ArticleIn vivo (Athens, Greece)
Potential Contribution of Epithelial Growth Factor Receptor to PI3K/AKT Pathway Dysregulation in Canine Soft Tissue Sarcoma.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimSoft tissue sarcoma (STS) is a mesenchymal tumor affecting multiple organs in dogs. Previous studies identified activation of the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (PKB, AKT) pathway in canine STS cell lines and clinical samples, but the underlying mechanism remains unclear. This study investigated PTEN loss, PIK3CA mutation, and EGFR over-expression as potential drivers of PI3K/AKT pathway activation in STS. MATERIALS AND
methodsWe analyzed 36 canine STS samples. PTEN and EGFR expression were evaluated using immunohistochemistry, while PIK3CA and EGFR mutations were assessed through DNA sequencing.
resultsPTEN was expressed in all analyzed samples, with no evidence of loss. Weak PTEN expression was observed in 12 (33.3%) samples, while 24 (66.7%) showed normal expression. DNA sequencing of PIK3CA revealed a single point mutation (c.554 A>C, H554P) in one case, but no hotspot mutations were identified. High EGFR expression was significantly correlated with elevated phospho-AKT levels (p<0.0001). Immunolabelling indicated that 30 samples (83.3%) were EGFR-positive, and 27 of these also showed positive phospho-AKT labeling. Accordingly, one missense point mutation in exon 21 of EGFR (E868K) was identified in one of 12 samples.
conclusionEGFR over-expression, rather than PTEN loss or PIK3CA mutations, may contribute to PI3K/AKT pathway dysregulation in canine STS. Further studies with larger sample sizes and additional validation techniques are necessary to confirm these findings.
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.