ArticleBMC genomic data2025
Profiling the full-length transcriptome of plasma cell mastitis via nanopore sequencing.
Article in BMC genomic data, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
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Who cites it
3 citing papers in PubMed.
- Plasma cell mastitis: a comprehensive review of etiological advances and future directions.Frontiers in immunology · 2026Review
- Recent Advances in Pathogenesis, Diagnosis and Integrated Traditional Chinese Medicine Therapy for Plasma Cell Mastitis.International journal of general medicine · 2026Review
- Molecular Targeted Therapy for Chronic Non-Bacterial Mastitis: New Insights into Pathophysiology and Therapeutic Strategies.International journal of women's health · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
introductionIn this study, we aimed to determine the transcriptomic profile of plasma cell mastitis (PCM) and elucidate its underlying mechanisms using nanopore sequencing technology (ONT). METHODS AND
resultsThrough comparisons and analyses of redundantly removed transcripts with known reference genome annotations, we identified 39,408 novel transcripts and 20,980 genes. By exploring full-length transcriptome data, we characterized selective splicing, selective polyadenylation events, and simple sequence repeat (SSR) site information, which enhanced our understanding of genome annotation and gene structure in plasma cell mastitis. Additionally, we investigated predicted transcription factors and LncRNAs, screening those with differences for further investigations. The GO and KEGG enrichment analysis of differentially expressed genes (DEGs) and differentially expressed transcripts (DETs) revealed subtle distinctions between them, with primary enrichments being in immune response and intercellular interactions. Our protein-protein interaction (PPI) analysis of hub proteins from DETs indicated up-regulated genes' involvement in immune response and down-regulated genes' role in cell adhesion. Furthermore, we assessed immune cell infiltration in plasma cell mastitis, observing various immune cells, such as B cells, T cells, and DC cells.
conclusionThese preliminary findings offer novel insights into the pathogenesis of plasma cell mastitis and present promising ideas for optimizing personalized treatment approaches, warranting further exploration and follow-up studies.
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