ArticleOncogene2023
ICAM2 initiates trans-blood-CSF barrier migration and stemness properties in leptomeningeal metastasis of triple-negative breast cancer.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Dysregulation of the inside-out signaling pathway in CNS-infiltrated pediatric T-cell acute lymphoblastic leukemia.Research square · 2026Article
- ICAM2 promotes endocrine resistance via dynein-mediated OXPHOS activation in ER-positive breast cancer.Cell death & disease · 2026Article
- Integrating Magnetic Resonance Chemical Shift Imaging for Localized Prostate Cancer Risk Stratification on the Basis of the Impact of Periprostatic Brown Adipocytes Within Tumor Microenvironment.Annals of surgical oncology · 2025Article
- Primary and secondary metastatic dissemination: multiple routes to cancer-related death.Molecular cancer · 2025Review
- Association of gut microbiota and immune gene expression with response to targeted therapy in BRAF mutated melanoma.Scientific reports · 2025Observational
- Proteomics uncovers ICAM2 (CD102) as a novel serum biomarker of proliferative lupus nephritis.Lupus science & medicine · 2025Article
- The research progress on meningeal metastasis in solid tumors.Discover oncology · 2025Review
- Leptomeningeal metastatic disease: new frontiers and future directions.Nature reviews. Clinical oncology · 2025Review
- Review
- Family-Wide Photoproximity Profiling of Integrin Protein Social Networks in Cancer.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leptomeningeal metastasis (LM) occurs when tumor cells spread to the leptomeningeal space surrounding the brain and the spinal cord, thereby causing poor clinical outcomes. The triple-negative breast cancer (TNBC) has been associated with symptoms of LM and mechanism remained unclear. Through proteomic analysis, we identified high expression of ICAM2 in leptomeningeal metastatic TNBC cells, which promoted the colonization of the spinal cord and resulted in poor survival in vivo. Two-way demonstration indicated that high levels of ICAM2 promoted blood-cerebrospinal fluid barrier (BCB) adhesion, trans-BCB migration, and stemness abilities and determined the specificity of LM in vivo. Furthermore, pull-down and antibody neutralizing assay revealed that ICAM2 determined the specificity of LM through interactions with ICAM1 in the choroid plexus epithelial cells. Therefore, neutralizing ICAM2 can attenuate the progression of LM and prolong survival in vivo. The results suggested that targeting ICAM2 is a potential therapeutic strategy for LM in TNBC.
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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 Socratic graph.