ArticleBone reports2020
GNAS mutated thyroid carcinoma in a patient with Mc Cune Albright syndrome.
Article in Bone reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- 2025 American Thyroid Association Management Guidelines for Adult Patients with Differentiated Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2025Guideline
- Somatic genomic profiling reveals clinically relevant heterogeneity inJournal of clinical & translational endocrinology · 2026Article
- Contract to kill: GNAS mutation.Molecular cancer · 2025Review
- Clinical spectrum and uncommon features of McCune-Albright syndrome in children: a cohort study from a National Referral Center.Frontiers in endocrinology · 2025Article
- A recurrent somatic missense mutation in GNAS gene identified in familial thyroid follicular cell carcinomas in German longhaired pointer dogs.BMC genomics · 2022Article
- Case report: Surgical treatment of McCune-Albright syndrome with hyperthyroidism and retrosternal goiter: A case report and literature review.Frontiers in surgery · 2022Article
- Peutz-Jeghers syndrome: Skin manifestations and endocrine anomalies (Review).Experimental and therapeutic medicine · 2021Review
- Review
- Thyroid Scan Conundrum in a Rare Case of McCune-Albright Syndrome.Indian journal of nuclear medicine : IJNM : the official journal of the Society of Nuclear Medicine, IndiaArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mc Cune-Albright syndrome (MAS) is a rare disorder defined by the triad of polyostotic fibrous dysplasia, "café au lait" skin hyperpigmentation and hyperfunctioning endocrinopathies, such as precocious puberty. MAS is caused by an activating post zygotic somatic mutation of GNAS gene, coding for the alpha-subunit of the stimulatory G protein (Gsalpha). In endocrine tissues, this mutation results in overproduction of hormones and endocrine cell hyperfunction and proliferation. Whereas the association of hyperthyroidism and thyroid adenomas is well known in MAS, the relation with thyroid carcinoma has rarely been observed. We report the occurrence of a thyroid carcinoma in an 18-years old woman with MAS, revealed by subclinical hyperthyroidism detected during her systematic annual follow-up. Ultrasound and thyroid scintigraphy revealed the presence of a nodule in the right lobe. Pathology on hemithyroidectomy revealed an unexpected thyroid follicular carcinoma. Neoplastic thyroid cells harbored the GNAS R201C activating mutation. This observation suggests that MAS may predispose patients to thyroid carcinomas and supports the importance of thyroid assessment by physical examination, hormonal blood test and ultrasound, in the follow-up of patients with MAS. Because ultrasound diagnostic is challenging in MAS, needle puncture of palpable nodules should be advised.
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