Evidence map›Paper›PMID 41293263›Full record

ArticleFrontiers in oncology2025

BTBD19 promotes colorectal cancer progression and correlates with adverse clinical outcomes.

Changjiang Yang, Xuhua Geng, Zihan Zhao

Abstract read
In one paragraph

Article in Frontiers in oncology, 2025. 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

3 authors.

Changjiang YangAerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China.
Xuhua GengSchool of Public Health, Boston University, Boston, MA, United States.
Zihan ZhaoAerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide. The identification of novel prognostic biomarkers and therapeutic targets is crucial for improving clinical management and patient outcomes. Members of the BTBD (BTB/POZ domain-containing) protein family have been implicated in tumorigenesis, but the role of BTBD19 in CRC remains poorly understood. Objective: This study aimed to investigate the expression pattern of BTBD19 in CRC, its association with clinicopathological features and prognosis, and its potential molecular mechanisms involving functional pathways and immune infiltration. Methods: BTBD19 expression was analyzed using public datasets (TCGA, GEO) and clinical tissue microarrays. Immunohistochemistry (IHC) was performed to validate protein expression. Survival analysis (OS, DSS, PFI) was conducted to assess prognostic significance. Functional enrichment analyses (GO/KEGG/GSEA) and immune infiltration analyses (ESTIMATE, ssGSEA, CIBERSORT) were used to explore underlying molecular mechanisms and immune-related associations. Results: BTBD19 was significantly upregulated in CRC tissues at both mRNA and protein levels compared to normal tissues. High BTBD19 expression was associated with advanced pathologic stages and poor prognosis (OS, DSS, PFI; all p<0.05). Functional analyses revealed that BTBD19-associated genes were enriched in pathways related to extracellular matrix organization, focal adhesion, and epithelial-mesenchymal transition. Immune infiltration analysis showed positive correlations between BTBD19 expression and stromal/immune scores, M2 macrophage infiltration, and expression of immune checkpoints (CD274, PDCD1). Conclusion: BTBD19 is upregulated in CRC and promotes tumor progression. It may serve as a potential prognostic biomarker for CRC, with implications for understanding CRC pathogenesis and immune microenvironment regulation.

Indexed as

BTBD19colorectal cancerimmune checkpointsimmune infiltrationmetastasisprognosis

Identifiers

PMID41293263
PMCPMC12640813

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