Evidence map›Paper›PMID 38523373›Full record

ArticleBMB reports2024

CDKN2 expression is a potential biomarker for T cell exhaustion in hepatocellular carcinoma.

Shibo Wei, Yan Zhang, Baeki E Kang, Wonyoung Park, He Guo, Seungyoon Nam, Jong-Sun Kang, Jee-Heon Jeong, Yunju Jo, Dongryeol Ryu and 2 more

Open access · goldAbstract readNews
PubMed Full text at PMC
In one paragraph

Article in BMB reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

12 authors at 6 institutions in 2 countries.

Shibo WeiDepartment of Precision Medicine, Sungkyunkwan University School of Medicine, Suwon 16419, Korea.
Yan ZhangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419, Korea.
Baeki E KangDepartment of Physiology, Sungkyunkwan University School of Medicine, Suwon 16419, Korea.
Wonyoung ParkDepartment of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan 50612, Korea.
He GuoDepartment of Obstetrics and Gynecology, The Second Hospital of Jilin University, Changchun 130041, China.
Seungyoon NamDepartment of Genome Medicine and Science, AI Convergence Center for Medical Science, Gachon University Gil Medical Center, Gachon University College of Medicine, Incheon 21565, Korea.
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419, Korea.
Jee-Heon JeongDepartment of Precision Medicine, Sungkyunkwan University School of Medicine, Suwon 16419, Korea.
Yunju JoDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju 61005, Korea.
Dongryeol RyuDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju 61005, Korea.
Yikun JiangDepartment of Orthopedics, The Second Hospital of Jilin University, Changchun 130041, China.
Ki-Tae HaDepartment of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan 50612, Korea.
Sungkyunkwan University · KRGwangju Institute of Science and Technology · KRSecond Affiliated Hospital of Jilin University · CNGachon University Gil Medical Center · KRJilin University · CNPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular Carcinoma (HCC), the predominant primary hepatic malignancy, is the prime contributor to mortality. Despite the availability of multiple surgical interventions, patient outcomes remain suboptimal. Immunotherapies have emerged as effective strategies for HCC treatment with multiple clinical advantages. However, their curative efficacy is not always satisfactory, limited by the dysfunctional T cell status. Thus, there is a pressing need to discover novel potential biomarkers indicative of T cell exhaustion (Tex) for personalized immunotherapies. One promising target is Cyclin-dependent kinase inhibitor 2 (CDKN2) gene, a key cell cycle regulator with aberrant expression in HCC. However, its specific involvement remains unclear. Herein, we assessed the potential of CDKN2 expression as a promising biomarker for HCC progression, particularly for exhausted T cells. Our transcriptome analysis of CDKN2 in HCC revealed its significant role involving in HCC development. Remarkably, single-cell transcriptomic analysis revealed a notable correlation between CDKN2 expression, particularly CDKN2A, and Tex markers, which was further validated by a human cohort study using human HCC tissue microarray, highlighting CDKN2 expression as a potential biomarker for Tex within the intricate landscape of HCC progression. These findings provide novel perspectives that hold promise for addressing the unmet therapeutic need within HCC treatment. [BMB Reports 2024; 57(6): 287-292].

Indexed as

Biomarkers, TumorCarcinoma, HepatocellularLiver NeoplasmsT-LymphocytesGene Expression ProfilingGene Expression Regulation, NeoplasticHumansT-Cell ExhaustionBiomarkers, Tumor

Identifiers

PMID38523373
PMCPMC11214889
OpenAlexW4391985655

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.