ArticleScientific reports2025
Proteomics characterization of triple-negative apocrine carcinoma reveals molecular features of progression and chemotherapy response.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Triple-negative apocrine carcinoma (TNAC) is a rare and chemotherapy-insensitive subtype of triple-negative breast cancer (TNBC), characterized by specific morphology and molecular features. Despite limited chemotherapy response, TNAC shows favorable long-term survival, suggesting distinct resistance mechanisms. In this study, we present the first proteomics-based profiling of TNAC formalin-fixed paraffin-embedded (FFPE) samples using mass spectrometry. Our analysis reveals progressive activation of PI3K/AKT and androgen receptor (AR) signaling, along with upregulation of GTPase-related proteins, suggesting enhanced invasiveness. Post-chemotherapy TNAC displays increased inflammation and mixed ribosomal regulation, pointing to a metabolic shift in survival strategy. These findings support the rationale for exploring chemotherapy de-escalation strategies in TNAC, and highlight the potential utility of PI3K/AKT inhibitors and AR antagonists, possibly in combination with GTPase inhibitors, metabolic disruptors, or immunotherapy.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.