ArticleHuman mutation2018
Genotype-specific progression of hereditary medullary thyroid cancer.
Article in Human mutation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Article
- Population Prevalence of the Major Thyroid Cancer-Associated Syndromes.The Journal of clinical endocrinology and metabolism · 2025Article
- Geospatial inheritance across the breath of the RET mutational landscape of multiple endocrine neoplasia 2A.Endocrine · 2025Article
- Article
- MEN2: surgical precision in the era of precision medicine.Endocrine-related cancer · 2025Review
- Article
- Surgical Treatment of Medullary Thyroid Cancer.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025Review
- Article
- [Precision medicine in endocrinology exemplified by medullary thyroid cancer].Innere Medizin (Heidelberg, Germany) · 2024Review
- Does Genotype-Specific Phenotype in Patients with Multiple Endocrine Neoplasia Type 2 Occur as Current Guidelines Predict?Cancers · 2024Article
- Clinical presentation of MEN 2A in index vs. non-index patients.Endocrine · 2023Article
- [Hereditary medullary thyroid cancer].Chirurgie (Heidelberg, Germany) · 2023Review
- Article
- Article
- Thyroidectomy Outcomes in Patients Identified With RET Pathogenic Variants Through a Population Genomic Screening Program.JAMA otolaryngology-- head & neck surgery · 2023Article
- Clinical characteristics of a large familial cohort with Medullary thyroid cancer and germline Cys618ArgFrontiers in endocrinology · 2023Article
- Medullary thyroid cancer and pheochromocytoma in MEN2A: are there parent of origin effects on disease expression?Familial cancer · 2022Article
- Review
- Active Surveillance inCancers · 2021Article
- Hereditary medullary thyroid carcinoma syndromes: experience from western India.Familial cancer · 2021Article
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Although already 25 years into the genomic era, age-related progression of hereditary medullary thyroid cancer (MTC), the prevalence of which is estimated at one in 80,000 inhabitants, remains to be delineated for most unique RET (REarranged during Transfection) mutations. Included in this study were 567 RET carriers. The age-related progression of MTC across histopathological groups (normal thyroid/C-cell hyperplasia; node-negative MTC; node-positive MTC) was statistically significant for 13 unique RET mutations (p.Cys611Phe/c.1832G > T; p.Cys611Tyr; p.Cys618Ser/c.1852T > A; p.Cys620Arg; p.Cys634Arg; p.Cys634Phe; p.Cys634Ser; p.Cys634Tyr; p.Glu768Asp; p.Leu790Phe/c.2370G > T; p.Val804Met; p.Ser891Ala; p.Met918Thr), whereas two unique RET mutations (p.Cys618Phe; p.Cys634Gly) trended toward statistical significance. When grouped by mutational risk (highest; high; moderate-high; low-moderate; polymorphism), the age-related progression of MTC was significant for all four categories of RET mutations, which differed significantly across and within the three histopathological groups. For high, for moderate-high, and for low-moderate risk RET mutations, the age-related progression of MTC by mutated codon was broadly comparable across and within the three histopathological groups, and essentially unaffected by the amino acid substitutions examined. These data argue in favor of splitting the American Thyroid Association's moderate-risk category into moderate-high and low-moderate risk categories, while emphasizing the need to contradistinguish the latter from rare nonpathogenic polymorphisms.
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