ReviewDiscover oncology2025
PTEN defects in cancer, from gene to protein molecular causes and therapeutic targets.
Review in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Novel lncRNA Signature (UFC1/PTENP1) as a Molecular Biomarker for the Diagnosis and Prognosis of Hepatocellular Carcinoma in an Egyptian Cohort.Current issues in molecular biology · 2026Article
- Donor-specific assemblies enhance somatic structural variant detection in complex genomic regions.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms, translational opportunities for diabetic polyneuropathy.Frontiers in endocrinology · 2026Review
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
No grant is acknowledged in the PubMed record.
Abstract
Recently, cancer has become a leading cause of death worldwide, prompting increased research to understand the pathways involved in cancer development and to identify solutions for its treatment. The PI3K/AKT pathway has garnered significant attention because of its involvement in promoting cell proliferation and inhibiting programmed cell death. The protein phosphatase and tensin homolog on chromosome 10 (PTEN) plays a crucial role in inhibiting this pathway, thereby limiting uncontrolled cell proliferation. PTEN gene expression is strictly regulated at the transcriptional, posttranscriptional, and posttranslational levels, and recent research has focused on PTEN due to its reduced levels in cancer cells. This review aims to provide a deep understanding of the PTEN protein from structural and regulatory perspectives, its mutated forms, and its interactions with the occurrence of various malignant tumors to summarize the recent work performed to combat cancers via molecular strategies to enhance PTEN.
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.