Kohlberger P D, Kieback D G, Mian C, Wiener H, Kainz C, Gitsch G, Breitenecker G
Department of Gynecology and Obstetrics, University of Vienna, Medical School, Austria.
J Soc Gynecol Investig. 1997 Sep-Oct;4(5):262-4.
Ovarian tumors of low malignant potential (borderline tumors) have a 5-year survival rate of 69-98%, illustrating that while the prognosis is better than in the typical epithelial carcinoma, a significant number of women still succumb to this disease. The aim of our study was to elucidate the role of numerical chromosomal aberrations in borderline tumors of the ovary in comparison with benign and malignant epithelial tumors in an effort to develop parameters to differentiate prospectively borderline lesions from benign and invasive tumors.
Cytologic imprints of surgical specimens of 46 ovarian tumors of low-malignant potential, 17 invasive epithelial carcinomas of the ovary, and 18 benign epithelial tumors of the ovary were examined for numerical chromosomal aberrations (trisomy 7, trisomy 12, and trisomy 17) by fluorescence in situ hybridization (FISH).
In benign tumors no evidence of trisomy 7 and 17 was present. Trisomy 12 was detected in six cases (33.3%). We did not find p53 protein overexpression in any case. Ki-67 stained positive in three cases (16.7%). In borderline tumors trisomy 12 was detected in 33 patients (71.7%). Numerical aberrations of chromosome 17 were absent in all cases. Fourteen patients (30.4%) showed trisomy 7. No immunohistochemical staining reaction for p53 protein was found. Staining of the proliferation marker Ki-67 was observed in two cases (4.3%). In malignant epithelial tumors of the ovary, trisomy 7, trisomy 12, and trisomy 17 were detected in 14 (82.3%), 11 (64.7%), and 5 (29.4%) cases, respectively. Four tumors (23.5%) showed immunohistochemically detected p53 protein overexpression. Thirteen tumors (76.5%) stained for Ki-67.
Our results indicate that trisomy 7 argues against benign disease. Trisomy 17 was specific for invasive disease, while trisomy 12 is common in borderline tumors of the ovary.
低恶性潜能卵巢肿瘤(交界性肿瘤)的5年生存率为69% - 98%,这表明虽然其预后优于典型的上皮性癌,但仍有相当数量的女性死于这种疾病。我们研究的目的是阐明染色体数目异常在卵巢交界性肿瘤中的作用,并与良性和恶性上皮性肿瘤进行比较,以期制定出前瞻性区分交界性病变与良性及浸润性肿瘤的参数。
通过荧光原位杂交(FISH)对46例低恶性潜能卵巢肿瘤、17例浸润性卵巢上皮癌和18例卵巢良性上皮性肿瘤的手术标本细胞学印片进行染色体数目异常(7号染色体三体、12号染色体三体和17号染色体三体)检测。
在良性肿瘤中未发现7号和17号染色体三体的证据。12号染色体三体在6例(33.3%)中被检测到。我们在任何病例中均未发现p53蛋白过表达。Ki-67在3例(16.7%)中呈阳性染色。在交界性肿瘤中,33例(71.7%)检测到12号染色体三体。所有病例均未出现17号染色体数目异常。14例(30.4%)显示7号染色体三体。未发现p53蛋白的免疫组化染色反应。增殖标志物Ki-67染色在2例(4.3%)中被观察到。在卵巢恶性上皮性肿瘤中,7号染色体三体、12号染色体三体和17号染色体三体分别在14例(82.3%)、11例(64.7%)和5例(29.4%)中被检测到。4例肿瘤(23.5%)显示免疫组化检测到p53蛋白过表达。13例肿瘤(76.5%)Ki-67染色阳性。
我们的结果表明,7号染色体三体不支持良性疾病。17号染色体三体是浸润性疾病所特有的,而12号染色体三体在卵巢交界性肿瘤中很常见。