ArticlePloS one2013
Post-transcriptional dysregulation by miRNAs is implicated in the pathogenesis of gastrointestinal stromal tumor [GIST].
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- miRNAs expression pattern and machine learning models elucidate risk for gastric GIST.Cancer biomarkers : section A of Disease markers · 2022Article
- Review
- Overview of microRNAs as liquid biopsy biomarkers for colorectal cancer sub-type profiling and chemoresistance.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Non-Coding RNAs, a Novel Paradigm for the Management of Gastrointestinal Stromal Tumors.International journal of molecular sciences · 2020Review
- Survivin is a novel transcription regulator of KIT and is downregulated by miRNA-494 in gastrointestinal stromal tumors.International journal of cancer · 2018Article
- miR-148b-3p functions as a tumor suppressor in GISTs by directly targeting KIT.Cell communication and signaling : CCS · 2018Article
- Small Molecules in Rare Tumors: Emerging Role of MicroRNAs in GIST.International journal of molecular sciences · 2018Review
- Article
- The progressive fragmentation of the KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GIST).Journal of translational medicine · 2017Article
- Down-regulation of 14q32-encoded miRNAs and tumor suppressor role for miR-654-3p in papillary thyroid cancer.Oncotarget · 2017Article
- miRNA-221 and miRNA-222 induce apoptosis via the KIT/AKT signalling pathway in gastrointestinal stromal tumours.Molecular oncology · 2015Article
- What Do We Know about the Role of miRNAs in Pediatric Sarcoma?International journal of molecular sciences · 2015Review
- Rare childhood cancers--an increasing entity requiring the need for global consensus and collaboration.Cancer medicine · 2015Article
- Good survival outcome of metastatic SDH-deficient gastrointestinal stromal tumors harboring SDHA mutations.Genetics in medicine : official journal of the American College of Medical Genetics · 2015Article
- Succinate dehydrogenase-deficient gastrointestinal stromal tumors.World journal of gastroenterology · 2015Review
- MicroRNAs as potential target in human bone and soft tissue sarcoma therapeutics.Frontiers in molecular biosciences · 2015Review
- Quadruple wild-type (WT) GIST: defining the subset of GIST that lacks abnormalities of KIT, PDGFRA, SDH, or RAS signaling pathways.Cancer medicine · 2015Article
- The genetic landscape of gastrointestinal stromal tumor lacking KIT and PDGFRA mutations.Endocrine · 2014Review
- MiR-137 regulates epithelial-mesenchymal transition in gastrointestinal stromal tumor.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
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13 authors.
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Abstract
In contrast to adult mutant gastrointestinal stromal tumors [GISTs], pediatric/wild-type GISTs remain poorly understood overall, given their lack of oncogenic activating tyrosine kinase mutations. These GISTs, with a predilection for gastric origin in female patients, show limited response to therapy with tyrosine kinase inhibitors and generally pursue a more indolent course, but still may prove fatal. Defective cellular respiration appears to underpin tumor development in these wild-type cases, which as a group lack expression of succinate dehydrogenase [SDH] B, a surrogate marker for respiratory chain metabolism. Yet, only a small subset of the wild-type tumors show mutations in the genes coding for the SDH subunits [SDHx]. To explore additional pathogenetic mechanisms in these wild-type GISTs, we elected to investigate post-transcriptional regulation of these tumors by conducting microRNA (miRNA) profiling of a mixed cohort of 73 cases including 18 gastric pediatric wild-type, 25 (20 gastric, 4 small bowel and 1 retroperitoneal) adult wild-type GISTs and 30 gastric adult mutant GISTs. By this approach we have identified distinct signatures for GIST subtypes which correlate tightly with clinico-pathological parameters. A cluster of miRNAs on 14q32 show strikingly different expression patterns amongst GISTs, a finding which appears to be explained at least in part by differential allelic methylation of this imprinted region. Small bowel and retroperitoneal wild-type GISTs segregate with adult mutant GISTs and express SDHB, while adult wild-type gastric GISTs are dispersed amongst adult mutant and pediatric wild-type cases, clustering in this situation on the basis of SDHB expression. Interestingly, global methylation analysis has recently similarly demonstrated that these wild-type, SDHB-immunonegative tumors show a distinct pattern compared with KIT and PDGFRA mutant tumors, which as a rule do express SDHB. All cases with Carney triad within our cohort cluster together tightly.
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