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Histogenesis of carcinosarcoma of the uterine corpus

子宫体癌肉瘤的组织发生

基本信息

批准号：
09671678
负责人：
ENOMOTO Takayuki
金额：
$ 2.3万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671678/
关键词：
Carcinosarcoma Clonality K-ras p53 HUMURA クロナリティー HUMARA

项目摘要

Carcinosacomas of the uterus is relatively uncommon, accounting for less Than 10% of uterine malignancies.Three theories (collision tumor theory, combination tumor theory and composition tumor theory) have been proposed for the pathogenesis of these tumors.We applied molecular techniques to determine the pathogenesis of uterine carcinosarcomas.The patterns of X-chromosome inactivation were analyzed, targeting a portion of exon 1 of the human androgen receptor (HUMARA) in malignant epithelial and mesenchymal components.The presence of p53 and K-ras mutations was also analyzed.DNAs were obtained from both epithelial and non-epithelial lesions from carcinosarcomas.Following treatment with methylation sensitive restriction endonuclease (Hha I or Hpa II), PCR amplification was performed using nested primers targeted to The HUMARA locus.We demonstrated that 85% of carcinosarcomas represent combination tumors, and 15% of those represent collision tumors.Mutations in the p53 gene and K-ras gene were found in 32% and 24% of the tumors, respectively.We correlated the histogenesis of individual carcinosarcomas with clinical outcome, and found that collision tumors had poorer prognosis than combination tumors.These observations show that the determination of histogenesis in individual cases of carcinosarcoma using molecular markers may be worthwhile, since the result could help predict the prognosis of individual cases and help guide clinical management.We further applied our methodology to determine the histogenesis of carcinosarcoma of the breast, vagina and ovary and showed that most of these tumors also represented combination tumors.

子宫癌是一种相对少见的肿瘤，占子宫恶性肿瘤的10%以下。本文应用分子生物学技术对子宫癌的发病机制进行了研究，分析了子宫癌X染色体失活的模式，用甲基化敏感的限制性内切酶处理恶性上皮细胞和间质细胞中的人雄激素受体（HUMARA）外显子1的一部分，并分析p53和K-ras突变的存在。Hha Ⅰ或Hpa Ⅱ基因，使用靶向HUMARA基因座的巢式引物进行PCR扩增。我们发现85%的癌细胞瘤为混合性肿瘤，15%为碰撞性肿瘤。分别在32%和24%的肿瘤中发现p53基因和K-ras基因突变。我们将单个癌细胞瘤的组织发生与临床结果联系起来，结果表明，碰撞肿瘤的预后比混合肿瘤差。这些观察表明，使用分子标记物确定癌肉瘤个体病例的组织发生可能是值得的，因为其结果有助于预测个体病例的预后并有助于指导临床治疗。我们进一步应用我们的方法确定乳腺癌肉瘤的组织发生，阴道和卵巢，并表明这些肿瘤大多数也代表联合肿瘤。