ReviewCold Spring Harbor perspectives in biology2018
Loss of E-Cadherin-Dependent Cell-Cell Adhesion and the Development and Progression of Cancer.
Review in Cold Spring Harbor perspectives in biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
118 citing papers in PubMed, 216 citations in OpenAlex.
- Invasive lobular breast cancer in young patients without adjuvant systemic treatment: 15-year survival outcomes.Breast cancer research and treatment · 2026Article
- Article
- Metabolic maintenance of breast cancer cells and metastases through E-cadherin/YAP-dependent pyruvate carboxylase expression.bioRxiv : the preprint server for biology · 2026Article
- SELE is associated with reduced breast cancer susceptibility: Evidence from Mendelian randomization and single-cell transcriptome.Translational oncology · 2026Article
- Extracellular and Membrane Protein: Structure, Biological Functions, Diseases, and an Emerging Modality for Drug Discovery.MedComm · 2026Review
- Integrins in cancer: insights into mechanisms and therapeutic potential.Cell communication and signaling : CCS · 2026Review
- 3D "Emboli" Culture Models Epithelial Breast Cancer Cell Oxidative Mitochondrial Metabolism with Relevance for Lung Metastasis.Cancer research communications · 2026Article
- Anoikis resistance and metastasis of ovarian cancer can be overcome by CDK8/19 mediator kinase inhibition.JCI insight · 2026Article
- Correlation of G protein-coupled receptor and tumor microenvironment with gastric cancer outcomes and therapies.Chinese medical journal · 2026Article
- THSD7B promotes tumor progression and is associated with prognosis in gastric adenocarcinoma.PloS one · 2026Article
- Multi-omics analysis and functional validation of CHEK1 as an independent prognostic biomarker in Pancreatic cancer.PloS one · 2026Article
- Article
- Epithelial-Mesenchymal Transition in Human Alveolar Cells Exposed to Indium Chloride.Journal of applied toxicology : JAT · 2025Article
- The therapeutic potential of high-intensity interval training in a breast cancer model: focus on the Hippo signaling pathway.Breast cancer (Tokyo, Japan) · 2025Article
- Anoikis resistance in gastric cancer: a comprehensive review.Cell death & disease · 2025Review
- Ubiquitin-like with phd and ring finger domains 1 as a potential therapeutic target in smoking-associated oral squamous cell carcinoma.Journal of dental sciences · 2025Article
- Article
- Influence ofIranian journal of microbiology · 2025Article
- Article
- Afadin loss induces breast cancer metastasis through destabilisation of E-cadherin to F-actin linkage.The Journal of pathology · 2025Article
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classical cadherins are the key molecules that control cell-cell adhesion. Notwithstanding this function, it is also clear that classical cadherins are more than just the "glue" that keeps the cells together. Cadherins are essential regulators of tissue homeostasis that govern multiple facets of cellular function and development, by transducing adhesive signals to a complex network of signaling effectors and transcriptional programs. In cancer, cadherins are often inactivated or functionally inhibited, resulting in disease development and/or progression. This review focuses on E-cadherin and its causal role in the development and progression of breast and gastric cancer. We provide a summary of the biochemical consequences and consider the conceptual impact of early (mutational) E-cadherin loss in cancer. We advocate that carcinomas driven by E-cadherin loss should be considered "actin-diseases," caused by the specific disruption of the E-cadherin-actin connection and a subsequent dependence on sustained actomyosin contraction for tumor progression. Based on the available data from mouse and human studies we discuss opportunities for targeted clinical intervention.
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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.