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• W2766853710 abstract "Journal of Pathology J Pathol 2002; 198: 157–162. Published online 24 July 2002 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/path.1185 Original Paper Immunohistochemical expression of cyclin D1, E2F-1, and Ki-67 in benign and malignant thyroid lesions Antonio D Saiz, Maria Olvera, Sherif Rezk, Barbara A Florentine, Althea McCourty and Russell K Brynes* Department of Pathology, Los Angeles County and USC Medical Center, Los Angeles, California, USA *Correspondence to: Russell K Brynes, MD, University of Southern California, Department of Pathology, HMR 209, 2011 Zonal Avenue, Los Angeles, CA 90033, USA. E-mail: Brynes@hsc.usc.edu Received: 4 January 2002 Accepted: 25 April 2002 Abstract Cyclin D1 and E2F-1 proteins are essential for the regulation of the G1/S transition through the cell cycle. Cyclin D1, a product of the bcl-1 gene, phosphorylates the retinoblastoma protein, releasing E2F-1, which in turn activates genes involved in DNA synthesis. Expression patterns of E2F-1 protein in thyroid proliferations have not been reported. This study used monoclonal antibodies for cyclin D1 and E2F-1 proteins to immunostain sections of normal thyroid, hyperplastic (cellular) nodules, follicular adenomas, follicular carcinomas, and papillary carcinomas. The proliferation rate was examined using an antibody specific for the Ki-67 antigen. Fluorescence in situ hybridization (FISH) methods and chromosome 11-specific probes were also employed to determine chromosome copy number and to assess for evidence of amplification at the 11q13 locus in papillary and follicular carcinomas with cyclin D1 overexpression. Concurrent overexpression of Ki-67, cyclin D1, and E2F-1 was found in the majority of benign and malignant thyroid lesions, compared with normal thyroid tissue. Cyclin D1 up-regulation was not due to extra copies of chromosome 11, or bcl-1 gene amplification. Malignant tumours showed the highest expression for all three markers, particularly papillary carcinomas. E2F-1 was detected at the same or slightly lower levels than cyclin D1. It was only found when cyclin D1 was overexpressed. Because cyclin D1 normally activates E2F-1, up-regulation of cyclin D1 may lead to E2F-1 overexpression in benign and malignant thyroid lesions. Copyright  2002 John Wiley & Sons, Ltd. Keywords: cyclin D1; E2F-1; Ki-67; cell-cycle proteins; thyroid neoplasms Introduction Cyclin D1 plays a key role in the regulation of the G1/S transition through the cell cycle. In conjunction with cyclin-dependent kinases, cyclin D1 phosphory- lates the retinoblastoma protein, releasing E2F-1, a promoter of G1/S cell-cycle progression [1–6]. Cyclin D1 is the product of the bcl-1 (PRAD, CCND-1) gene located on chromosome 11q13. Translocation or amplification of bcl-1 or the 11q13 locus can result in overexpression of cyclin D1 and has been associ- ated with several types of neoplasms, including breast carcinomas, advanced head and neck squamous cell carcinomas, and bladder carcinomas [7–11]. Mantle cell lymphomas express the t(11;14)(q13;q32) and typ- ically have increased levels of cyclin D1, which is a useful marker in the differential diagnosis of small lymphoid cell neoplasms [12,13]. Overexpression of cyclin D1 protein has been reported in malignant thy- roid tumours, especially papillary carcinoma [14–21]. E2F-1 is the best-characterized member of the E2F transduction factor family and serves as the ultimate mediator of the G1/S transition [1–6]. When released by phosphorylated retinoblastoma protein, free E2F- 1 mediates G1/S progression by binding to promoter sequences of genes necessary for DNA replication and cell-cycle control [1,2,5]. In addition to driving S-phase entry, E2F-1 has also been found to induce Copyright  2002 John Wiley & Sons, Ltd. apoptosis [1,5]. Overexpression of E2F-1 has been reported in multiple myeloma and in mantle cell lymphoma, where it closely correlates with cyclin D1 up-regulation [22–24]. E2F-1 expression patterns in benign and malignant thyroid lesions have not been previously reported. In this study, we compared the immunostaining patterns of cyclin D1, E2F-1, and Ki-67, a well- characterized proliferation marker, in benign and malignant thyroid lesions. In thyroid carcinomas with cyclin D1 overexpression, we utilized fluorescence in situ hybridization (FISH) methods and chromosome 11-specific probes to determine chromosome copy number and to assess for evidence of amplification at the 11q13 locus. Materials and methods Specimen selection Paraffin blocks from 45 thyroidectomy specimens were selected from the surgical pathology files of the Department of Pathology at the Los Angeles County and USC Medical Center. These included eight hyperplastic nodules, ten follicular adenomas, 19 papillary carcinomas, and eight follicular carcinomas. Six normal thyroid sections taken from biopsies for different conditions served as controls." @default.
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