Educational Case: Endocrine Neoplasm

Segura, Sheila; Ramos‐Rivera, Gloria; Suhrland, Mark J.

doi:10.1177/2374289518775722

Cited by 4 publications

(4 citation statements)

References 7 publications

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“…Following isotopic transplanta.on of quail neural tube into chick host embryos, they observed quail neural crestderived cells within the host ul.mobranchial gland that appeared to exhibit cytoplasmic secretory granules characteris.c of C-cells 25 , formaldehyde-induced fluorescence characteris.c of some neuroendocrine cell types 26 , and posi.ve immunostaining with an an.-calcitonin an.body 27 . These findings led to assump.on of a neural crest origin of C-cells in all vertebrates (including mammals), of C-cell-derived cancers like MTC [28][29][30] , and more broadly, of other biochemically similar neuroendocrine cell types (the amine precursor uptake and decarboxyla.on or APUD series) that are distributed throughout the body in disparate organs and .ssues [31][32][33] .…”

Section: Introduconmentioning

confidence: 99%

A pre-vertebrate endodermal origin of calcitonin-producing neuroendocrine cells

Rees,

Kirk,

Gattoni

et al. 2024

Preprint

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SummaryVertebrate calcitonin-producing cells (C-cells) are neuroendocrine cells that secrete the small peptide hormone calcitonin in response to elevated blood calcium levels. C-cells are crucial for maintenance of calcium homeostasis, yet the embryonic and evolutionary origins of this cell type remain contentious. Whereas mouse C-cells reside within the thyroid gland and derive from pharyngeal endoderm, avian C-cells are located within ultimobranchial glands and were reported to derive from the neural crest. We use a comparative cell lineage tracing approach in a range of vertebrate model systems to resolve the ancestral embryonic origin of vertebrate C-cells. We find, contrary to previous studies, that chick C-cells derive from pharyngeal endoderm, with neural crest-derived cells instead contributing to connective tissue intimately associated with C-cells in the ultimobranchial gland. This endodermal origin of C-cells is conserved in a ray-finned bony fish (zebrafish) and a cartilaginous fish (the little skate,Leucoraja erinacea). Furthermore, we discover putative C-cell homologues within the endodermally-derived pharyngeal epithelium of the ascidianCiona intestinalisand the amphioxusBranchiostoma lanceolatum, two invertebrate chordates that lack neural crest cells. Our findings point to a conserved endodermal origin of C-cells across vertebrates and to a pre-vertebrate origin of this cell type along the chordate stem.

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Section: Introduconmentioning

confidence: 99%

A pre-vertebrate endodermal origin of calcitonin-producing neuroendocrine cells

Rees,

Kirk,

Gattoni

et al. 2024

Preprint

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“…Medullary thyroid cancer (MTC) is an infrequent neuroendocrine tumor that originates from C cells (formerly known as parafollicular cells), which stem from the neural crest cells that migrate into the thyroid gland from the third and fourth branchial pouches [ 1 , 2 ]. It was first reported as a specific entity in 1959, when Hazard et al reviewed 600 cases of an atypical thyroid cancer with non-follicular histology and amyloid-containing stroma [ 3 ].…”

Section: ⧉ Introductionmentioning

confidence: 99%

“…It was first reported as a specific entity in 1959, when Hazard et al reviewed 600 cases of an atypical thyroid cancer with non-follicular histology and amyloid-containing stroma [ 3 ]. Although these cells are placed throughout the thyroid gland, they are predominant at the junction of the upper and middle third of each lobe, where most of the MTCs are located [ 1 ]. Parafollicular cells produce mainly calcitonin (Ct), which serves not only in diagnosis but as a prognostic marker as well [ 4 ].…”

Section: ⧉ Introductionmentioning

confidence: 99%

Medullary thyroid cancer: molecular factors, management and treatment

Pavlidis

Sapalidis²,

Chatzinikolaou³

et al. 2021

Rom J Morphol Embryol

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Medullary thyroid cancer (MTC) is an infrequent neuroendocrine tumor, which amounts to 3–5% of all thyroid malignancies. Approximately 75–80% of MTCs are sporadic neoplasms. The rest of 20–25% are familial cases that belong to multiple endocrine neoplasia (MEN) syndromes, specifically MEN2 and MEN3. These cases of familial MTC are attributed to an activating germline mutation of a tyrosine kinase receptor gene, the rearranged during transfection ( RET ) proto-oncogene, located on chromosome 10q11.21. These mutations are also found in some cases of sporadic MTC. This review sets forth in summary the accepted guidelines and approaches regarding diagnosis, management, and treatment of MTC. Surgical resection is the standard care, and an early, prophylactic intervention is performed in genetic cases. Further investigation and understanding of the molecular pathways involved in the growth and advancement of MTC is required in order to provide efficient therapy in cases of progressive disease.

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“…Recently activating somatic mutations in the BRAF proto-oncogene has been discovered in various malignancies, such as in melanoma (60–70% of cases) [1, 2], colon cancer (10%) [3, 4] including thyroid cancer (35–70%) [5, 6]. Thyroid tumors are the most frequent neoplasms of the endocrine system [7]. Well-differentiated thyroid carcinomas account for > 85% of all thyroid cancers including papillary and follicular carcinomas.…”

Section: Introductionmentioning

confidence: 99%

Low dose radiation regulates BRAF-induced thyroid cellular dysfunction and transformation

et al. 2019

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BackgroundThe existence of differentiated thyroid cells is critical to respond radioactive iodide treatment strategy in thyroid cancer, and loss of the differentiated phenotype is a trademark of iodide-refractive thyroid disease. While high-dose therapy has been beneficial to several cancer patients, many studies have indicated this clinical benefit was limited to patients having BRAF mutation. BRAF-targeted paired box gene-8 (PAX8), a thyroid-specific transcription factor, generally dysregulated in BRAF-mutated thyroid cancer.MethodsIn this study, thyroid iodine-metabolizing gene levels were detected in BRAF-transformed thyroid cells after low and high dose of ionizing radiation. Also, an mRNA-targeted approach was used to figure out the underlying mechanism of low (0.01Gyx10 or 0.1Gy) and high (2Gy) radiation function on thyroid cancer cells after BRAFV600E mutation.ResultsLow dose radiation (LDR)-induced PAX8 upregulation restores not only BRAF-suppressive sodium/iodide symporter (NIS) expression, one of the major protein necessary for iodine uptake in healthy thyroid, on plasma membrane but also regulate other thyroid metabolizing genes levels. Importantly, LDR-induced PAX8 results in decreased cellular transformation in BRAF-mutated thyroid cells.ConclusionThe present findings provide evidence that LDR-induced PAX8 acts as an important regulator for suppression of thyroid carcinogenesis through novel STAT3/miR-330-5p pathway in thyroid cancers.Electronic supplementary materialThe online version of this article (10.1186/s12964-019-0322-x) contains supplementary material, which is available to authorized users.

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Educational Case: Endocrine Neoplasm

Cited by 4 publications

References 7 publications

A pre-vertebrate endodermal origin of calcitonin-producing neuroendocrine cells

A pre-vertebrate endodermal origin of calcitonin-producing neuroendocrine cells

Medullary thyroid cancer: molecular factors, management and treatment

Low dose radiation regulates BRAF-induced thyroid cellular dysfunction and transformation

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