ReviewJournal of mammary gland biology and neoplasia1996
The role of cadherin-mediated adhesion in breast cancer.
Review in Journal of mammary gland biology and neoplasia, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
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.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Unusual Infiltration into the Common Bile Duct: A Rare Case of Diffuse Hepatic Metastases from Breast Cancer.Internal medicine (Tokyo, Japan) · 2025Article
- An Evaluation of Matrix-Containing and Humanised Matrix-Free 3-Dimensional Cell Culture Systems for Studying Breast Cancer.PloS one · 2016Article
- Expression of N-cadherin proteins in myocardial hypertrophy in rats.Experimental and therapeutic medicine · 2014Article
- The role and function of cadherins in the mammary gland.Breast cancer research : BCR · 2012Review
- Circulating levels of cell adhesion molecule L1 as a prognostic marker in gastrointestinal stromal tumor patients.BMC cancer · 2011Article
- MUC4 mucin-induced epithelial to mesenchymal transition: a novel mechanism for metastasis of human ovarian cancer cells.Oncogene · 2010Article
- Activated leukocyte cell adhesion molecule: a novel biomarker for breast cancer.International journal of cancer · 2009Article
- Deregulation of MUC4 in gastric adenocarcinoma: potential pathobiological implication in poorly differentiated non-signet ring cell type gastric cancer.British journal of cancer · 2008Article
- TTYH2, a human homologue of the Drosophila melanogaster gene tweety, is up-regulated in colon carcinoma and involved in cell proliferation and cell aggregation.World journal of gastroenterology · 2007Article
- E-, N- and P-cadherin, and alpha-, beta- and gamma-catenin protein expression in normal, hyperplastic and carcinomatous human prostate.The Histochemical journal · 2000Article
- Tissue architecture: the ultimate regulator of epithelial function?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1998Review
- Reversion of the malignant phenotype of human breast cells in three-dimensional culture and in vivo by integrin blocking antibodies.The Journal of cell biology · 1997Article
- Cell adhesion molecules in the normal and cancerous mammary gland.Journal of mammary gland biology and neoplasia · 1996Review
- The importance of the microenvironment in breast cancer progression: recapitulation of mammary tumorigenesis using a unique human mammary epithelial cell model and a three-dimensional culture assay.Biochemistry and cell biology = Biochimie et biologie cellulaire · 1996Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cell adhesion molecule E-cadherin is expressed on the basolateral surfaces of normal mammary epithelial cells and is lost in a subset of breast cancers. Loss of E-cadherin expression has been postulated to facilitate tumor cell detachment from a primary tumor ultimately leading to metastasis. In this paper, I review the published in vitro data that initially supported this "invasion suppressor" role for E-cadherin as well as more recent in vitro and in vivo data showing that E-cadherin-positive tumor cells can metastasize. I examine other molecules required for E-cadherin function and discuss how defects in the expression or function of these molecules might alter E-cadherin function in E-cadherin-positive tumor cells. For example, loss of expression or function of catenins, intracellular molecules that interact with E-cadherin, can result in the loss of E-cadherin-mediated adhesion and a more invasive phenotype. Altered phosphorylation of E-cadherin or catenins can also influence E-cadherin function. Finally, expression of other cell surface molecules such as mucins may interfere with E-cadherin function. The collective effect of these molecules on the adhesive phenotype of breast cancer cells may be one determinant of metastatic potential.
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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.