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(American Journal of Pathology. 2000;157:579-586.)
© 2000 American Society for Investigative Pathology

Regular Articles

Patterns of Chromosomal Imbalances in Parathyroid Carcinomas

Soili Kytölä^*, Filip Farnebo^*, Takao Obara, Jorma Isola, Lars Grimelius^§, Lars-Ove Farnebo^¶, Kerstin Sandelin^¶ and Catharina Larsson^*

From the Department of Molecular Medicine,^*
Endocrine Genetics Unit, and the Departments of Surgery
and Pathology,^§
Karolinska Hospital, Stockholm, Sweden; the Department of Endocrine Surgery,
Tokyo Women’s Medical University, Tokyo, Japan; and The Laboratory of Cancer Genetics,^¶
Institute of Medical Technology, University of Tampere and Tampere University Hospital, Tampere, Finland

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 seen in >40% of the cases. The commonly occurring regions of loss were assigned 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 alterations supports the idea of a progression of genetic events in the development of parathyroid carcinoma, where gains of Xq and 1q would represent relatively early events that are followed by loss of 13q, 9p, and 1p, and by gain of 19p. A sex-dependent distribution was also evident for two of the common alterations with preferential gain of 1q 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 gains of 1q, 9q, 16p, 19p and Xq were significantly more common in the carcinomas 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 candidate locations for tumor suppressor genes and oncogenes that are potentially involved in parathyroid carcinogenesis.

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