ArticleScientific reports2017
Differences in the transcriptome of medullary thyroid cancer regarding the status and type of RET gene mutations.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Resolving thyroid lineage cell trajectories merging into a dual endocrine gland in mammals.Nature communications · 2026Article
- Review
- Article
- Current status of the prognostic molecular markers in medullary thyroid carcinoma.Endocrine connections · 2020Review
- MEN2-related pheochromocytoma: current state of knowledge, specific characteristics in MEN2B, and perspectives.Endocrine · 2020Review
- Two GEO MicroRNA Expression Profile Based High-Throughput Screen to Identify MicroRNA-31-3p Regulating Growth of Medullary Thyroid Carcinoma Cell by Targeting RASA2.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Update on Multiple Endocrine Neoplasia Type 2: Focus on Medullary Thyroid Carcinoma.Journal of the Endocrine Society · 2018Review
- Recent advances in the biology and therapy of medullary thyroid carcinoma.F1000Research · 2017Review
- Changing pattern of pheochromocytoma and paraganglioma in a stable UK population.Acta endocrinologica (Bucharest, Romania : 2005)Article
- Analysis of lncRNA and mRNA Transcriptomes Expression in Thyroid Cancer Tissues Among Patients With Exposure of Medical Occupational Radiation.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medullary thyroid cancer (MTC) can be caused by germline mutations of the RET proto-oncogene or occurs as a sporadic form. It is well known that RET mutations affecting the cysteine-rich region of the protein (MEN2A-like mutations) are correlated with different phenotypes than those in the kinase domain (MEN2B-like mutations). Our aim was to analyse the whole-gene expression profile of MTC with regard to the type of RET gene mutation and the cancer genetic background (hereditary vs sporadic). We studied 86 MTC samples. We demonstrated that there were no distinct differences in the gene expression profiles of hereditary and sporadic MTCs. This suggests a homogeneous nature of MTC. We also noticed that the site of the RET gene mutation slightly influenced the gene expression profile of MTC. We found a significant association between the localization of RET mutations and the expression of three genes: NNAT (suggested to be a tumour suppressor gene), CDC14B (involved in cell cycle control) and NTRK3 (tyrosine receptor kinase that undergoes rearrangement in papillary thyroid cancer). This study suggests that these genes are significantly deregulated in tumours with MEN2A-like and MEN2B-like mutations; however, further investigations are necessary to demonstrate any clinical impact of these findings.
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