• 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

人类前列腺癌中apc和mcc基因表达缺失及等位基因缺失的高频率。

High-frequency of loss of expression and allelic deletion of the apc and mcc genes in human prostate-cancer.

作者信息

Gao X, Zacharek A, Grignon D, Liu H, Sakr W, Porter A, Chen Y, Honn K

机构信息

WAYNE STATE UNIV,SCH MED,DEPT PATHOL,DETROIT,MI 48201. WAYNE STATE UNIV,DEPT CHEM,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT RADIAT ONCOL,DIV CANC BIOL,DETROIT,MI 48201.

出版信息

Int J Oncol. 1995 Jan;6(1):111-7. doi: 10.3892/ijo.6.1.111.

DOI:10.3892/ijo.6.1.111
PMID:21556510
Abstract

Loss of heterozygosity (LOH) or allelic deletion at various loci has been reported in the majority of human tumors. The frequently deleted targets are believed to be tumor suppressor genes. Recent studies have identified the APC and MCC genes at 5q21, as putative tumor suppressor genes. The APC and MCC genes have been implicated in the development of familial adenomatous polyposis coli and cancers of the gastrointestinal tract, ovary, breast and lung. In the present study, we investigated a possible role of the APC and MCC genes in prostate cancer development. mRNA expression of the APC and MCC genes and LOH at the APC and MCC loci were determined in prostate cancer tissues from 28 patients and 5 human prostatic adenocarcinoma cell lines. Of the informative cases, the frequency of LOH at the APC and MCC loci was 63% (10/16) and 54% (7/13), respectively. Overall, 65% (15/23) of the informative cases showed LOH at the APC and/or MCC gene. All prostate cancer cell lines showed homozygosity at all APC and MCC polymorphic sites studied. Approximately half (57%) of the tumor tissues examined showed a decreased expression of APC and MCC mRNA. Our data suggest that the APC and MCC genes may be involved in the formation of human prostate cancer (HPC).

摘要

在大多数人类肿瘤中都报道了不同位点的杂合性缺失(LOH)或等位基因缺失。频繁缺失的靶点被认为是肿瘤抑制基因。最近的研究已确定位于5q21的APC和MCC基因为假定的肿瘤抑制基因。APC和MCC基因与家族性腺瘤性息肉病以及胃肠道、卵巢、乳腺和肺癌有关。在本研究中,我们调查了APC和MCC基因在前列腺癌发生中的可能作用。测定了28例患者的前列腺癌组织和5个人前列腺腺癌细胞系中APC和MCC基因的mRNA表达以及APC和MCC位点的LOH。在信息充分的病例中,APC和MCC位点的LOH频率分别为63%(10/16)和54%(7/13)。总体而言,65%(15/23)的信息充分病例在APC和/或MCC基因处显示LOH。所有前列腺癌细胞系在所研究的所有APC和MCC多态性位点均显示纯合性。大约一半(57%)的检测肿瘤组织显示APC和MCC mRNA表达降低。我们的数据表明,APC和MCC基因可能参与了人类前列腺癌(HPC)的形成。

