ArticleGenes, chromosomes & cancer2016
HRAS mutation prevalence and associated expression patterns in pheochromocytoma.
Article in Genes, chromosomes & cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Genotype-phenotype correlations in pheochromocytoma and paraganglioma: a systematic review and individual patient meta-analysis.Endocrine-related cancer · 2019Pooled it
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- Genetic variants and down-regulation of CACNA1H in pheochromocytoma.Endocrine-related cancer · 2024Article
- TOP2A Expression in Pheochromocytoma and Abdominal Paraganglioma: a Marker of Poor Clinical Outcome?Endocrine pathology · 2023Article
- HRAS Q61L Mutation as a Possible Target for Non-Small Cell Lung Cancer: Case Series and Review of Literature.Current oncology (Toronto, Ont.) · 2022Review
- Genetics of Pheochromocytomas and Paragangliomas Determine the Therapeutical Approach.International journal of molecular sciences · 2022Review
- Composite pheochromocytoma/paraganglioma-ganglioneuroma: analysis of SDH and ATRX status, and identification of frequent HRAS and BRAF mutations.Endocrine connections · 2021Article
- A Critical Appraisal of Contemporary and Novel Biomarkers in Pheochromocytomas and Adrenocortical Tumors.Biology · 2021Review
- What Have We Learned from Molecular Biology of Paragangliomas and Pheochromocytomas?Endocrine pathology · 2021Review
- Activation of RAS Signalling is Associated with Altered Cell Adhesion in Phaeochromocytoma.International journal of molecular sciences · 2020Article
- Catecholamine-Secreting Tumors in Pediatric Patients With Cyanotic Congenital Heart Disease.Journal of the Endocrine Society · 2019Review
- Precision Surgery for Pheochromocytomas and Paragangliomas.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2019Review
- Pheochromocytoma and paraganglioma: genotype versus anatomic location as determinants of tumor phenotype.Cell and tissue research · 2018Review
- Activating FGFR1 Mutations in Sporadic Pheochromocytomas.World journal of surgery · 2018Article
- Treatment for Patients With Malignant Pheochromocytomas and Paragangliomas: A Perspective From the Hallmarks of Cancer.Frontiers in endocrinology · 2018Review
- A Clinical Roadmap to Investigate the Genetic Basis of Pediatric Pheochromocytoma: Which Genes Should Physicians Think About?International journal of endocrinology · 2018Review
- Metabologenomics of Phaeochromocytoma and Paraganglioma: An Integrated Approach for Personalised Biochemical and Genetic Testing.The Clinical biochemist. Reviews · 2017Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pheochromocytomas (PCC) and abdominal paragangliomas (PGL) display a highly diverse genetic background and recent gene expression profiling studies have shown that PCC and PGL (together PPGL) alter either kinase signaling pathways or the pseudo-hypoxia response pathway dependent of the genetic composition. Recurrent mutations in the Harvey rat sarcoma viral oncogene homolog (HRAS) have recently been verified in sporadic PPGLs. In order to further establish the HRAS mutation frequency and to characterize the associated expression profiles of HRAS mutated tumors, 156 PPGLs for exon 2 and 3 hotspot mutations in the HRAS gene was screened, and compared with microarray-based gene expression profiles for 93 of the cases. The activating HRAS mutations G13R, Q61R, and Q61K were found in 10/142 PCC (7.0%) and a Q61L mutation was revealed in 1/14 PGL (7.1%). All HRAS mutated cases included in the mRNA expression profiling grouped in Cluster 2, and 21 transcripts were identified as altered when comparing the mutated tumors with 91 HRAS wild-type PPGL. Somatic HRAS mutations were not revealed in cases with known PPGL susceptibility gene mutations and all HRAS mutated cases were benign. The HRAS mutation prevalence of all PPGL published up to date is 5.2% (49/950), and 8.8% (48/548) among cases without a known PPGL susceptibility gene mutation. The findings support a role of HRAS mutations as a somatic driver event in benign PPGL without other known susceptibility gene mutations. HRAS mutated PPGL cluster together with NF1- and RET-mutated tumors associated with activation of kinase-signaling pathways.
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