Kiechle-Schwarz M, Bauknecht T, Schmidt J, Walz L, Pfleiderer A
Department of Gynecology and Obstetrics, Albert-Ludwigs University, Freiburg, Germany.
Cancer Detect Prev. 1995;19(3):234-43.
Successful cytogenetic analysis was performed on short-term cultures of 62 malignant ovarian tumors from 42 patients. Twenty-three tumors from 18 patients revealed clonal chromosome abnormalities. Five cases showed nonclonal chromosome changes. In the remaining 19 cases, a normal female karyotype was found. Numerical or single structural changes were found in only 11 carcinomas from nine patients. Trisomy 12 and 7 were each the sole abnormality in two cases a piece. One tumor showed a trisomy 6 as the only karyotypic change. Four tumors revealed simple translocations and deletions affecting the chromosomes X, 1, 2, 6, and 7. Twelve of the cytogenetically abnormal tumor samples showed complex karyotypes with both numerical and structural aberrations leading to hyperdiploid, near-triploid, and near-tetraploid stemlines. The recurrent numerical imbalances were losses of the chromosomes 1 (N = 5), X (N = 3), and 17 (N = 3), and gains of the chromosomes 12 (N = 5) and 20 (N = 3). Regarding structural rearrangements, the chromosome bands 11p13-14 and 19p13 were the most frequently affected regions. 11p13-14 was rearranged in four tumors. In two cases, a deletion 11p13-14 was found. Two tumors revealed a nonreciprocal translocation involving 11p13-14 and leading to the loss of distal 11p material. The most consistent finding was a 19p+ marker chromosome, which was present in five different ovarian carcinomas. Our results are in accordance with a recent cytogenetic report describing a 19p+ marker and loss of 11p material as consistent cytogenetic aberrations in human ovarian carcinomas.
对42例患者的62个恶性卵巢肿瘤进行了短期培养,并成功进行了细胞遗传学分析。18例患者的23个肿瘤显示出克隆性染色体异常。5例显示非克隆性染色体变化。在其余19例中,发现正常女性核型。仅在9例患者的11个癌中发现了数值或单一结构变化。12号和7号三体分别在2例中各为唯一异常。1个肿瘤显示6号三体为唯一的核型变化。4个肿瘤显示涉及X、1、2、6和7号染色体的简单易位和缺失。12个细胞遗传学异常的肿瘤样本显示出复杂核型,伴有数值和结构畸变,导致超二倍体、近三倍体和近四倍体干细胞系。反复出现的数值失衡是1号染色体缺失(N = 5)、X号染色体缺失(N = 3)和17号染色体缺失(N = 3),以及12号染色体增加(N = 5)和20号染色体增加(N = 3)。关于结构重排,11p13 - 14和19p13染色体带是最常受影响的区域。11p13 - 14在4个肿瘤中发生重排。2例中发现11p13 - 14缺失。2个肿瘤显示涉及11p13 - 14的非相互易位,导致11p远端物质丢失。最一致的发现是一个19p +标记染色体,存在于5种不同的卵巢癌中。我们的结果与最近一份细胞遗传学报告一致,该报告描述19p +标记和11p物质丢失是人类卵巢癌中一致的细胞遗传学畸变。