Endocrine changes associated with the human aging process: III. Effect of age on the number of calcitonin immunoreactive cells in the thyroid gland

O’Toole, Kathleen; Fenoglio‐Preiser, Cecilia M.; Pushparaj, Neela

doi:10.1016/s0046-8177(85)80276-8

Cited by 61 publications

(28 citation statements)

References 35 publications

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“…26,27 The present study, conducted on aspirates, confirmed these histologic findings since we demonstrated the existence of a greater concentration of C cells (140, or 86.9%) in the middle and upper third of the lateral lobes of the gland. How- ever, in contrast to studies carried out on histologic material, 10,22 we detected cells in the lower third (eight cases) and in the isthmus (four cases), although in small numbers. Several investigators 6,13,18,24 have mentioned the difficulty in observing C cells when using common histochemical staining methods, with identification of these cells on the basis of purely morphologic aspects almost impossible.…”

Section: Discussioncontrasting

confidence: 99%

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C Cells in Normal Thyroid Aspirates

Lima¹,

Santos²,

Tiveron³

et al. 1999

Acta Cytologica

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Section: Discussioncontrasting

confidence: 99%

“…However, O'Toole et al 22 proposed that the number of C cells varies widely after 60 years of age, with a tendency toward hyperplasia. Among the 19 glands studied here, 7 were from patients older than 60 (nos.…”

Section: Discussionmentioning

confidence: 99%

C Cells in Normal Thyroid Aspirates

Lima¹,

Santos²,

Tiveron³

et al. 1999

Acta Cytologica

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“…Several conditions such as hyperparathyroidism, hypercalcemia, infancy and chronic lymphatic thyroiditis (Wolfe et al, 1975a,b;Gibson et al, 1980;DeLellis, 1992;Tomita and Millard, 1992), are now admittedly associated with CCH, whereas others, such as age and sex, are still subject to controversy (Gibson et al, 1982;O'Toole et al, 1985;Albores-Saavedra et al, 1988;Scopsi et al, 1991;Guyetant et al, 1997;Harach, 1997). In our patients with a history of external radiation, no correlation has been seen in the sex ratio between the CCH positive and CCH negative groups (1.66 and 1.6 respectively).…”

Section: Discussionmentioning

confidence: 99%

Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue

et al. 2002

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The RET proto-oncogene encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain. In human thyroid gland, the RET proto-oncogene is normally expressed in parafollicular C-cells. Thyroid C-cell hyperplasia is associated with inherited medullary thyroid carcinomas and is considered as a pre-neoplastic stage of C-cells disease. It has also been observed in thyroid tissues adjacent to follicular and papillary carcinomas. In order to study the relationship between a misfunctioning of the RET proto-oncogene and the presence of C-cell hyperplasia, we compared a series of thyroid glands presenting sporadic or radiation-associated tumours, as well as samples of unrelated normal thyroid tissues, for alteration in exons 10 and 11 of the gene and for the presence or absence of C-cell hyperplasia. Here we report a significantly higher frequency of C-cell hyperplasia present in peritumoural thyroid tissues of radiation-induced epithelial thyroid tumours, than in peritumoural of sporadic thyroid tumours or in control normal thyroid tissues (P=0.001). A G691S RET polymorphism was present with a higher frequency in radiation-induced epithelial thyroid tumours (55%) than in sporadic tumours (20%) and in control normal thyroid tissues (15%). Interestingly, this polymorphism was associated in the majority (88%) of radiation-induced tumours with a C-cell hyperplasia in the peritumoural tissues. Several explanations for this association are discussed.

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“…Since MEN2 is defined as a hereditary MTC disorder and some MEN2 clinical features, such as pheo, HPT, or Marfanoid body habitus, can be caused by mutations within other genes besides RET [Frank-Raue et al, 2005;Neumann et al, 2002]; at least one of the affected family members must have MTC to define the sequence change as a mutation . Individuals with only C-cell hyperplasia or elevated calcitonin were not considered clinically affected for the purpose of classifying mutations, since C-cell hyperplasia and elevated calcitonin can occur within the general population and in MEN2 family members that did not inherit the RET mutation (not all C-cell hyperplasia proceeds to MTC) [Baumgartner-Parzer et al, 2005;Gibson et al, 1982;Hazard, 1977;Lips et al, 1994;O'Toole et al, 1985]. Family members were also not considered affected if they had suspected but unconfirmed MEN2 clinical features.…”

Section: Classification Of Pathogenicitymentioning

confidence: 99%

Multiple endocrine neoplasia type 2RETprotooncogene database: Repository of MEN2-associatedRETsequence variation and reference for genotype/phenotype correlations

et al. 2009

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Multiple endocrine neoplasia type 2 (MEN2) is an inherited, autosomal-dominant disorder caused by deleterious mutations within the RET protooncogene. MEN2 RET mutations are mainly heterozygous, missense sequence changes found in RETexons 10, 11, and 13-16. Our group has developed the publicly available, searchable MEN2 RET database to aid in genotype/phenotype correlations, using Human Genome Variation Society recommendations for sequence variation nomenclature and database content. The MEN2 RET database catalogs all RET sequence variation relevant to the MEN2 syndromes, with associated clinical information. Each database entry lists a RET sequence variation's location within the RET gene, genotype, pathogenicity classification, MEN2 phenotype, first literature reference, and comments (which may contain information on other clinical features, complex genotypes, and additional literature references). The MEN2 phenotype definitions were derived from the International RET Mutation Consortium guidelines for classification of MEN2 disease phenotypes. Although nearly all of the 132 RET sequence variation entries initially cataloged in the database were from literature reports, novel sequence variation and updated phenotypic information for any existing database entry can be submitted electronically on the database website. The database website also contains links to selected MEN2 literature reviews, gene and protein information, and RET reference sequences. The MEN2 RET database (www.arup.utah.edu/database/MEN2/ MEN2_welcome.php) will serve as a repository for MEN2-associated RET sequence variation and reference for RET genotype/MEN2 phenotype correlations.

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Endocrine changes associated with the human aging process: III. Effect of age on the number of calcitonin immunoreactive cells in the thyroid gland

Cited by 61 publications

References 35 publications

C Cells in Normal Thyroid Aspirates

C Cells in Normal Thyroid Aspirates

Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue

Multiple endocrine neoplasia type 2RETprotooncogene database: Repository of MEN2-associatedRETsequence variation and reference for genotype/phenotype correlations

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