The clonality of nodules in recurrent goiters at second surgery

Harrer, P.; Bröcker, Martina; Zint, Antje; Derwahl, Michael; Barbera, L.; Zumtobel, V.

doi:10.1007/s004230050159

Cited by 22 publications

(11 citation statements)

References 5 publications

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“…In these lesions, the presence of a TSH receptor mutation may be important (Krohn et al 1998): 10/11 cases showed monoclonality on HUMARA analysis, but only 6/12 toxic nodules with no TSH receptor mutation are clonal, raising the possibility that during thyroid hyperplasia a cell with a mutation at this locus leads to the initiation of autonomous growth. In recurrent goitres, nodules are predominantly polyclonal (Harrer et al 1998a). In several studies of clonality in multinodular goitre, the proportion of clonal nodules varies, and it is clear that clonal and polyclonal nodules can coexist in the same gland (Namba et al 1990;Bamburger et al 1993;Kim et al 1998), with no apparent correlation with morphology, although clonal nodules might be larger (Kim et al 1998).…”

Section: Current Statusmentioning

confidence: 99%

The clonal origin and clonal evolution of epithelial tumours

Garcia

Novelli

Wright

2000

Int J Experimental Path

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While the origin of tumours, whether from one cell or many, has been a source of fascination for experimental oncologists for some time, in recent years there has been a veritable explosion of information about the clonal architecture of tumours and their antecedents, stimulated, in the main, by the ready accessibility of new molecular techniques. While most of these new results have apparently confirmed the monoclonal origin of human epithelial (and other) tumours, there are a significant number of studies in which this conclusion just cannot be made. Moreover, analysis of many articles show that the potential impact of such considerations as patch size and clonal evolution on determinations of clonality have largely been ignored, with the result that a number of these studies are confounded. However, the clonal architecture of preneoplastic lesions provide some interesting insights --many lesions which might have been hitherto regarded as hyperplasias are apparently clonal in derivation. If this is indeed true, it calls into some question our hopeful corollary that a monoclonal origin presages a neoplastic habitus. Finally, it is clear, for many reasons, that methods of analysis which involve the disaggregation of tissues, albeit microdissected, are far from ideal and we should be putting more effort into techniques where the clonal architecture of normal tissues, preneoplastic and preinvasive lesions and their derivative tumours can be directly visualized in situ.

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Section: Current Statusmentioning

confidence: 99%

The clonal origin and clonal evolution of epithelial tumours

Garcia

Novelli

Wright

2000

Int J Experimental Path

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“…Some studies showed that in multinodular goitres clonal and polyclonal nodules coexist. Interestingly, nodules in recurrent goitres are predominantly polyclonal, while many thyroid cancers are polyclonal [22][23][24]. The collected data suggest that both benign and malignant nodules have their origin in a de novo proliferation of different cohorts of thyrocytes supporting the presence of subtle alterations within the clinically and sonographically normal perinodular tissue.…”

Section: Discussionmentioning

confidence: 79%

Analysis of tissue surrounding thyroid nodules by ultrasound digital images

Trimboli

Bini

Andrioli³

et al. 2014

Endocrine

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Since US is not easily reproducible, the digital image analysis (IA) has been proposed so that the image evaluation is not subjective. In fact, IA meets the criteria of objectivity, accurateness, and reproducibility by a matrix of pixels whose value is displayed in a gray level. This study aims at evaluating via IA the tissue surrounding a thyroid nodule (backyard tissue, BT) from goitres with benign (b-BT) and malignant (m-BT) lesions. Sixty-nine US images of thyroid nodules surrounded by adequate thyroid tissue was classified as normoechoic and homogeneous were enrolled as study group. Forty-three US images from normal thyroid (NT) glands were included as controls. Digital images of 800 × 652 pixels were acquired at a resolution of eight bits with a 256 gray levels depth. By one-way ANOVA, the 43 NT glands were not statistically different (P = 0.91). Mean gray level of normal glands was significantly higher than b-BT (P = 0.026), and m-BT (P = 0.0001), while no difference was found between b-BT and m-BT (P = 0.321). NT tissue boundary external to the nodule was found at 6.0 ± 0.5 mm in cancers and 4.0 ± 0.5 mm in benignancies (P = 0.001). These data should indicate that the tissue surrounding a thyroid nodule may be damaged even when assessed as normal by US. This is of interest to investigate the extranodular effects of thyroid tumors.

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“…Prior studies have used X-inactivation (HUMARA) analyses to prove that the patch size in thyroid is actually quite large. 32,33 And, in fact, nodules from nodular goiter can have evidence of monoclonal origin. 34 Thus, we do know that single cells can be progenitors for fairly large nodular areas within the thyroid.…”

Section: Discussionmentioning

confidence: 99%

Thyroidectomies from patients with history of therapeutic radiation during childhood and adolescence have a unique mutational profile

2008

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Radiation in childhood is a known risk factor for thyroid carcinoma, but may also be related to benign nodular hyperplasias. Recent evidence from comparative genomic hybridization indicates that radiation can induce clonal DNA damage in cultured rat thyrocytes. We used a loss of heterozygosity analysis for the loci identified by comparative genomic hybridization to study human thyroids. Thyroids from patients with a history of radiation, patients who had recent therapeutic external beam radiation for laryngeal carcinoma, and patients who had no radiation and underwent incidental thyroidectomy with laryngectomy for laryngeal carcinoma were included. PCR was performed for 18 different genetic loci defined by prior reported comparative genomic hybridization study. A semiquantitative capillary electrophoresis analysis was used and frequency of allelic loss was calculated from the number of losses/the number of informative loci. A total of 40 cases of thyroids from patients with childhood radiation, 12 cases of recently radiated thyroids, and 15 cases of nonradiated thyroids were included. In the nonradiated and recently radiated thyroids, the mean frequency of allelic loss was 2.3%. In the thyroids from patients radiated as children, the mean frequency of allelic loss was 39%. Losses were seen at every locus with a range of 7-100% of the cases analyzed (mean 49.6%). Radiation in childhood was associated with both benign nodular disease and carcinomas of the thyroid. The frequency of allelic loss was very high in all lesions in these patients, as compared to control thyroid glands. These data from human thyroids support prior cell culture experiments and show that radiation induces genetic mutational damage even in benign proliferative processes in these thyroids.

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The clonality of nodules in recurrent goiters at second surgery

Abstract: The finding that nodules in recurrent goiters are predominantly polyclonal suggests that these lesions have their origin in a de novo proliferation of different cohorts of thyrocytes due to unknown growth stimulating molecular events.

Cited by 22 publications

References 5 publications

The clonal origin and clonal evolution of epithelial tumours

The clonal origin and clonal evolution of epithelial tumours

Analysis of tissue surrounding thyroid nodules by ultrasound digital images

Thyroidectomies from patients with history of therapeutic radiation during childhood and adolescence have a unique mutational profile

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