ReviewCurrent oncology reports2013
Exploring novel therapeutic targets in GIST: focus on the PI3K/Akt/mTOR pathway.
Review in Current oncology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- In vitro analysis of PI3K pathway activation genes for exploring novel biomarkers and therapeutic targets in clear cell renal carcinoma.American journal of translational research · 2023Article
- Transcriptomic study of gastrointestinal stromal tumors with liver metastasis.Frontiers in genetics · 2023Article
- PI3K/Akt pathway and Nanog maintain cancer stem cells in sarcomas.Oncogenesis · 2021Article
- Preclinical model-based evaluation of Imatinib resistance induced byAmerican journal of translational research · 2021Article
- Inhibition of AKT-Signaling Sensitizes Soft Tissue Sarcomas (STS) and Gastrointestinal Stromal Tumors (GIST) to Doxorubicin via Targeting of Homology-Mediated DNA Repair.International journal of molecular sciences · 2020Article
- Therapeutic Potential of PI3K/AKT/mTOR Pathway in Gastrointestinal Stromal Tumors: Rationale and Progress.Cancers · 2020Review
- Effects of COSurgical endoscopy · 2019Article
- Prognostic Role of miR-221 and miR-222 Expression in Cancer Patients: A Systematic Review and Meta-Analysis.Cancers · 2019Review
- Mechanisms of resistance to a PI3K inhibitor in gastrointestinal stromal tumors: anCancer management and research · 2019Article
- Succinate Dehydrogenase-Deficient Gastrointestinal Stromal Tumors: Small Steps Toward Personalized Medicine?Epigenetics insights · 2019Article
- Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate.Oncology letters · 2018Article
- miR-148b-3p functions as a tumor suppressor in GISTs by directly targeting KIT.Cell communication and signaling : CCS · 2018Article
- Expression and phosphorylation of FOXO1 influences cell proliferation and apoptosis in the gastrointestinal stromal tumor cell line GIST-T1.Experimental and therapeutic medicine · 2018Article
- Ghrelin and gastrointestinal stromal tumors.World journal of gastroenterology · 2017Review
- Phytochemicals and PI3K Inhibitors in Cancer-An Insight.Frontiers in pharmacology · 2017Review
- Combination of Imatinib Mesylate and AKT Inhibitor Provides Synergistic Effects in Preclinical Study of Gastrointestinal Stromal Tumor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Molecular Pathogenesis and Diagnostic, Prognostic and Predictive Molecular Markers in Sarcoma.Surgical pathology clinics · 2016Review
- The influence of subclonal resistance mutations on targeted cancer therapy.Nature reviews. Clinical oncology · 2016Review
- Analysis of PI3K pathway components in human cancers.Oncology letters · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal stromal tumors (GISTs) are the most common soft tissue sarcoma, and most feature abnormalities in two genes encoding the receptor tyrosine kinases (RTKs), KIT, and PDGFRA. The RTK inhibitor imatinib revolutionized treatment in GIST; however, drug resistance remains a challenge. Constitutive autophosphorylation of RTKs is linked to phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway hyperactivation, which is central to oncogenic signaling, and known to be dysregulated in GIST. Preclinical experiments have confirmed that inhibiting the PI3K/Akt/mTOR pathway is a rational target for therapy. Early studies using mTOR inhibitors have shown limited success, which may be due to the activation of Akt that occurs following mTORC1 inhibition. Therefore, targeting PI3K or Akt, which lie upstream of mTORC1, may translate into more complete pathway inhibition. Several treatment strategies are currently being developed in phase 1 and 2 clinical trials. Compounds currently in development include pan-Class I PI3K inhibitors, dual PI3K/mTOR inhibitors, and Akt inhibitors. The aim of this review is to highlight the evidence for targeting PI3K/Akt/mTOR-dependent mechanisms in GIST and to evaluate the existing preclinical and clinical data supporting this strategy.
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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.