Recurrent Mutations of Chromatin-Remodeling Genes and Kinase Receptors in Pheochromocytomas and Paragangliomas
Clinical Cancer Research, ISSN: 1557-3265, Vol: 22, Issue: 9, Page: 2301-2310
2016
- 115Citations
- 87Captures
- 2Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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- Citations115
- Citation Indexes113
- 113
- CrossRef80
- Clinical Citations1
- PubMed Guidelines1
- Policy Citations1
- Policy Citation1
- Captures87
- Readers87
- 87
- Mentions2
- News Mentions1
- News1
- References1
- Wikipedia1
Most Recent News
Therapies Targeting the Signal Pathways of Pheochromocytoma and Paraganglioma
Abstract:Pheochromocytoma and paraganglioma (PCC/PGL) are rare tumors that originate from adrenal or extra-adrenal chromaffin cells. A significant clinical manifestation of PCC/PGL is that the tumors
Article Description
Purpose: Pheochromocytomas and paragangliomas (PPGL) are genetically heterogeneous tumors of neural crest origin, but the molecular basis of most PPGLs is unknown. Experimental Design: We performed exome or transcriptome sequencing of 43 samples from 41 patients. A validation set of 136 PPGLs was used for amplicon-specific resequencing. In addition, a subset of these tumors was subjected to microarray-based transcription, protein expression, and histone methylation analysis by Western blotting or immunohistochemistry. In vitro analysis of mutants was performed in cell lines. Results: We detected mutations in chromatin-remodeling genes, including histone-methyltransferases, histone-demethylases, and histones in 11 samples from 8 patients (20%). In particular, we characterized a new cancer syndrome involving PPGLs and giant cell tumors of bone (GCT) caused by a postzygotic G34W mutation of the histone 3.3 gene, H3F3A. Furthermore, mutations in kinase genes were detected in samples from 15 patients (37%). Among those, a novel germline kinase domain mutation of MERTK detected in a patient with PPGL and medullary thyroid carcinoma was found to activate signaling downstream of this receptor. Recurrent germline and somatic mutations were also detected in MET, including a familial case and sporadic PPGLs. Importantly, in each of these three genes, mutations were also detected in the validation group. In addition, a somatic oncogenic hotspot FGFR1 mutation was found in a sporadic tumor. Conclusions: This study implicates chromatin-remodeling and kinase variants as frequent genetic events in PPGLs, many of which have no other known germline driver mutation. MERTK, MET, and H3F3A emerge as novel PPGL susceptibility genes.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84968830210&origin=inward; http://dx.doi.org/10.1158/1078-0432.ccr-15-1841; http://www.ncbi.nlm.nih.gov/pubmed/26700204; http://clincancerres.aacrjournals.org/cgi/doi/10.1158/1078-0432.CCR-15-1841; https://syndication.highwire.org/content/doi/10.1158/1078-0432.CCR-15-1841; https://aacrjournals.org/clincancerres/article/22/9/2301/79888/Recurrent-Mutations-of-Chromatin-Remodeling-Genes; https://dx.doi.org/10.1158/1078-0432.ccr-15-1841; https://clincancerres.aacrjournals.org/content/22/9/2301
American Association for Cancer Research (AACR)
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