期刊文献+

转录因子E2F-4的表达与乳腺癌分级、分期及预后的关系 被引量:1

Expression of transcription factor E2F-4 in breast cancer and its relationship with histological grading, clinical staging and prognosis
下载PDF
导出
摘要 目的:探讨乳腺癌中转录因子E2F-4的表达与临床分期、病理组织学分级及其预后等参数的关系。方法:采用免疫组化学的方法检测乳腺癌组织中E2F-4的表达,半定量分析E2F-4的表达与肿瘤分期、分级、术后生存时间等临床病理学参数的关系;以正常乳腺组织作为对照。结果:正常乳腺小叶及导管上皮细胞之E2F-4表达呈阴性;65例乳腺癌中33例(50.8%)呈E2F-4高表达;E2F-4高表达与乳腺癌的病理学分级、类型、临床分期以及术后生存时间有关(P<0.05)。结论:E2F-4作为肿瘤的相关基因,参与了乳腺癌的发生、发展。E2F-4的高表达可能是评判乳腺癌恶性程度、转移、复发及预后的较好指标。 Objective To investigate the relationship between the expression of transcription factor E2F-4 in breast cancer and its clinico-pathological parameters including histological grading, clinical staging and prognosis. Methods The expression of E2F-4 protein in breast cancer was detected by immunohistochemical staining. The relationship between E2F4 expression and clinico-pathological parameters. Normal mammary tissues were used as controls. Results Absence of E2F-4 expression was found in normal mammary tissues. Overexpression of E2F-4 protein was found in 50.8% of the breast cancer cases (33/65). Over-expression of transcription factor E2F-4 in breast cancer was closely related with the histological grading, clinical staging and poor prognosis(P〈0.05). Conclusions E2F-4 may be involved in the carcinogenesis and staging of breast cancer. The over-expression of E2F-4 might be used as a new marker to predict the metastatic potential and outcome of breast cancer.
出处 《外科理论与实践》 2008年第2期141-144,共4页 Journal of Surgery Concepts & Practice
关键词 转录因子E2F-4 乳腺肿瘤 预后 肿瘤分期 Transcription factor, E2F-4 Breast neoplasms Prognosis Neoplasm staging
  • 相关文献

参考文献13

  • 1Chen X, Weaver J, Bore BA, et al. Allelic Imbalance in BRCA1 and BRCA2 Gene Expression Is Associated with an Increased Breast Cancer Risk [J]. Hum Mol Genet, 2008,Epub ahead of print.
  • 2Ho GH, Calvano JE, Bisogna M, et al. Expression of E2F-1 and E2F-4 is reduced in primary and metastatic breast carcinomas [J]. Breast Cancer Res Treat,2001,69 (2):115-122.
  • 3Beijersbergen RL, Kerkhoven RM, Zhu L, et al. E2F-4, a new member of the E2F gene family, has oncogenic activity and associates with p107 in vivo [J]. Genes Dev, 1994,8(22):2680-2690.
  • 4Black MM, Barclay TH, Hankey BF. Prognosis in breast cancer utilizing histologic characteristics of the primary tumor[J]. Cancer, 1975,36(6):2048-2055.
  • 5Maiti B, Li J, de Bruin A, et al. Cloning and characterization of mouse E2F8, a novel mammalian E2F family member capable of blocking cellular proliferation [J]. J Biol Chem,2005,280(18):18211-18220.
  • 6Ezhevsky SA, Ho A, Becker-Hapak M, et al. Differential regulation of retinoblastoma tumor suppressor protein by G(1) cyclin-dependent kinase complexes in vivo[J]. Mol Cell Biol,2001,21 (14):4773-4784.
  • 7Takashima H, Matsumoto Y, Matsubara N, et al. Effect of naturally occurring E2F-4 alterations on transcriptional activation and proliferation in transfected cells [J]. Lab Invest,2001,81(11):1565-1573.
  • 8Chen C, Wells AD. Comparative analysis of E2F family member oncogenic activity[J]. PLoS ONE,2007,2(9):e912.
  • 9Rakha EA, Armour JA, Pinder SE, et al. High-resolution analysis of 16q22.1 in breast carcinoma using DNA amplifiable probes (multiplex amplifiable probe hybridization technique) and immunohistochemistry[J]. Int J Cancer,2005,114(5):720-729.
  • 10Ma Y, Freeman SN, Cress WD. E2F4 deficiency promotes drug-induced apoptosis[J], Cancer Biol Ther,2004, 3(12):1262-1269.

同被引文献26

  • 1Skonier J, Neubauer M, Madisen L, et al. cDNA cloning and sequence analysis of beta ig-h3, a novel gene induced in a human adenocarcinoma cell line after treatment with transforming growth factor-beta [J]. DNA Cell Biol, 1992,11(7) :511-522.
  • 2Soini Y. Tight junctions in lung cancer and lung metasta- sis:a review[J]. Int J Clin Exp Pathol,2012,5 (2):126- 136.
  • 3Schorderet DF, Menasche M, Morand S, et al. Genomic characterization and embryonic expression of the mouse bigh3(Tgfbi) gene[J] Biochem Biophys Res Commun, 2000,274(2) : 267-274.
  • 4Ma CY, Rong Y, Radiloff DR, et al. Extracellular matrix protein betaig-h3/TGFBI promotes metastasis of colon cancer by enhancing cell extravasation[J]. Genes Dev, 2008,22(3) :308-321.
  • 5Gomis RR, Alarc6n C, Nadat C, et al. C/EBPbeta at the core of the TGFbeta cytostatic response and its evasion i.n metastatic breast cancer cells[J] Cancer Cell, 2006, 10 (3) .. 203-214.
  • 6Beavon IR. The E-cadherin-catenin complex in tumour metas- tasis: structure, function and regulation[J]. Eur J Cancer, 2000,36(13) : 1607-1620.
  • 7Hoersch S, Andrade-Navarro MA. Periostin shows increased evolutionary plasticity in its alternatively spliced region[J]. BMC Evol Biol,2010,28(1):10-30.
  • 8Hourihan RN, O'Sullivan GC, Morgan JG. Transcriptionalgene expression profiles of oesophageal adenocarcinoma and normal oesophageal tissues [J]. Anti Cancer Res, 2003,23(1A) :161-165.
  • 9Jemal A,Siegel R,Ward E,et al. Cancer statistics, 2008[J]. CA Cancer J Clin,2008,58(2) :71-96.
  • 10Ivanov SV, Ivanova AV, Salnikow K, et al. Two novel VHL targets, TGFBI (BIGH3) and its transactivator KLF10,are up-regulated in renal clear cell carcinoma and other tumors[J]. Biochem Biophys Res Commun, 2008, 370(4) :536-540.

引证文献1

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部