Evidence map›Paper›PMID 42109651›Full record

ArticleFrontiers in oncology2026

SPC24 boosts tumor progression and correlates with immune infiltrates in pancreatic adenocarcinoma.

Wenhui Chen, Xianyu Huang, Jiaxin Liu, Yonghui Liao, Dingwen Zhong

Abstract read
In one paragraph

Article in Frontiers in oncology, 2026. 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
–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

1 citing paper in PubMed.

  1. Article
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

5 authors.

Wenhui ChenDepartment of Hepatobiliary and Pancreatic Surgery, The Affliated Ganzhou Hospital of Nanchang University (Ganzhou People's Hospital), Ganzhou, Jiangxi, China.
Xianyu HuangDepartment of Hepatobiliary and Pancreatic Surgery, The Affliated Ganzhou Hospital of Nanchang University (Ganzhou People's Hospital), Ganzhou, Jiangxi, China.
Jiaxin LiuDepartment of Hepatobiliary and Pancreatic Surgery, The Affliated Ganzhou Hospital of Nanchang University (Ganzhou People's Hospital), Ganzhou, Jiangxi, China.
Yonghui LiaoDepartment of Hepatobiliary and Pancreatic Surgery, The Affliated Ganzhou Hospital of Nanchang University (Ganzhou People's Hospital), Ganzhou, Jiangxi, China.
Dingwen ZhongDepartment of Hepatobiliary and Pancreatic Surgery, The Affliated Ganzhou Hospital of Nanchang University (Ganzhou People's Hospital), Ganzhou, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Pancreatic ductal adenocarcinoma (PDAC) is known for its highly aggressive nature, difficult diagnosis, and resistance to treatment, resulting in a long-term five-year survival rate of less than 10%. This study focuses on the expression and function of mitotic spindle core component SPC24 in PDAC, systematically revealing its important role in tumor progression and prognosis. Methods: Based on TCGA, GEO, and single-cell RNA sequencing data, SPC24 was significantly overexpressed in PDAC tissues and malignant cell subsets, and its expression level was significantly negatively correlated with overall survival (OS) and progression-free survival (PFS). Results: Bioinformatics analysis showed that SPC24-related genes were mainly enriched in cell cycle regulation, chromosome segregation and spindle assembly pathways, suggesting that SPC 24-related genes play a driving role in genomic instability and tumor clone evolution. Immunoinfiltration analysis revealed that high SPC24 expression was associated with immunosuppressive microenvironment features, such as increased M2 tumor-associated macrophages and regulatory T cells, and decreased CD8 + T cells and NK cells. Single-cell communication analysis further suggests that SPC24 may facilitate immune escape by regulating ligand-receptor interactions between tumor cells and immune cells in TME. In addition, Conclusion: SPC24, as an important oncogenic factor and prognostic marker of PDAC, promotes tumor progression and treatment resistance by regulating mitotic abnormalities, metabolic reprogramming and immune microenvironment, and is worthy of being a candidate molecule for new strategies and diagnostic monitoring of targeted therapy. Future studies are needed to further explore its molecular mechanisms and potential for combination therapy to improve clinical outcomes in patients with PDAC.

Indexed as

Immune escapemitosispancreatic ductal adenocarcinoma (PDAC)single cell sequencingSPC24tumor immune microenvironment

Identifiers

PMID42109651
PMCPMC13149173

What OpenQuestion holds

Textmetadata
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.