Patterns of chromosomal imbalances in parathyroid carcinomas

Citation
S. Kytola et al., Patterns of chromosomal imbalances in parathyroid carcinomas, AM J PATH, 157(2), 2000, pp. 579-586
Citations number
31
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
AMERICAN JOURNAL OF PATHOLOGY
ISSN journal
00029440 → ACNP
Volume
157
Issue
2
Year of publication
2000
Pages
579 - 586
Database
ISI
SICI code
0002-9440(200008)157:2<579:POCIIP>2.0.ZU;2-6
Abstract
In this study we have characterized chromosomal imbalances in a panel of 29 parathyroid carcinomas using comparative genomic hybridization (CGH). The most frequently detected imbalances were losses of 1p and 13q that were see n in >40% of the cases. The commonly occurring regions of loss were assigne d to 1p21-p22 (41%), 13q14-q31 (41%), 9p21-pter (28%), 6q22-q24 (24%), and 4q24 (21%), whereas gains preferentially involved 19p (45%), Xc-q13 (28%), 9q33-qter (24%), 1q31-q32 (21%) and 16p (21%). The distribution of CGH alte rations supports the idea of a progression of genetic events in the develop ment of parathyroid carcinoma, where gains of Xq and 1q would represent rel atively early events that are followed by loss of 13q, 9p, and 1p, and by g ain of 19p. A sex-dependent distribution was also evident for two of the co mmon alterations with preferential gain of Iq in female cases and of Xq in male cases. When the CGH profiles for the 29 carcinomas were compared with our previously published results for sporadic parathyroid adenomas, highly significant differences were revealed. Loss of 1p, 4q, and 13q as well as g ains of 1q, 9q, 16p, 19p and Xq were significantly more common in the carci nomas than in the adenomas. In contrast, loss of the 11q13 region, which is the most common CGH abnormality in sporadic adenomas, was not detected in any of the carcinomas. Taken together, the findings identify several candid ate locations for tumor suppressor genes and oncogenes that are potentially involved in parathyroid carcinogenesis.