ReviewPediatric blood & cancer2025
RAS Pathway Mutations and Therapeutics in Vascular Anomalies.
Review in Pediatric blood & cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- RAS Inhibitor RMC-7977 Blocks Vascular Overgrowth of NRASJournal of cellular and molecular medicine · 2026Article
- Sirolimus outperforms alpelisib in models ofBlood vessels, thrombosis & hemostasis · 2026Article
- Factors influencing somatic genetic testing for vascular anomalies at 2 academic centers.Blood vessels, thrombosis & hemostasis · 2026Article
- Pathogenic mechanism of extracranial arteriovenous malformations: insights from clinical, pathological, and genetic analyses.Virchows Archiv : an international journal of pathology · 2026Article
- MEK Inhibition Reduces Vascular Malformations and Gene Dysregulation in NRASPediatric blood & cancer · 2026Article
- KRAS-dependent glycolytic reprogramming of endothelial cells in sporadic arteriovenous malformations.EMBO molecular medicine · 2026Article
- Generation of Human Haematopoietic Model Cell Lines Revealed Distinct Replication Stress Tolerance Between Two OncogenicBiomolecules · 2026Article
- Human Lymphatic Endothelial Cells Expressing NRASPediatric blood & cancer · 2025Article
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.
Funding
Abstract
Vascular anomalies (VAs) are a diverse group of vascular tumors and vascular malformations (VMs). VMs are characterized by abnormal vessel development, overgrowth, and dysfunction. Coagulopathy, edema, and effusions can cause severe morbidity and mortality in children and adults with these diseases. Germline or somatic mutations in the RAS/RAF/MAPK pathway have been identified in multiple types of VAs. RAS genes (KRAS, NRAS, and HRAS) are small GTPase proteins that play an important role in normal development and cell function. In healthy cells, RAS proteins cycle between GDP (inactive) and GTP (active) states that regulate important functions such as proliferation, migration, and survival. "Hot spot" mutations in codons 12, 13, or 61 of RAS genes are found in multiple tumor types and VAs. RAS mutations often cause excessive MAP kinase signaling, driving unchecked cell proliferation. In this review, we discuss the different RAS pathway mutations discovered in VAs and the role that these may play using insights from cell and animal models. Current therapies targeting RAS pathways are presented. In the future, a better understanding of the role of RAS pathway mutations may advance therapeutic strategies for people with VAs.
Indexed as
Identifiers
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.