Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com Original Article Cytogenet Genome Res 115:16–22 (2006) DOI: 10.1159/000094796 Chromosomal alterations in 98 endometrioid adenocarcinomas analyzed with comparative genomic hybridization K. Levan a K. Partheen a L. Österberg a K. Helou a G. Horvath a, b a Department of Oncology, Göteborg University, and b Gynecological Oncology Section, Department of Oncology, Sahlgrenska University Hospital, Göteborg (Sweden) esis pathways of which differ. Tumors of endometrioid type represent over 80% of all endometrial cancers; they are usu- ally well-differentiated and low-stage (Sherman, 2000; Lax, 2004). Furthermore, these tumors tend to be rich in steroid receptors and to lack p53 immunoreactivity (Sherman, 2000) . The remaining 20% are usually poorly differentiated and of non-endometrioid type (Soslow et al., 1998). In 1988, the committee of the International Federation of Gynecology and Obstetrics (FIGO) recommended surgi- cal staging of endometrial carcinoma; the size and localiza- tion of the tumor determine the surgical stage (I–IV) (Creas- man et al., 2001). When patients are diagnosed with endometrial cancer, the standard procedure is to surgically remove the tumor and evaluate the level of risk to which the patient is exposed. Abstract. The aim of the present study was to investigate chromosomal alterations in a large set of homogeneous tu- mors, 98 endometrioid adenocarcinomas. We also wanted to evaluate differences in chromosomal alterations in the different groups of tumors in relation to stage, survival and invasive or metastatic properties of the tumors. Compara- tive genomic hybridization (CGH) was used to detect chro- mosomal alterations in tissue samples from 98 endometri- oid adenocarcinomas. All chromosomes were involved in DNA copy number variations at least once in the tumor ma- terial, but certain changes were recurrent and rather spe- cific. Among the specific changes, it was possible to iden- tify 39 chromosomal regions displaying frequent DNA copy number alterations. The most frequent alteration was de- tected at 1q25 ] q42, in which gains were found in 30 cases (30%). Gains at 19pter ] p13.1 were detected in 26 tumors Request reprints from György Horvath Department of Oncology, Institute of Selected Clinical Sciences Göteborg University, SE-413 45 Gothenburg (Sweden) telephone: +46 31 324 31 45; fax: +46 31 41 72 05 e-mail: gyorgy.horvath@oncology.gu.se © 2006 S. Karger AG, Basel 1424–8581/06/1151–0016$23.50/0 Accessible online at: www.karger.com/cgr (26%) and at 19q13.1 ] q13.3 in 19 tumors (19%). Increased copy numbers were also detected at 8q (8q21 ] q22 and 8q22 ] qter), at a relatively high rate, in 17 cases (17%). Fur- thermore, gains at 10q21 ] q23 and 10p were found in 14 (14%) and 13 cases (13%), respectively. The most common losses were found in the three regions 4q22 ] qter, 16q21 ] qter and 18q21 ] qter, all of which were detected in eight of the 98 tumors (8%). We also detected differences between the tumors from deceased patients and from sur- vivors. Gain at 1q25 ] q42 was more commonly detected in the tumors from patients who died of cancer. We noted that the regions most affected differed in the different surgical stages (I–IV). The results of the CGH analysis identify spe- cific chromosomal regions affected by copy number chang- es, appropriate objects for further genetic studies. Copyright © 2006 S. Karger AG, Basel Carcinoma of the endometrium, also known as endome- trial or corpus cancer, is the most frequently diagnosed ma- lignancy of the female reproductive tract in western coun- tries. In Sweden, approximately 1,300 women (27 per 100,000 women) are diagnosed annually. Recently, several authors have suggested that there are at least two distinct types of endometrial carcinoma, the molecular carcinogen- Supported by The King Gustav V Jubilee Clinic Cancer Research Foundation. Manuscript received 12 September 2005; accepted in revised form for publication by A. Geurts van Kessel, 28 February 2006.