ArticleMolecular carcinogenesis2020
Loss of myoepithelial calponin-1 characterizes high-risk ductal carcinoma in situ cases, which are further stratified by T cell composition.
Article in Molecular carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Gap junction communication regulates luminal-myoepithelial crosstalk and cell differentiation in a bilayered human mammary epithelial cell model.Biology methods & protocols · 2026Article
- The Microenvironment in DCIS and Its Role in Disease Progression.Advances in experimental medicine and biology · 2025Review
- Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance.Signal transduction and targeted therapy · 2024Review
- Article
- Neurotrophin signaling is a central mechanism of salivary dysfunction after irradiation that disrupts myoepithelial cells.NPJ Regenerative medicine · 2023Article
- TGFβ-mediated MMP13 secretion drives myoepithelial cell dependent breast cancer progression.NPJ breast cancer · 2023Article
- Identifying recurrences and metastasis after ductal carcinoma in situ (DCIS) of the breast.Histopathology · 2023Review
- Re-evaluation of the myoepithelial cells roles in the breast cancer progression.Cancer cell international · 2022Review
- Article
- Ductal Carcinoma in Situ: Molecular Changes Accompanying Disease Progression.Journal of mammary gland biology and neoplasia · 2022Review
- Immune response and stromal changes in ductal carcinoma in situ of the breast are subtype dependent.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Loss of myoepithelial calponin-1 characterizes high-risk ductal carcinoma in situ cases, which are further stratified by T cell composition.Molecular carcinogenesis · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
A hallmark of ductal carcinoma in situ (DCIS) progression is a loss of the surrounding ductal myoepithelium. However, whether compromise in myoepithelial differentiation, rather than overt cellular loss, can be used to predict the risk of DCIS progression is unknown. Here we address this question utilizing pure and mixed DCIS cases (N = 30) as surrogates for DCIS at low and high risk for progression, respectively. We used multiplex immunohistochemical staining to evaluate the relationship between myoepithelial cell differentiation and lymphoid immune cell types associated with poor prognostic DCIS. Our results show that myoepithelial calponin-1 discriminates between pure and mixed DCIS lesions better than histological subtype, presence of necrosis, or nuclear grade. Additionally, focal loss of myoepithelial cells associated with increased PD-1+CD8+ T cells, which suggests a link between the myoepithelium and immune surveillance. To identify associations between calponin-1 expression and immune response, we performed unsupervised hierarchical clustering of myoepithelial and immune cell biomarkers on 219 DCIS lesions from 30 cases. Notably, the majority of pure (low-risk) DCIS lesions clustered in a high calponin-1, T cell low group, whereas the majority of mixed (high-risk) DCIS lesions clustered in a low calponin-1, T cell high group, specifically with CD8+ and PD-1+CD8+ T cells. However, a subset of pure DCIS lesions had a similar calponin-1 and immune signature as the majority of mixed DCIS lesions, which have low calponin-1 and T cell enrichment-raising the possibility that these pure DCIS lesions might be at a high risk for progression.
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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 OpenQuestion graph.