Evidence map›Paper›PMID 41465457›Full record

ArticleInternational journal of molecular sciences2025

Elucidating Pancreatic Ductal Adenocarcinoma Carcinogenesis at Single-Cell Resolution and Identifying Subtype Specific Drug Candidates.

Jing Chen, Hui Jiang, Hui Chen, Kuan Yang, Kaiyue Yang, Mingyao Sun, Na Lv, Bolin Ren, Xinyi Lin, Xia Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jing ChenCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Hui JiangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Hui ChenCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.ORCID 0009-0009-1699-2706
Kuan YangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Kaiyue YangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Mingyao SunCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Na LvCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Bolin RenCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Xinyi LinCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.ORCID 0009-0003-5331-8872
Xia LiCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.
Yunpeng ZhangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.ORCID 0000-0002-3709-3656
Congxue HuCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.

Funding

China Postdoctoral Science Foundation 2024M760709Heilongjiang Postdoctoral Fund LBH-Z24210Key Research and Development Program of Heilongjiang Province 2024ZX12C27Longjiang New Era Outstanding Doctoral Dissertation Project Grant LJYXL2024-069National Natural Science Foundation of China 62472131, 62172131, U23A20166, 32570792, 62502128National Science and Technology Major Program 2024ZD0530500STI2030-Major Projects-2021ZD0202400 Not applicable
6 · The paper itself

Abstract

Although single-cell analyses have advanced our understanding of pancreatic ductal adenocarcinoma (PDAC), most studies to date have focused on primary and metastatic tumors. Here, we map cell composition, phenotypic plasticity, and microenvironmental remodeling from human normal pancreas through preneoplastic lesions to PDAC, with the preneoplastic phase recognized as a critical window for carcinogenesis. We pinpoint genes that are persistently dysregulated throughout malignant transformation and are associated with a poor prognosis. Focusing on ductal and acinar cells as the principal origins of PDAC, we delineate malignant preneoplastic cell clusters that exhibit strong carcinogenic potential. Immune profiling reveals marked expansion and functional reprogramming of macrophages during disease progression. Integrative analysis with human PDAC bulk transcriptomic cohorts identifies candidate compounds, such as Brefeldin A, with potential for intervention in preneoplastic disease. Together, our study elucidates dynamic molecular and cellular mechanisms underlying PDAC carcinogenesis and provides actionable insights for early intervention and targeted therapy.

Indexed as

Antineoplastic AgentsCarcinogenesisCarcinoma, Pancreatic DuctalPancreatic NeoplasmsSingle-Cell AnalysisCell Transformation, NeoplasticGene Expression ProfilingGene Expression Regulation, NeoplasticHumansTumor MicroenvironmentAntineoplastic Agentscarcinogenesisdrug candidatePDACpreneoplastic stagescRNA-seq

Identifiers

PMID41465457
PMCPMC12732769

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.