ArticleThe Journal of clinical endocrinology and metabolism2008
High resolution array-comparative genomic hybridization profiling reveals deoxyribonucleic acid copy number alterations associated with medullary thyroid carcinoma.
Article in The Journal of clinical endocrinology and metabolism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Thyroid C-Cell Biology and Oncogenic Transformation.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025Review
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- Identification of Three Prognosis-Related Differentially Expressed lncRNAs Driven by Copy Number Variation in Thyroid Cancer.Journal of immunology research · 2022Article
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- Article
- The pathogenic role of the GIP/GIPR axis in human endocrine tumors: emerging clinical mechanisms beyond diabetes.Reviews in endocrine & metabolic disorders · 2020Review
- Article
- Outcomes of Children and Adolescents with Advanced Hereditary Medullary Thyroid Carcinoma Treated with Vandetanib.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Role of CDKN2C Fluorescence In Situ Hybridization in the Management of Medullary Thyroid Carcinoma.Annals of clinical and laboratory science · 2017Article
- ATF4 Targets RET for Degradation and Is a Candidate Tumor Suppressor Gene in Medullary Thyroid Cancer.The Journal of clinical endocrinology and metabolism · 2017Article
- Postmortem Examination of an Aggressive Case of Medullary Thyroid Carcinoma Characterized by Catastrophic Genomic Abnormalities.JCO precision oncology · 2017Article
- Medullary Thyroid Carcinoma: Recent Advances Including MicroRNA Expression.Endocrine pathology · 2016Review
- Role of CDKN2C Copy Number in Sporadic Medullary Thyroid Carcinoma.Thyroid : official journal of the American Thyroid Association · 2016Article
- Thyroid C-Cell Biology and Oncogenic Transformation.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2015Review
- The role of Cdk5 in neuroendocrine thyroid cancer.Cancer cell · 2013Article
- Article
- Genetic alterations in a primary medullary thyroid carcinoma and its lymph node metastasis in a patient with 15 years follow-up.Diagnostic pathology · 2012Article
- Genomic analysis using high-resolution single-nucleotide polymorphism arrays reveals novel microdeletions associated with premature ovarian failure.Fertility and sterility · 2011Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
contextActivating mutations in the RET protooncogene have been demonstrated in multiple endocrine neoplasia 2 and sporadic medullary thyroid carcinoma (MTC). However, the complete genetic etiology underlying MTC tumorigenesis remains unclear.
objectiveOur objective was to define more precisely the chromosomal regions and uncover novel genes associated with MTC tumorigenesis. DESIGN AND
settingIn this study, we used high resolution array-based comparative genomic hybridization to define tumor-associated copy number alterations (CNA) in 30 primary MTCs: 20 sporadic tumors (50% of which harbored RET mutation), and 10 hereditary.
resultsWe identified 98 CNA, including 76 genomic allelic losses, two gains, and 20 copy number variations associated with MTC. Across sporadic and hereditary groups, there was a similar and overlapping pattern of predominant allelic loss. There were 29 regions containing at least 30% CNA in the 30 tumor samples. The most frequent allelic loss occurred in four loci, 7q36.1, 12p13.31, 13q12.11, and 19p13.3-11. No regions were found to be uniquely altered in the hereditary tumors. There were 21 CNA specific to sporadic MTC, with loss of 11q23.3 uniquely altered in RET negative tumors. Pathway analysis found cellular growth and proliferation as the most significant overall target, and cell death as the most significant pathway targeted in sporadic MTC.
conclusionsOur findings underscore the importance of candidate tumor suppressor genes together with RET alterations in MTCs. Despite of RET status, all MTC might share similar oncogenetic mechanisms. Dysfunction of cell proliferation and cell death may both be involved in MTC tumorigenesis.
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