ReviewMolecules (Basel, Switzerland)2018
Targeting GLI Transcription Factors in Cancer.
Review in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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
46 citing papers in PubMed, 71 citations in OpenAlex.
- Smoothened signaling in microglia: canonical or not, and does it promote or limit inflammation?Acta pharmacologica Sinica · 2026Article
- SHH pathway inhibition and astrocyte co-culture induce distinct responses in glioblastoma and cancer stem cells.Scientific reports · 2026Article
- High-grade uterine endometrial stromal sarcoma harboring GLI1 and MDM2/CDK4 co-amplifications.Diagnostic pathology · 2025Article
- G Protein-Coupled Receptor Signaling: Implications and Therapeutic Development Advances in Cancers.MedComm · 2025Review
- Multiple signaling pathways in the frontiers of lung cancer progression.Frontiers in immunology · 2025Review
- Current progress and future perspective of super-enhancers: a viable and effective bridge between the transcriptional apparatus and disease.Frontiers in genetics · 2025Review
- A Comprehensive Clinicopathologic and Molecular Reappraisal of GLI1 -altered Mesenchymal Tumors with Pooled Outcome Analysis Showing Poor Survival in GLI1 - amplified Versus GLI1- rearranged Tumors.The American journal of surgical pathology · 2024Article
- Identification of Novel GANT61 Analogs with Activity in Hedgehog Functional Assays and GLI1-Dependent Cancer Cells.Molecules (Basel, Switzerland) · 2024Article
- The value of GLI1 and p16 immunohistochemistry in the premolecular screening for GLI1-altered mesenchymal neoplasms.Virchows Archiv : an international journal of pathology · 2024Article
- Ultraviolet Radiation Biological and Medical Implications.Current issues in molecular biology · 2024Review
- An Insight into the Role of GLIS1 in Embryonic Development, iPSC Generation, and Cancer.Advances in experimental medicine and biology · 2024Review
- The immunoreactivity of GLI1 and VEGFA is a potential prognostic factor in kidney renal clear cell carcinoma.BMC cancer · 2023Article
- Landscape of Druggable Molecular Pathways Downstream of Genomic CDH1/Cadherin-1 Alterations in Gastric Cancer.Journal of personalized medicine · 2022Article
- Topical Delivery of Hedgehog Inhibitors: Current Status and Perspectives.International journal of molecular sciences · 2022Review
- The immune microenvironment in gastric adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2022Review
- Cancer stem cells, not bulk tumor cells, determine mechanisms of resistance to SMO inhibitors.Cancer research communications · 2022Article
- A Data Science Approach for the Identification of Molecular Signatures of Aggressive Cancers.Cancers · 2022Article
- Article
- Review
- Horizontal transfer of the stemness-related markers EZH2 and GLI1 by neuroblastoma-derived extracellular vesicles in stromal cells.Translational research : the journal of laboratory and clinical medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of hedgehog (Hh) signaling has been observed in a wide variety of tumors and accounts for more than 25% of human cancer deaths. Inhibitors targeting the Hh signal transducer Smoothened (SMO) are widely used and display a good initial efficacy in patients suffering from basal cell carcinoma (BCC); however, a large number of patients relapse. Though SMO mutations may explain acquired therapy resistance, a growing body of evidence suggests that the non-canonical, SMO-independent activation of the Hh pathway in BCC patients can also account for this adverse effect. In this review, we highlight the importance of glioma-associated oncogene (GLI) transcription factors (the main downstream effectors of the canonical and the non-canonical Hh cascade) and their putative role in the regulation of multiple oncogenic signaling pathways. Moreover, we discuss the contribution of the Hh signaling to malignant transformation and propose GLIs as central hubs in tumor signaling networks and thus attractive molecular targets in anti-cancer therapies.
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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.