ArticleCancers2025
A Validated Proteomic Signature of Basal-like Triple-Negative Breast Cancer Subtypes Obtained from Publicly Available Data.
Article in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Emerging Breast Cancer Subpopulations: Functional Heterogeneity Beyond the Classical Subtypes.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBasal-like breast cancer (BLBC) is a highly aggressive molecular subtype characterized by the strong expression of a gene cluster found in the basal or outer epithelial layer of the adult mammary gland. Patients with BLBC typically face a poor prognosis, with a shorter disease-free period and overall survival.
methodsIn this study, we explored the proteomic profiles of BLBC patients using publicly available data from two large cohorts of breast cancer patients. By integrating cluster analysis, predictive modeling, protein differential abundance expression, and network analysis, we identified and validated the presence of two distinct subgroups, characterized by 256 upregulated and 99 downregulated proteins.
resultsWe report the upregulation of spliceosome components, especially SNRPG and its partners (BUD13, CWC15, SNRNP70, ZMAT12), indicating altered splicing activity between TNBC subgroups. Collagen proteins (COL1A1, COL1A2, COL3A1, COL11A1) were associated with tumor progression and metastasis. Proteins in the CCT complex and microtubule-associated proteins (TUBA1C, TUBB) were linked to cytoskeletal structure and chemotherapy resistance. Aminoacyl-tRNA synthetases (DARS1, IARS1, KARS1) may also play a role in TNBC development.
conclusionsThese findings suggest the existence of novel molecular signatures that could improve TNBC classification, prognosis, and potential therapeutic targeting.
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