Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (563 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Adhesion Molecules, Cell; Molecules, Cell Adhesion; Cell Adhesion Molecule; Adhesion Molecule, Cell; Molecule, Cell Adhesion; Saccharide-Mediated Cell Adhesion Molecules; Saccharide Mediated Cell Adhesion Molecules; Intercellular Adhesion Molecules.
Where it fits in the MeSH classification
- Broader topics
- Membrane Glycoproteins; Antigens, Surface
- Narrower topics
- 12E7 Antigen; Cadherin Related Proteins; Cadherins; Carcinoembryonic Antigen; CD11 Antigens; CD146 Antigen; CD24 Antigen; CD4 Immunoadhesins; CEACAM1 Protein; Cell Adhesion Molecule-1; Cell Adhesion Molecules, Neuronal; DC-Specific ICAM-3 Grabbing Nonintegrin; Endolyn; Epithelial Cell Adhesion Molecule
- See also
- Integrins
Research landscape
PubMed indexes 161,106 records tagged with the MeSH heading “Cell Adhesion Molecules” (counts retrieved 2026-10-31). 22,551 of them (14.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 53,744 records.
Reviews account for 13,557 records (8.4%) and meta-analyses for 494. Randomized controlled trials number 1,799 (1.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 36,377 |
| 2000-2009 | 48,434 |
| 2010-2019 | 53,744 |
| 2020 onward | 22,551 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 13,557 | 8.4% |
| Meta-analyses | 494 | 0.3% |
| Randomized controlled trials | 1,799 | 1.1% |
Method: PubMed query "Cell Adhesion Molecules"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42410113 · DOI · PMC13364714 |
| RET receptor tyrosine kinase architecture, assemblies, and activation | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 41921038 · DOI · PMC7619074 |
| Cadherin 17 and digestive cancers: from diagnostic to therapeutic opportunities | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 41928253 · DOI · PMC13169878 |
CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Cells under high confinement migrate efficiently in low-adhesion environments by forming stable, polarized, hydrostatic pressure-driven leader blebs.
- Closing excerpt
- Together, these findings define the biophysical and molecular mechanisms that underlie polarity in bleb-based migration and highlight how alternative spatial organization of signalling modules supports distinct migration modes in different microenvironments.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (179 words)
Cells under high confinement migrate efficiently in low-adhesion environments by forming stable, polarized, hydrostatic pressure-driven leader blebs. Here we investigated the basis of polarized bleb morphology in metastatic melanoma cells migrating under low-adhesive and highly confined microenvironments. Using high-resolution live imaging, molecular perturbations and biosensors, we show that EGF signalling through PI3K stabilizes and maintains polarized leader blebs. EGFR and PI3K activities form a gradient within leader blebs that decreases from rear to front, promoting phosphatidylinositol 3,4,5-trisphosphate and Rac1-GTP accumulation at the bleb rear, whereas phosphatidylinositol 4,5-bisphosphate and RhoA-GTP concentrate at the bleb tip, the inverse of the organization observed in integrin-dependent mesenchymal migration. Optogenetic disruption of this gradient triggers bleb retraction, underscoring its functional importance. Mathematical modelling and experiments identified a mechanism whereby during bleb initiation, CD44 and ERM proteins restrict EGFR mobility within a membrane-apposed cortical actin meshwork at the bleb rear, establishing the EGFR-PI3K-Rac gradient. Together, these findings define the biophysical and molecular mechanisms that underlie polarity in bleb-based migration and highlight how alternative spatial organization of signalling modules supports distinct migration modes in different microenvironments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42410113 · DOI · PMC13364714
RET receptor tyrosine kinase architecture, assemblies, and activation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Among the 58 human receptor tyrosine kinases that are known, only the RET (REarrangement during Transfection) receptor contains cadherin-like domains in its extracellular portion.
- Closing excerpt
- It then discusses current views on how distinct assemblies of GFL-GFR⍺-RET receptor complexes are able to activate the intrinsic RET tyrosine kinase function to relay intracellular signals.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (131 words)
Among the 58 human receptor tyrosine kinases that are known, only the RET (REarrangement during Transfection) receptor contains cadherin-like domains in its extracellular portion. This multidomain extracellular module contains a binding site for a family of five related heterodimeric ligands. Each heterodimer comprises a secreted glial cell line-derived neurotrophic factor (GDNF) family ligand (GFL) and a membrane-anchored co-receptor GFR⍺ (GDNF family receptor alpha). Once a GFL-GFR⍺ ligand is bound to RET, this stimulates the activation of the receptor through tyrosine-based autophosphorylation. This mini review explores how the shape and architecture of RET encode a flexible GFL-GFR⍺-binding site, summarising recent progress in understanding RET structure. It then discusses current views on how distinct assemblies of GFL-GFR⍺-RET receptor complexes are able to activate the intrinsic RET tyrosine kinase function to relay intracellular signals.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41921038 · DOI · PMC7619074
Cadherin 17 and digestive cancers: from diagnostic to therapeutic opportunities [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cadherin-17 (CDH17, LI-cadherin) is a non-classical cadherin with restricted expression in normal gastrointestinal epithelium, emerging as a multifunctional molecule in cancer.
