Evidence map›Paper›PMID 40484878›Full record

ArticleSignal transduction and targeted therapy2025

Single-cell transcriptional dissection illuminates an evolution of immunosuppressive microenvironment during pancreatic ductal adenocarcinoma metastasis.

Xiaowei Liu, Jinen Song, Meiling Yuan, Fengli Zuo, Huihui Li, Leyi Tang, Xinmin Wang, Xueyan Wang, Qian Xiao, Li Li and 6 more

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 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

16 authors.

Xiaowei Liu *Institute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Jinen Song *Institute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Meiling YuanInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Fengli ZuoInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Huihui LiInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Leyi TangInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Xinmin WangInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Xueyan WangInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Qian XiaoInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Li LiInstitute of Clinical Pathology, West China Hospital of Sichuan University, Chengdu, China.
Xinyu LiuInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Zhankun YangCollege of Chemical Engineering, Shijiazhuang University, Shijiazhuang, Hebei, China.
Jianlin WuState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.ORCID 0000-0002-3875-185X
Jing JingInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China. jingjing@wchscu.edu.cn.
Xuelei MaDepartment of Biotherapy, West China Hospital and State Key Laboratory of Biotherapy, Sichuan University, Chengdu, Sichuan, China. drmaxuelei@gmail.com.ORCID 0000-0002-9148-5001
Hubing ShiInstitute for Breast Health Medicine, State Key Laboratory of Biotherapy, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China. shihb@scu.edu.cn.ORCID 0000-0002-2926-3440

Funding

National Natural Science Foundation of China (National Science Foundation of China) 22105137National Natural Science Foundation of China (National Science Foundation of China) 82172634
6 · The paper itself

Abstract

How the host immune system loses its surveillance function during the evolution from normal cell to malignancy is still largely unknown. Here, we investigate the dynamics changes of the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment by profiling 132,115 single-cell transcriptomes derived from 51 tissues, including healthy pancreatic tissue, non-metastatic PDAC primary tumors, metastatic primary tumors, and patient-matched liver metastases. The cellular proportion, bio-functional, and interaction between each cell type are carefully characterized. Aberrant copy number variations (CNVs) indicating malignant intensity are identified at chromosomes 7 and 20 of epithelial cells during tumor development. A bio-functional transition of predominant genes from physiology to pancreatic oncogenesis and metastasis is observed. Combinatorial analysis of epithelial cells and immunocytes indicates a gradient loss of immune surveillance during the malignant transformation. By dissecting cellular interaction, we unravel an incremental tumor cell-triggered apoptosis of DCs through molecular pair ANXA1-FPR1/3. Consequently, the activation and infiltration of cytotoxic CD8

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsTumor MicroenvironmentCD8-Positive T-LymphocytesDNA Copy Number VariationsFemaleGene Expression Regulation, NeoplasticHumansKiller Cells, NaturalMaleNeoplasm MetastasisSingle-Cell AnalysisTranscriptome

Identifiers

PMID40484878
PMCPMC12146409

What OpenQuestion holds

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LicenceCC BY
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.