Evidence map›Paper›PMID 39384651›Full record

ArticleCell biology and toxicology2024

Mechanisms of HIF1A-mediated immune evasion in gastric cancer and the impact on therapy resistance.

Hao Qi, Xiaoyu Ma, Yu Ma, Liuyu Jia, Kuncong Liu, Honghu Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell biology and toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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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

6 authors.

Hao QiDepartment of Surgical Oncology, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning Province, China.
Xiaoyu MaDepartments of Gastrointestinal Endoscopy, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Yu MaDepartment of Nuclear Medicine, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Liuyu JiaDepartment of Surgical Oncology, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning Province, China.
Kuncong LiuDepartment of Surgical Oncology, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning Province, China.
Honghu WangDepartment of Surgical Oncology, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning Province, China. hgwang@cmu.edu.cn.

Funding

National Natural Science Foundation of China No. 82373271, 82303040
6 · The paper itself

Abstract

backgroundThe high prevalence and detrimental effects on patient outcomes make gastric cancer (GC) a significant health issue that persists internationally. Existing treatment modalities exhibit limited efficacy, prompting the exploration of immune checkpoint inhibitors as a novel therapeutic approach. However, resistance to immunotherapy poses a significant challenge in GC management, necessitating a profound grasp of the intrinsic molecular pathways.

methodsThis study focuses on investigating the immunosuppressive mechanisms of quiescent cancer cells (QCCs) in GC, particularly their resistance to T-cell-mediated immune responses. Utilizing mouse models, gene editing techniques, and transcriptome sequencing, we aim to elucidate the interactions between QCCs, immune cells, and key regulatory factors like HIF1A. Functional enrichment analysis will further underscore the role of glycolysis-related genes in mediating immunosuppression by QCCs.

resultsThe cancer cells that survived GC treated with T-cell therapy lost their proliferative ability. QCCs, as the main resistance force to immunotherapy, exhibit stronger resistance to CD8

conclusionUnraveling the molecular mechanisms by which QCCs resist T-cell-mediated immune responses through immunosuppression holds promising implications for refining treatment strategies and enhancing patient outcomes in GC. By delineating these intricate interactions, this study contributes crucial insights into precision medicine and improved therapeutic outcomes in GC management.

Indexed as

Hypoxia-Inducible Factor 1, alpha SubunitStomach NeoplasmsTumor MicroenvironmentAnimalsCell Line, TumorDrug Resistance, NeoplasmGlycolysisHumansImmune EvasionImmunotherapyMiceMice, Inbred C57BLTumor EscapeHypoxia-Inducible Factor 1, alpha SubunitDrug resistanceGastric cancerGlycolysisHIF1AImmune-suppressive microenvironmentQuiescent cancer cellsSingle-cell sequencingT cells

Identifiers

PMID39384651
PMCPMC11464584

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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.