- Closing excerpt
- By integrating current findings and addressing existing challenges, we aim to provide a comprehensive overview of its multifaceted roles and to emphasize emerging strategies to harness this molecule for clinical applications in cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (253 words)
Cadherin-17 (CDH17, LI-cadherin) is a non-classical cadherin with restricted expression in normal gastrointestinal epithelium, emerging as a multifunctional molecule in cancer. CDH17 regulates cell–cell adhesion, modulates key signaling pathways, and interacts with the tumor microenvironment, collectively influencing proliferation, invasion, metastasis, therapeutic resistance, and immune evasion. Its expression is highly context-dependent and dynamically regulated, with both upregulation and loss linked to distinct features of tumor aggressiveness and differentiation. CDH17 also interfaces with pathways governing stemness and cellular plasticity, suggesting a role in modulating therapeutic response and resistance mechanisms.Beyond its biological functions, CDH17 has been investigated as a diagnostic marker, with tissue-based detection, circulating biomarkers, and radiolabeled imaging probes exploiting its tumor-restricted expression and membrane localization, offering opportunities for noninvasive tumor detection, staging, and monitoring. CDH17 also holds potential prognostic significance, although its clinical relevance varies according to molecular context and tumor differentiation status, emphasizing the need for integrative biomarker assessment. Finally, the tumor-specific expression of CDH17 has inspired multiple therapeutic strategies, including cellular immunotherapies, antibody–drug conjugates, immunotoxins, radiolabeled agents, and engineered delivery platforms, all designed to selectively target CDH17-expressing cells while minimizing off-target toxicity. Such strategies highlight the translational potential of CDH17 as both a therapeutic target and a platform for precision oncology.In this review, we summarize the molecular mechanisms, biological functions, diagnostic and prognostic relevance, and therapeutic applications of CDH17. By integrating current findings and addressing existing challenges, we aim to provide a comprehensive overview of its multifaceted roles and to emphasize emerging strategies to harness this molecule for clinical applications in cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41928253 · DOI · PMC13169878
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens [4]
- Research article Tumor-associated neutrophils as a new prognostic factor in cancer: a systematic review and meta-analysis [5]
- Research article A nonsynonymous functional variant in integrin-alpha(M) (encoded by ITGAM) is associated with systemic lupus erythematosus [6]
- Research article Meta-analysis of Genome-wide Association Studies for Neuroticism, and the Polygenic Association With Major Depressive Disorder [7]
- Research article Blood CEA levels for detecting recurrent colorectal cancer [8]
- Research article Impact of TROP2 expression on prognosis in solid tumors: A Systematic Review and Meta-analysis [9]
References
- Jha A, Chandra A, Farahani PE, Toettcher JE, Pasapera AM, Haugh JM, et al.. CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration. . 2026. PMID 42410113 · DOI · PMC13364714
- Zol-Hanlon M, McDonald NQ. RET receptor tyrosine kinase architecture, assemblies, and activation. . 2026. PMID 41921038 · DOI · PMC7619074
- Fernandez B, Lopez L, Matis T, Dabernat S, Amintas S. Cadherin 17 and digestive cancers: from diagnostic to therapeutic opportunities. . 2026. PMID 41928253 · DOI · PMC13169878
- Kiryluk K, Li Y, Scolari F, Sanna-Cherchi S, Choi M, Verbitsky M, et al.. Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens. Nat Genet. 2014. PMID 25305756 · DOI · PMC4213311
- Shen M, Hu P, Donskov F, Wang G, Liu Q, Du J. Tumor-associated neutrophils as a new prognostic factor in cancer: a systematic review and meta-analysis. PLoS One. 2014. PMID 24906014 · DOI · PMC4048155
- Nath SK, Han S, Kim-Howard X, Kelly JA, Viswanathan P, Gilkeson GS, et al.. A nonsynonymous functional variant in integrin-alpha(M) (encoded by ITGAM) is associated with systemic lupus erythematosus. Nat Genet. 2008. PMID 18204448 · DOI
- Genetics of Personality Consortium, de Moor MH, van den Berg SM, Verweij KJ, Krueger RF, Luciano M, et al.. Meta-analysis of Genome-wide Association Studies for Neuroticism, and the Polygenic Association With Major Depressive Disorder. JAMA Psychiatry. 2015. PMID 25993607 · DOI · PMC4667957
- Nicholson BD, Shinkins B, Pathiraja I, Roberts NW, James TJ, Mallett S, et al.. Blood CEA levels for detecting recurrent colorectal cancer. Cochrane Database Syst Rev. 2015. PMID 26661580 · DOI · PMC7092609
- Zeng P, Chen MB, Zhou LN, Tang M, Liu CY, Lu PH. Impact of TROP2 expression on prognosis in solid tumors: A Systematic Review and Meta-analysis. Sci Rep. 2016. PMID 27645103 · DOI · PMC5028884
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.