ReviewFrontiers in oncology2020
Targeting the Extra-Cellular Matrix-Tumor Cell Crosstalk for Anti-Cancer Therapy: Emerging Alternatives to Integrin Inhibitors.
Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- Proteoglycans as Molecular Regulators of Bone Metastasis: Extracellular Matrix Remodeling, Tumor-Bone Crosstalk, Dormancy, and Therapeutic Opportunities.Biomolecules · 2026Review
- Microenvironmental and Molecular Pathways Driving Dormancy Escape in Bone Metastases.International journal of molecular sciences · 2025Review
- In vivo CRISPR screening in head and neck cancer reveals Uchl5 as an immunotherapy target.Nature communications · 2025Article
- Targeting breast tumor extracellular matrix and stroma utilizing nanoparticles.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Computational approaches identify a transcriptomic fingerprint of drug-induced structural cardiotoxicity.Cell biology and toxicology · 2024Article
- Deletion of Tmem268 in mice suppresses anti-infectious immune responses by downregulating CD11b signaling.EMBO reports · 2024Article
- Article
- Review
- Regulation of tumor immunity and immunotherapy by the tumor collagen extracellular matrix.Frontiers in immunology · 2023Review
- Towards a potential pan-cancer prognostic signature for gene expression based on probesets and ensemble machine learning.BioData mining · 2022Article
- Inhibitory effect of phenolic extract from squirting cucumber (RSC advances · 2022Article
- Review
- An Osteosarcoma Model by 3D Printed Polyurethane Scaffold and In Vitro Generated Bone Extracellular Matrix.Cancers · 2022Article
- Epigenetic regulation and targeting of ECM for cancer therapy.American journal of physiology. Cell physiology · 2022Review
- The complex interactions between the cellular and non-cellular components of the brain tumor microenvironmental landscape and their therapeutic implications.Frontiers in oncology · 2022Review
- Article
- The potential prognostic values of the ADAMTS-like protein family: an integrative pan-cancer analysis.Annals of translational medicine · 2021Article
- The Yin and Yang of Discoidin Domain Receptors (DDRs): Implications in Tumor Growth and Metastasis Development.Cancers · 2021Review
- Integrin signaling gene alterations and outcomes of cancer patients receiving immune checkpoint inhibitors.American journal of translational research · 2021Article
- Tumor-Associated Extracellular Matrix: How to Be a Potential Aide to Anti-tumor Immunotherapy?Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) is a complex network composed of a multitude of different macromolecules. ECM components typically provide a supportive structure to the tissue and engender positional information and crosstalk with neighboring cells in a dynamic reciprocal manner, thereby regulating tissue development and homeostasis. During tumor progression, tumor cells commonly modify and hijack the surrounding ECM to sustain anchorage-dependent growth and survival, guide migration, store pro-tumorigenic cell-derived molecules and present them to enhance receptor activation. Thereby, ECM potentially supports tumor progression at various steps from initiation, to local growth, invasion, and systemic dissemination and ECM-tumor cells interactions have long been considered promising targets for cancer therapy. Integrins represent key surface receptors for the tumor cell to sense and interact with the ECM. Yet, attempts to therapeutically impinge on these interactions using integrin inhibitors have failed to deliver anticipated results, and integrin inhibitors are still missing in the emerging arsenal of drugs for targeted therapies. This paradox situation should urge the field to reconsider the role of integrins in cancer and their targeting, but also to envisage alternative strategies. Here, we review the therapeutic targets implicated in tumor cell adhesion to the ECM, whose inhibitors are currently in clinical trials and may offer alternatives to integrin inhibition.
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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.