Abstract
BackgroundMost of the steps involved in the initiation and progression of Hürthle (oncocytic, oxyphilic) cell carcinomas of the thyroid remain unknown.MethodsUsing differential display and semiquantitative RT-PCR we found, among other alterations, overexpression of the gene encoding the Core I subunit of the complex III of the mitochondrial respiratory chain in a follicular carcinoma composed of Hürthle cells.ResultsSimilar high levels of Core I gene expression were detected in nine follicular carcinomas (seven with Hürthle cell features), in seven microfollicular adenomas (one with Hürthle cell features) and in one micro/macrofollicular adenoma, in contrast to a lower/normal expression in nine papillary carcinomas (three with Hürthle cell features) and five macrofollicular adenomas (one of which displaying Hürthle cell features). No significative correlation was found between Core I overexpression and the proliferative activity of the lesions.ConclusionsWe conclude that Core I overexpression in thyroid tumours is not associated with malignancy, Hürthle cells or proliferative activity. The pathogenetic mechanism linking Core I overexpression to the microfollicular pattern of growth of thyroid tumours remains to be clarified.
Highlights
Most of the steps involved in the initiation and progression of Hürthle cell carcinomas of the thyroid remain unknown
Differential display (DD) The DD analysis of mRNA revealed seven bands differentially expressed in normal thyroid tissue and in the follicular Hürthle cell carcinoma
We found overexpression of the gene encoding the Core I subunit of the complex III of mitochondrial respiratory chain (MRC) in follicular carcinomas and microfollicular adenomas of the thyroid with or without Hürthle cells features, in contrast with its underexpression in macrofollicular adenomas and its near-normal levels in papillary carcinomas
Summary
Most of the steps involved in the initiation and progression of Hürthle (oncocytic, oxyphilic) cell carcinomas of the thyroid remain unknown. Neoplastic progression is a prolonged and stepwise process involving a series of molecular alterations that culminate in invasion and metastasis. Such molecular alterations usually result in the modification of gene expression in cancer cells. Some consistent molecular changes have been previously described in functioning thyroid adenomas – TShR and Gs alpha gene mutations – [1] as well as in papillary thyroid carcinomas: RET/PTC and trk rearrangement [2,3] and BRAF mutation [4]. Carcinomas with Hürthle (oncocytic, oxyphilic) cell features typically harbour the genetic alterations associated to the predominant histotype of the lesion – e.g. the high prevalence of RET/PTC rearrangements and B-RAF mutations in the Hürthle cell variant of papillary thyroid carcinomas [4,8].
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