ReviewMolecular & cellular oncology
Role of G protein-coupled receptor kinase 2 in tumoral angiogenesis.
Review in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 11 citations in OpenAlex.
- Regulation of G protein-coupled receptor kinase 2 and its role in tumors.Journal of translational medicine · 2026Review
- Unveiling the Role of GRK2: From Immune Regulation to Cancer Therapeutics.Mediators of inflammation · 2025Review
- Exploring the potential biological function of GRK2 in colorectal cancer.Functional & integrative genomics · 2024Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Downregulation of G protein-coupled receptor kinase 2 (GRK2) in endothelial cells has recently been identified as a relevant event in the tumoral angiogenic switch. Based on the effects of altering GRK2 dosage in cell and animal models, this kinase appears to act as a hub in key signaling pathways involved in vascular stabilization and remodeling. Accordingly, decreased GRK2 expression in endothelial cells accelerates tumor growth in mice by impairing the pericytes ensheathing the vessels, thereby promoting hypoxia and macrophage infiltration. These results raise new questions regarding the mechanisms by which transformed cells trigger the decrease in GRK2 observed in human breast cancer vessels and how GRK2 modulates the interactions between different cell types that occur in the tumor microenvironment.
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What OpenQuestion holds
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.