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首页> 外文会议>International Multidisciplinary Congress >Overexpression of pl6~(INK4a) in HPV Positive and Negative Infiltrating Cervical Adenocarcinomas
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Overexpression of pl6~(INK4a) in HPV Positive and Negative Infiltrating Cervical Adenocarcinomas

机译：HPV阳性和负浸润宫颈腺癌中PL6〜（INK4A）的过表达

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Cervical adenocarcinoma represents about 15% of cervical carcinomas and its incidence has increased during last decades, specially among young women8. Most important etiological factor is human papillomavirus (HPV) DNA, detected by PCR in a extremely variable percentage, between 76-100% of in situ adenocarcinomas and between 0-100% of different subtypes of infiltrating adenocarcinomas6. An important group of cervical glandular lesions seem to have same mechanisms of oncogenesis as the ones related to the better known squamous lesions, where it is most relevant the binding and functional inactivation of p53 and pRb by HPV oncoproteins E6 and E7, so Milde-Langosh et al~4 detected mRNA E6/E7 in 80% of a large group of HPV positive adenocarcinomas. Protein regulator p16~(INK4a) acts as a cyclin-dependant kinase (CDK) inhibitor, stopping cell cycle progression. CDKs inhibitors bind to CDK-kinase complexes in the Gl phase, so blocking the CDK kinase activity and preventing pRb phosphorylation and transition to S phase.
机译：宫颈腺癌代表宫颈癌的约15％，其发病率在上几十年中，特别是年轻妇女之间的增加。最重要的病因因子是人乳头瘤病毒（HPV）DNA，通过PCR以极其可变的百分比检测，在原位腺癌的76-100％之间，介于0-100％的渗透腺癌的不同亚型之间。一组重要的宫颈腺体病变似乎具有与与更好的已知鳞状病变有关的癌症机制，其中HPV癌蛋白E6和E7的P53和PRB的结合和功能灭活是最相关的，因此MILDE-LAN​​GOSH在大量HPV阳性腺癌中的80％中检测到mRNA e6 / E7。蛋白质调节剂P16〜（INK4A）充当细胞周期蛋白依赖性激酶（CDK）抑制剂，停止细胞周期进展。 CDKS抑制剂在GL相中与CDK-激酶复合物结合，因此阻断CDK激酶活性并防止PRB磷酸化并过渡到S期。

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