• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

[胰腺癌分子生物学研究的一般规则]

[General rules for the study of pancreatic cancer by molecular biological aspect].

作者信息

Omata M, Tada M

机构信息

Department of Gastroenterology, University of Tokyo, Japan.

出版信息

Nihon Geka Gakkai Zasshi. 2000 Feb;101(2):233-6.

PMID:10734643
Abstract

Genetic changes in K-ras, p53, p16, DPC4, and telomerase activity are frequent in pancreatic adenocarcinoma. The incidence of these changes has been reported to be approximately 80% for K-ras, 50% for p53, p16, and DPC4, and 90% for telomerase activity. Genetic abnormalities of APC and microsatellite instability are relatively rare (less than 10%) in pancreatic carcinoma. Among these genetic abnormalities, K-ras and telomerase activity have been used as molecular markers for the diagnosis of pancreatic carcinoma. K-ras mutation could be considered as an early event in the progression to malignancy and thus it has no clear association with the prognosis of the carcinoma. In contrast, mutation of p53 could be a prognostic indicator.

摘要

K-ras、p53、p16、DPC4基因改变以及端粒酶活性在胰腺腺癌中很常见。据报道,这些改变的发生率在K-ras约为80%,在p53、p16和DPC4约为50%,在端粒酶活性约为90%。APC基因异常和微卫星不稳定性在胰腺癌中相对少见(低于10%)。在这些基因异常中,K-ras和端粒酶活性已被用作胰腺癌诊断的分子标志物。K-ras突变可被视为恶性进展中的早期事件,因此它与癌的预后无明确关联。相比之下,p53突变可能是一个预后指标。

相似文献

1
[General rules for the study of pancreatic cancer by molecular biological aspect].[胰腺癌分子生物学研究的一般规则]
Nihon Geka Gakkai Zasshi. 2000 Feb;101(2):233-6.
2
[Genetics of pancreatic cancer: recent advances in molecular diagnosis].[胰腺癌的遗传学:分子诊断的最新进展]
Nihon Geka Gakkai Zasshi. 2002 Jun;103(6):476-81.
3
Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis.胰腺肿瘤:导管癌中涉及的分子途径参与壶腹癌的发生,但不参与外分泌非导管性或内分泌肿瘤的发生。
Br J Cancer. 2001 Jan;84(2):253-62. doi: 10.1054/bjoc.2000.1567.
4
Molecular diagnosis of pancreatic cancer.胰腺癌的分子诊断
Hepatogastroenterology. 2001 Jul-Aug;48(40):933-8.
5
SMAD4/DPC4 and pancreatic cancer survival. Commentary re: M. Tascilar et al., The SMAD4 protein and prognosis of pancreatic ductal adenocarcinoma. Clin. Cancer Res., 7: 4115-4121, 2001.SMAD4/DPC4与胰腺癌生存率。评论文章:M. 塔西拉尔等人,《SMAD4蛋白与胰腺导管腺癌的预后》。《临床癌症研究》,2001年第7卷,第4115 - 4121页
Clin Cancer Res. 2001 Dec;7(12):3853-6.
6
Immunohistochemical and genetic analysis of non-small cell and small cell gallbladder carcinoma and their precursor lesions.非小细胞和小细胞胆囊癌及其前驱病变的免疫组织化学和基因分析
Mod Pathol. 2003 Apr;16(4):299-308. doi: 10.1097/01.MP.0000062656.60581.AA.
7
Tumor-suppressive pathways in pancreatic carcinoma.胰腺癌中的肿瘤抑制途径。
Cancer Res. 1997 May 1;57(9):1731-4.
8
K-ras, p53, and DPC4 (MAD4) alterations in fine-needle aspirates of the pancreas: a molecular panel correlates with and supplements cytologic diagnosis.胰腺细针穿刺抽吸物中K-ras、p53和DPC4(MAD4)改变:分子检测组合与细胞学诊断相关并补充其诊断。
Am J Clin Pathol. 2002 May;117(5):755-65. doi: 10.1309/5RQ0-JCQU-5XF2-51LQ.
9
Comparative analysis of K-ras point mutation, telomerase activity, and p53 overexpression in pancreatic tumours.胰腺肿瘤中K-ras点突变、端粒酶活性及p53过表达的比较分析
Oncol Rep. 2003 Mar-Apr;10(2):277-83.
10
Mutation status of K-ras, p53 and allelic losses at 9p and 18q are not prognostic markers in patients with pancreatic cancer.K-ras、p53的突变状态以及9号染色体短臂和18号染色体长臂的等位基因缺失并非胰腺癌患者的预后标志物。
Anticancer Res. 2009 May;29(5):1803-10.