相似文献

1
High-frequency of loss of expression and allelic deletion of the apc and mcc genes in human prostate-cancer.人类前列腺癌中apc和mcc基因表达缺失及等位基因缺失的高频率。
Int J Oncol. 1995 Jan;6(1):111-7. doi: 10.3892/ijo.6.1.111.
2
Loss of heterozygosity affecting the APC and MCC genetic loci in patients with primary breast carcinomas.原发性乳腺癌患者中影响APC和MCC基因位点的杂合性缺失。
Cancer Epidemiol Biomarkers Prev. 1994 Jun;3(4):331-3.
3
Loss of heterozygosity involving the APC and MCC genetic loci occurs in the majority of human esophageal cancers.大多数人类食管癌中会出现涉及腺瘤性息肉病(APC)基因座和微卫星不稳定相关基因(MCC)基因座的杂合性缺失。
Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3385-8. doi: 10.1073/pnas.89.8.3385.
4
Loss of heterozygosity of multiple tumor suppressor genes in human gastric cancers by polymerase chain reaction.通过聚合酶链反应检测人类胃癌中多个肿瘤抑制基因的杂合性缺失
Lab Invest. 1996 Apr;74(4):835-41.
5
Loss of heterozygosity of APC and MCC genes in oral squamous cell carcinomas in Taiwan.
J Oral Pathol Med. 1997 Aug;26(7):322-6. doi: 10.1111/j.1600-0714.1997.tb00223.x.
6
Loss of heterozygosity of MCC is not associated with mutation of the retained allele in sporadic colorectal cancer.
Hum Mol Genet. 1994 Mar;3(3):443-6. doi: 10.1093/hmg/3.3.443.
7
Loss of heterozygosity of the Mutated in Colorectal Cancer gene is not associated with promoter methylation in non-small cell lung cancer.Mutated in Colorectal Cancer 基因杂合性缺失与非小细胞肺癌启动子甲基化无关。
Lung Cancer. 2012 Aug;77(2):272-6. doi: 10.1016/j.lungcan.2012.04.001. Epub 2012 Apr 26.
8
Decreased expression of the adenomatous polyposis coli (Apc) and mutated in colorectal cancer (Mcc) genes in mouse lung neoplasia.小鼠肺肿瘤中腺瘤性息肉病 coli(Apc)和结直肠癌突变(Mcc)基因的表达降低。
Mol Carcinog. 1998 Jan;21(1):37-49.
9
Loss of heterozygosity affecting the p53, Rb, and mcc/apc tumor suppressor gene loci in dysplastic and cancerous ulcerative colitis.发育异常和癌变的溃疡性结肠炎中影响p53、Rb和mcc/apc肿瘤抑制基因位点的杂合性缺失
Cancer Res. 1992 Feb 1;52(3):741-5.
10
Allelic loss involving the tumor suppressor genes APC and MCC and expression of the APC protein in the development of dysplasia and carcinoma in Barrett esophagus.在巴雷特食管发育异常和癌的发生过程中涉及肿瘤抑制基因APC和MCC的等位基因缺失以及APC蛋白的表达。
Am J Clin Pathol. 2000 Dec;114(6):890-5. doi: 10.1309/L1Q3-E3AQ-APU9-NA0A.

引用本文的文献

1
Wnt/β-catenin signaling in cancers and targeted therapies.Wnt/β-连环蛋白信号通路在癌症和靶向治疗中的作用。
Signal Transduct Target Ther. 2021 Aug 30;6(1):307. doi: 10.1038/s41392-021-00701-5.
2
Transcript profiling in the testes and prostates of postnatal day 30 Sprague-Dawley rats exposed prenatally and lactationally to 2-hydroxy-4-methoxybenzophenone.暴露于 2-羟基-4-甲氧基二苯甲酮的新生 30 天 Sprague-Dawley 大鼠的睾丸和前列腺转录谱分析。
Reprod Toxicol. 2018 Dec;82:111-123. doi: 10.1016/j.reprotox.2018.10.001. Epub 2018 Oct 11.
3
Activation of Wnt-β-catenin pathway in basal-parabasal layers of normal cervical epithelium comparable during development of uterine cervical carcinoma.
Wnt-β-catenin 通路在正常宫颈上皮的基底层-副基底层中的激活与子宫颈癌的发展过程相当。
Mol Cell Biochem. 2018 Jun;443(1-2):121-130. doi: 10.1007/s11010-017-3216-5. Epub 2017 Oct 27.
4
Prostate cancer: the need for biomarkers and new therapeutic targets.前列腺癌:生物标志物和新治疗靶点的需求。
J Zhejiang Univ Sci B. 2014 Jan;15(1):16-42. doi: 10.1631/jzus.B1300106.
5
Prostate cancer old problems and new approaches : Part I. epidemiology, incidence and genetic alterations.前列腺癌的老问题与新方法:第一部分。流行病学、发病率和遗传改变。
Pathol Oncol Res. 1996 Mar;2(1-2):98-109. doi: 10.1007/BF02893960.
6
Recessive oncogenes: current status.隐性癌基因:现状
Pathol Oncol Res. 1995;1(1):7-22. doi: 10.1007/BF02893578.