0000-0003-0425-916X
Chia-Wei LiInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0000-0002-2531-2866
Institute of Biomedical Sciences, Academia Sinica · TWNational Taiwan University · TWChina Medical University · TWNational Tsing Hua University · TWNational Yang Ming Chiao Tung University · TWUniversity of Massachusetts Lowell · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of effector T cells leads to upregulation of PD-1, which can inhibit T-cell activity following engagement with its ligand PD-L1. Post-translational modifications (PTM), including glycosylation, phosphorylation, ubiquitination, and palmitoylation, play a significant role in regulating PD-1 protein stability, localization, and interprotein interactions. Targeting PTM of PD-1 in T cells has emerged as a potential strategy to overcome PD-1-mediated immunosuppression in cancer and enhances antitumor immunity. The regulatory signaling pathways that induce PTM of PD-1 can be suppressed with small-molecule inhibitors, and mAbs can directly target PD-1 PTMs. Preliminary outcomes from exploratory studies suggest that focusing on the PTM of PD-1 has strong therapeutic potential and can enhance the response to anti-PD-1.

Indexed as

NeoplasmsProgrammed Cell Death 1 ReceptorB7-H1 AntigenHumansImmunotherapyProtein Processing, Post-TranslationalUbiquitinationB7-H1 AntigenProgrammed Cell Death 1 Receptor

Identifiers

PMID38231470
PMCPMC10940856
OpenAlexW4390940871

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.