Breast cancer is characterised by a number of genetic aberrations. Our purpose was to use comparative genomic hybridisation (CGH) to screen breast carcinomas for copy number changes: 44 ductal and 8 lobular carcinomas were studied and a large number of genetic aberrations identified. Many of these s
Common genetic changes in hereditary and sporadic pituitary adenomas detected by comparative genomic hybridization
β Scribed by Svetlana D. Pack; Liu-Xiu Qin; Evgenia Pak; Yun Wang; David O. Ault; Poonam Mannan; Sivakumar Jaikumar; Constantine A. Stratakis; Edward H. Oldfield; Zhengping Zhuang; Robert J. Weil
- Book ID
- 102220214
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 332 KB
- Volume
- 43
- Category
- Article
- ISSN
- 1045-2257
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β¦ Synopsis
Twenty-four pituitary adenomas, both the sporadic type (n ΒΌ 18) and the type arising in association with either multiple endocrine neoplasia, type 1 (MEN1; n ΒΌ 2), or Carney complex (CNC, n ΒΌ 4) were analyzed by comparative genomic hybridization. Twenty-one (88%) tumors displayed chromosomal alterations. The number of chromosomal aberrations in each tumor varied from 2 to greater than 10. Several recurrent chromosomal abnormalities were identified in this study. The most frequently detected losses of chromosomal material involved 1p (14 of 24, 58%), 11p (11 of 24, 46%), 17 (10 of 24, 42%), 16p (9 of 24, 38%), 4 (8 of 24, 33%), 10p (6 of 24, 25%), 12 (6 of 24, 25%), 20 (6 of 24, 25%), 22q (6 of 24, 25%), 13q (5 of 24, 21%), and 9p (4 of 24, 17%). Copy number increases were detected on 4q (7 of 24, 29%), 17 (8 of 24, 33%), 19 (7 of 24, 29%), 1p (6 of 24, 25%), 5 (6 of 24, 25%), 20 (6 of 24, 25%), 6q (5 of 24, 21%), 13q21-qter (5 of 24, 21%), and 16p (5 of 24, 21%). Chromosome 11 loss, which involved 11p in all cases, was the most significant finding and was common to tumors arising sporadically and in association with MEN1 and CNC. In addition, the majority of the tumors (18 of 24, 75% overall and 86% of all tumors with chromosomal abnormalities) showed involvement of chromosome 1. Tumors had either loss (14 of 24, 58%) or gain (6 of 24, 25%) in the 1p32-1pter region. Finally, changes on chromosome 17, either loss or gain, occurred in 71% (17) of all 24 patients. In summary, all the tumors with chromosomal rearrangements (21 of 24, 88%), whether sporadic pituitary adenomas or those associated with MEN1 or CNC, had alteration(s) of 1p32, 11p, or 17. ' 2005 Wiley-Liss, Inc. abnormalities, the a-subunit of the guanine nucleotide-binding protein (GNAS), the tumorsuppressor gene MEN1 on chromosome band 11q13, and the 1a regulatory subunit of protein kinase A (PRKAR1A), respectively (Weinstein et al., 1991;
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