ArticleBreast cancer research : BCR2023
Transcriptomic alterations underlying metaplasia into specific metaplastic components in metaplastic breast carcinoma.
Article in Breast cancer research : BCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 53 citations in OpenAlex.
- Hormone therapy enhances anti-PD1 efficacy in premenopausal estrogen receptor-positive and HER2-negative advanced breast cancer.Cell reports. Medicine · 2025Trial
- Podoplanin-defined tumour plasticity and CCR7-mediated lymphatic metastasis in triple-negative breast cancer.British journal of cancer · 2026Article
- Carcinomas exhibiting epithelial-mesenchymal transition manifest an M2 macrophage-enriched tumor immune microenvironment.Breast cancer research : BCR · 2025Article
- Integrated profiling of metaplastic breast cancer identifies putative master regulators of intratumoral heterogeneity.NPJ breast cancer · 2025Article
- Case Report: Metaplastic breast carcinoma with osseous and chondrodifferentiation in liver metastasis: a rare case and review of literature.Frontiers in oncology · 2025Article
- Characteristics and transcriptional regulators of spontaneous epithelial-mesenchymal transition in genetically unperturbed patient-derived non-spindled breast carcinoma.Breast cancer research : BCR · 2024Article
- A comprehensive overview of metaplastic breast cancer: Features and treatments.Cancer science · 2024Review
- Translational Aspects in Metaplastic Breast Carcinoma.Cancers · 2024Review
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9 authors at 2 institutions in 1 country.
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Abstract
backgroundMetaplastic breast carcinoma (MpBC) typically consists of carcinoma of no special type (NST) with various metaplastic components. Although previous transcriptomic and proteomic studies have reported subtype-related heterogeneity, the intracase transcriptomic alterations between metaplastic components and paired NST components, which are critical for understanding the pathogenesis underlying the metaplastic processes, remain unclear.
methodsFifty-nine NST components and paired metaplastic components (spindle carcinomatous [SPS], matrix-producing, rhabdoid [RHA], and squamous carcinomatous [SQC] components) were microdissected from specimens obtained from 27 patients with MpBC for gene expression profiling using the NanoString Breast Cancer 360 Panel on a NanoString nCounter FLEX platform. BC360-defined signatures were scored using nSolver software.
resultsHierarchical clustering and principal component analysis revealed a heterogeneous gene expression profile (GEP) corresponding to the NST components, but the GEP of metaplastic components exhibited subtype dependence. Compared with the paired NST components, the SPS components demonstrated the upregulation of genes related to stem cells and epithelial-mesenchymal transition and displayed enrichment in claudin-low and macrophage signatures. Despite certain overlaps in the enriched functions and signatures between the RHA and SPS components, the specific differentially expressed genes differed. We observed the RHA-specific upregulation of genes associated with vascular endothelial growth factor signaling. The chondroid matrix-producing components demonstrated the upregulation of hypoxia-related genes and the downregulation of the immune-related MHC2 signature and the TIGIT gene. In the SQC components, TGF-β and genes associated with cell adhesion were upregulated. The differentially expressed genes among metaplastic components in the 22 MpBC cases with one or predominantly one metaplastic component clustered paired NST samples into clusters with correlation with their associated metaplastic types. These genes could be used to separate the 31 metaplastic components according to respective metaplastic types with an accuracy of 74.2%, suggesting that intrinsic signatures of NST may determine paired metaplastic type. Finally, the EMT activity and stem cell traits in the NST components were correlated with specimens displaying lymph node metastasis.
conclusionsWe presented the distinct transcriptomic alterations underlying metaplasia into specific metaplastic components in MpBCs, which contributes to the understanding of the pathogenesis underlying morphologically distinct metaplasia in MpBCs.
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