ArticleInternational journal of biological sciences2011
The myoepithelial cell layer may serve as a potential trigger factor for different outcomes of stage-matched invasive lobular and ductal breast cancers.
Article in International journal of biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed.
- Gap junction communication regulates luminal-myoepithelial crosstalk and cell differentiation in a bilayered human mammary epithelial cell model.Biology methods & protocols · 2026Article
- Clinical Evolution of Epithelial-Mesenchymal Transition in Human Carcinomas.Cancer research · 2020Observational
- Article
- Morphology of the myoepithelial cell: immunohistochemical characterization from resting to motile phase.TheScientificWorldJournal · 2012Article
- Malignant transformation and stromal invasion from normal or hyperplastic tissues: true or false?Journal of Cancer · 2011Article
- A component of lobular carcinoma in clinically lymph node-negative patients predicts for an increased likelihood of upstaging to pathologic stage III breast cancer.Advances in radiation oncologyArticle
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Authors and funding
4 authors.
Funding
Abstract
Invasive lobular cancer (ILC) tends to be significantly larger in size with significantly more positive lymph nodes, whereas ILC has a significantly more favorable outcome, compared to stage-matched invasive ductal carcinoma (IDC). The mechanism accounting for such differences remains elusive. Based on morphological, immunohistochemical, and molecular studies of over 1,000 cases of human breast cancers, we hypothesize that the differences may result from the structural and/or functional differences of their surrounding myoepithelial cell layers, which dictate lobular and ductal tumor cells to follow different pathways of invasion or metastasis. The background, rationale, supportive data, and implications of our hypothesis are presented and discussed.
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