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Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor
Published on: May 2, 2022
Non-Coding RNAs, a Novel Paradigm for the Management of Gastrointestinal Stromal Tumors
Azadeh Amirnasr1, Stefan Sleijfer1, Erik A C Wiemer1
1Department of Medical Oncology, Erasmus MC Cancer Institute, Erasmus University Medical Center, 3015 CN Rotterdam, The Netherlands.
Abstract:
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal malignancies found in the gastrointestinal tract. At a molecular level, most GISTs are characterized by gain-of-function mutations in V-Kit Hardy-Zuckerman 4 Feline Sarcoma Viral Oncogene Homolog (KIT) and Platelet Derived Growth Factor Receptor Alpha (PDGFRA), leading to constitutive activated signaling through these receptor tyrosine kinases, which drive GIST pathogenesis. In addition to surgery, treatment with the tyrosine kinase inhibitor imatinib forms the mainstay of GIST treatment, particularly in the advanced setting. Nevertheless, the majority of GISTs develop imatinib resistance. Biomarkers that indicate metastasis, drug resistance and disease progression early on could be of great clinical value. Likewise, novel treatment strategies that overcome resistance mechanisms are equally needed. Non-coding RNAs, particularly microRNAs, can be employed as diagnostic, prognostic or predictive biomarkers and have therapeutic potential. Here we review which non-coding RNAs are deregulated in GISTs, whether they can be linked to specific clinicopathological features and discuss how they can be used to improve the clinical management of GISTs.
Insights
Gastrointestinal stromal tumors (GISTs) involve KIT and PDGFRA mutations. Non-coding RNAs offer potential as biomarkers and therapeutics to overcome imatinib resistance in GIST patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal malignancies of the GI tract.
- Most GISTs arise from activating mutations in KIT or PDGFRA receptor tyrosine kinases.
- Imatinib is a primary treatment, but resistance frequently develops, necessitating new strategies.
Purpose of the Study:
- To review non-coding RNAs deregulated in GISTs.
- To explore the link between non-coding RNAs and GIST clinicopathological features.
- To discuss the potential of non-coding RNAs in GIST management.
Main Methods:
- Literature review of studies on non-coding RNAs in GISTs.
- Analysis of associations between non-coding RNA expression and GIST characteristics.
- Evaluation of non-coding RNAs as diagnostic, prognostic, and therapeutic tools.
Main Results:
- Non-coding RNAs, especially microRNAs, are frequently deregulated in GISTs.
- Specific non-coding RNAs correlate with GIST progression, metastasis, and imatinib resistance.
- Non-coding RNAs show promise as biomarkers and therapeutic targets.
Conclusions:
- Non-coding RNAs represent a significant area for improving GIST diagnosis and treatment.
- Targeting non-coding RNAs may overcome imatinib resistance and enhance patient outcomes.
- Further research into non-coding RNAs is crucial for advancing GIST clinical management.
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