Genetic analysis of ovarian germ cell tumors by comparative genomic hybridization.
Genetic analysis of ovarian germ cell tumors by comparative genomic hybridization.
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发表时间：
1998-07
期刊：
影响因子：
11.2
通讯作者：
M. Riopel;A. Spellerberg;Constance A. Griffin;Elizabeth J. Perlman
中科院分区：
文献类型：
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作者：
M. Riopel;A. Spellerberg;Constance A. Griffin;Elizabeth J. Perlman
卵巢生殖细胞肿瘤（OGCT）表现出在睾丸中未见的异质性，包括良性成熟囊性畸胎瘤、中期不成熟畸胎瘤、恶性生殖细胞肿瘤[GCT（无性细胞瘤、内胚窦瘤和混合型GCT）]和46，XY个体的生殖腺发育不良中出现的GCT。比较基因组杂交用于分析27个OGCT的相对增益或损失的区域。对21例恶性OGCT（12例无性细胞瘤，6例内胚窦瘤和3例混合型GCT）的分析表明，遗传改变与成人睾丸GCT中报告的相似。获得的最常见区域包括染色体12 p（21个肿瘤中的16个），21（21个肿瘤中的10个），8（21个肿瘤中的8个）和1 q（21个肿瘤中的6个）。最常见的丢失区域是13号染色体。在12 p11 -12和4 q11确定了高水平增益区域。该类别中不同组织学亚型的增益和损失特征相似。46，XY患者中出现1个肿瘤;该肿瘤为二倍体，显示12 p的增益。未成熟畸胎瘤（6例）仅显示1例异常，即14号染色体获得。我们的结论是，恶性OGCT在遗传上与成人睾丸中发现的相似，然而，未成熟畸胎瘤没有一致的收益或损失，因此与成人睾丸中存在的不同。文献综述表明，这一组的遗传异常可能预示着更差的预后。最后，发育不良性腺中的OGCT出现在二倍体而不是四倍体细胞系中，但它们也显示出12 p的增益。
Ovarian germ cell tumors (OGCTs) show a heterogeneity that is not seen in their testicular counterparts and include benign mature cystic teratomas, intermediate immature teratomas, malignant germ cell tumors [GCTs (dysgerminomas, endodermal sinus tumors, and mixed GCTs)], and GCTs arising in dysgenetic gonads of 46,XY individuals. Comparative genomic hybridization was used to analyze 27 OGCTs for regions of relative gain or loss. The analysis of 21 malignant OGCTs (12 dysgerminomas, 6 endodermal sinus tumors, and 3 mixed GCTs) demonstrated genetic alterations similar to those reported in adult testicular GCTs. The most common regions gained include chromosomes 12p (16 of 21 tumors), 21 (10 of 21 tumors), 8 (8 of 21 tumors), and 1q (6 of 21 tumors). The most common region lost was chromosome 13. Regions of high-level gain were identified at 12p11-12 and 4q11. The profile of gains and losses was similar in the different histological subtypes within this category. One tumor presented in a 46,XY patient; this tumor was diploid and showed a gain of 12p. Immature teratomas (six cases) showed only one case with an abnormality, which was a gain of chromosome 14. We conclude that malignant OGCTs are genetically similar to those found in the adult testis; however, immature teratomas show no consistent gains or losses and are therefore different from those presenting in the adult testis. A review of the literature suggests that genetic abnormalities in this group may herald a worse prognosis. Lastly, OGCTs in dysgenetic gonads arise in a diploid rather than a tetraploid cell line, yet they also show a gain of 12p.