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Follicular Tumours (follicular + tumour)

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Medical Sciences100%

Selected Abstracts

Frizzled-1 is down-regulated in follicular thyroid tumours and modulates growth and invasiveness,

THE JOURNAL OF PATHOLOGY, Issue 1 2008
A Ulivieri
Abstract The mechanisms of follicular thyroid carcinoma (FTC) transformation and progression are not well understood. Previously, we detected LOH at 7q21 in all FTCs examined, indicating that loss of genetic material in that region is a common trait in these lesions. To analyse the effects of LOH on gene expression, we performed an analysis of the mRNA expression levels of six different genes, located at 7q21.1,7q21.3. A total of 23 lesions, including eight follicular hyperplasias (FHs), eight follicular adenomas (FAs), two FTCs and five papillary thyroid carcinomas (PTCs) were analysed. The Frizzled-1 (FZD-1) gene, located at 7q21.13, showed the lowest levels of mRNA expression. Down-regulation of FZD-1 expression was also confirmed in an independent series of 69 follicular neoplastic lesions compared to 25 PTCs, analysed by quantitative RT,PCR. In vitro studies showed that FZD-1 expression was also markedly reduced at both protein and mRNA levels in three FTC-derived cell lines (FRO, WRO and FTC-133), while it was normal in the three PTC-derived cell lines (Ca300, Ca301 and K1) examined. We demonstrated that over-expression of FZD-1 in 3 FTC-derived cells decreased invasiveness and proliferation rate, indicating a possible pathogenetic role. In addition, FZD-1 RNA interference in the PTC-derived cell line K1 increased invasiveness. Our data indicated that FZD-1 is involved in growth of follicular tumours and may be considered as a novel marker of this type of tumour. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]

Immunohistochemical staining of cutaneous tumours with G-81, a monoclonal antibody to dermcidin

BRITISH JOURNAL OF DERMATOLOGY, Issue 1 2004
Y. Minami
Summary Background Recently, the novel antimicrobial peptide named dermcidin (DCD) was reported in human eccrine sweat glands. Objectives We investigated the expression of DCD in a variety of cutaneous tumours in order to assess the usefulness of the monoclonal antibody (G-81), which recognizes a fragment of DCD. Patients/methods We studied the immunoreactivity of the G-81 antibody on 197 cutaneous tumours. Results A total of 13 of 26 cutaneous mixed tumours showed substantial immunoreactivity. In contrast all the following cases were completely unreactive: (i) epithelial tumours (seborrhoeic keratosis, squamous cell carcinoma, Bowen's disease, actinic keratosis, genital Paget's disease); (ii) follicular tumours (basal cell carcinoma, trichilemmoma, trichoepithelioma, trichoblastoma, keratoacanthoma, proliferating trichilemmal tumour, pilomatricoma); (iii) melanocytic tumours (malignant melanoma, naevus cell naevus, Spitz naevus, blue naevus); (iv) neural tumours (schwannoma, neurofibroma, Merkel cell neoplasm); (v) mesenchymal tumours (soft fibroma, dermatofibroma, dermatofibrosarcoma protuberans, vascular leiomyoma, leiomyosarcoma, lipoma, juvenile xanthogranuloma, angiomyoma); and (vi) other sweat gland tumours (poroid neoplasms, syringoma, cylindroma, clear cell hidradenoma, spiradenoma, syringoid eccrine carcinoma, mucinous carcinoma, apocrine cystadenoma, syringocystadenoma papilliferum, apocrine adenocarcinoma). Twenty-six cutaneous mixed tumours were considered from histopathological findings to be the apocrine type, but 13 of 26 mixed tumours contained some DCD-immunopositive cells that possibly differentiate into eccrine secretory glands. Conclusions We found the expression of DCD in tubular structures of 50% of cutaneous mixed tumours with apocrine differentiation. These results suggest that a number of cutaneous mixed tumours show both eccrine and apocrine differentiation in the same neoplasm. [source]

Aneuploidy and RAS mutations are mutually exclusive events in the development of well-differentiated thyroid follicular tumours

CLINICAL ENDOCRINOLOGY, Issue 5 2007
Ana Banito
Summary Objective, Follicular thyroid tumours present several genetic alterations such as aneuploidy, RAS mutations and PAX8/PPAR,rearrangements. The molecular basis of aneuploidy remains undefined in the majority of human cancers. It has been proposed that mutations in RAS oncogenes could be related to chromosomal instability, although this issue remains controversial. The aim of our study was to investigate the correlation between aneuploidy, RAS mutations and PAX8/PPAR, gene rearrangement in thyroid follicular tumours. Design, Ploidy status was determined by flow cytometry in 111 thyroid lesions (42 follicular thyroid adenomas, 27 follicular thyroid carcinomas, 19 follicular variants of papillary thyroid carcinoma, 20 poorly differentiated thyroid carcinomas and 3 anaplastic thyroid carcinomas). RAS mutations and PAX8/PPAR, fusion gene were investigated in 101 and 87 of these samples, respectively. Results, Altogether, 12 of 50 (24%) diploid tumours presented RAS mutation which contrasts with 3 of 51 (5·9%; P = 0·0124) RAS mutations in the group of aneuploid tumours. The aneuploid tumours harbouring RAS mutations were two poorly differentiated carcinomas and one follicular variant of papillary thyroid carcinoma with poorly differentiated areas. None of the tumours with RAS mutations expressed the PAX8/PPAR, fusion gene. Three of five (60%) follicular thyroid adenomas and 1 of 7 (14%) follicular thyroid carcinomas, with the PAX8/PPAR, fusion gene, were aneuploid. Conclusions, Our data suggest that aneuploidy and RAS mutations are mutually exclusive events in the development of well-differentiated thyroid follicular tumours. [source]