ReviewCurrent health sciences journal
ELTD1 Review: New Regulator of Angiogenesis in Glioma.
Review in Current health sciences journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 2 citations in OpenAlex.
- STAT3 Signaling in Spinal Cord Injury: Neurochemical Mechanisms Linking Neuroinflammation, Mitochondrial Stress, and Glial Remodeling.Neurochemical research · 2026Review
- Identification of the adhesion GPCR ADGRL4/ELTD1 as a novel potential prognostic biomarker for cerebral cavernous malformation disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- Stigmasterol exerts antiglioma effects by regulating lipid metabolism.Molecular medicine reports · 2024Article
- Nuclear and membrane-bound hormone receptors in glioblastoma: Expression, functionality, and therapeutic implications.Neuro-oncology advancesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is a severe brain cancer in which angiogenesis is controlled by G protein-coupled receptors (GPCRs), such as Epidermal Growth Factor Latrophilin and seven transmembrane domain-containing protein 1 (ELTD1), which are crucial for tumor progression. ELTD1 is an understudied GPCR with a broad expression profile in various tissues, including the human brain, especially in the cerebral cortex. It plays a significant role in angiogenesis and tumorigenesis and is regulated by interconnected VEGF and DLL4/Notch pathways. ELTD1 also modulates the JAK/STAT3/HIF-1α signaling axis, affecting the response of cells to low-oxygen conditions and promoting cell proliferation. However, their specific ligands and functional mechanisms remain unclear. ELTD1 expression is associated with different outcomes in various cancers. For example, in GBM, higher ELTD1 levels are linked to more mature and less leaky blood vessels, potentially enhancing drug delivery and therapeutic success. It also has divergent prognostic implications in renal, ovarian, and colorectal cancer. Additionally, ELTD1 overexpression in central nervous system endothelial cells suggests that it is a potential biomarker for multiple sclerosis. Therapeutically, blocking ELTD1 inhibits vessel formation, possibly slowing tumor growth. Initial therapies used polyclonal antibodies, but the shift has been towards more targeted monoclonal antibodies, particularly in preclinical glioma models. This review aimed to translate these insights into effective clinical treatments. However, several gaps remain in our knowledge regarding ELTD1 ligands and their potential involvement in other physiological or pathological processes that future research can address to elucidate the role of ELTD1 in cancer, through angiogenesis and other intracellular pathways.
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.