期刊文献+

基因治疗联合放射治疗恶性肿瘤的分子机制

Molecular mechanism of genetherapy combined radiotherapy for malignant tumor
原文传递
导出
摘要 放射治疗是恶性肿瘤治疗的常规手段之一,对放射治疗的耐受性是影响放疗疗效的主要障碍之一。基因治疗联合放疗代表了恶性肿瘤治疗的一种新方式,在一系列联合治疗的研究中发现,基因治疗可以提高肿瘤的辐射敏感性,减少肿瘤的复发和转移,改善放射治疗的疗效。该文综述肿瘤基因治疗联合放射治疗的有关分子机制。 Radiotherapy is one of the routine treatment methods for malignant tumor. Resistance to radiation is one significant obstacle to the curative effects of radiotherapy. Genetherapy combined with radiotherapy represents a new approach to cancer treatment. A series of studies about combination therapy found that genetherapy could enhance tumor radiosensitivity, reduce recurrence and metastasis, and improve effects of radiotherapy. Review the relevant molecular mechanisms of genetherapy combined radiotherapy for malignant tumor.
出处 《国际放射医学核医学杂志》 2009年第2期113-116,共4页 International Journal of Radiation Medicine and Nuclear Medicine
关键词 肿瘤 基因疗法 放射疗法 辐射耐受性 Neoplasms Genetherapy Radiotherapy Radiation tolerance
  • 相关文献

参考文献23

  • 1Collis S J, DeWeese TL. Enhanced radiation response through directed molecular targeting approaches. Cancer Metastasis Rev, 2004, 23(3-4): 277-292.
  • 2Baker SJ, Markowitz S, Fearon ER, et al. Suppression of human colorectal carcinoma cell growth by wild-type p53. Science, 1990, 249(4971): 912-915.
  • 3Hanpt S, Haupt Y. Importance of p53 for cancer onset and therapy. Anticancer Drugs, 2006, 17(7): 725-732.
  • 4Mimeault M, Batra SK. Recent advances on multiple tumorigenic cascades involved in prostatic cancer progression and targeting therapies. Carcinogenesis, 2006, 27(1): 1-22.
  • 5Guha A, Mukherjee J. Advances in the biology of astrocytomas. Curt Opin Neurol, 2004, 17(6): 655-662.
  • 6肖绍文,张珊文,吕有勇,杨敬贤,杨新宇.外源性p53基因对人胃癌细胞的放射增敏作用[J].北京大学学报(医学版),2001,33(5):427-431. 被引量:13
  • 7Moon C, Oh Y, Roth JA. Current status of gene therapy for lung cancer and head and neck cancer. Clin Cancer Res, 2003, 9(14): 5055-5067.
  • 8Lavin MF, Khanna KK. ATM: the protein encoded by the gene mutated in the radiosen-sitive syndrome ataxia-telangiectasia. Int J Radiat Biol, 1999, 75(10): 1201-1214.
  • 9Fan Z, Chakravarty P, Alfieri A, et al. Adenovirus-mediated antisense ATM gene transfer sensitizes prostate cancer cells to radiation. Cancer Gene Ther, 2000, 7(10): 1307-1314.
  • 10Guha C, Guha U, Tribius S, et al. Antisense ATM gene therapy: a strategy to increase the radiosensitivity of human tumors. Gene Ther, 2000, 7(10): 852-858.

二级参考文献32

  • 1[1]Kamb A, Gruis NA, Weaver FJ, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science, 1994; 264:436.
  • 2[2]Graham F, Prevec L. Gene Transfer and Expression Protocols. In Clifton NJ,ed. Methods in Molecular Biology. Vol.7th, Totowa: Humana Press Inc, 1991:258 - 264.
  • 3[3]Serrano M, Hannon GJ, Beach D. A new regulatory motif in cell cycle control causing specific inhibition of cyclin D/CDK4. Nature, 1993; 366(6456):704.
  • 4[4]Nobori T, Mlura K, Wu DJ, et al. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature, 1994; 368(6473):753.
  • 5[5]Arap W, Nishikawa R, Furnari FB, et al. Replacement of the p16/CDKN2 gene suppresses human glioma cell growth. Cancer Res, 1995; 55:1351.
  • 6[6]Hama S, Sadatoma T, Yoshioka H, et al. Transformation of human glioma cell lines with the p16 gene inhibits cell proliferation. Anti-cancer Res, 1997; 17(30):1933.
  • 7[7]Jin XM, Nguyen D, Zhang WW, et al. Cell cycle arrest and inhibition of tumor cell proliferation by the p16ink4 gene mediated by an adenovirus vector. Cancer Res, 1995; 55:3250.
  • 8[8]Yeudall WA, Crawford RY, Enslay JF, et al. MTS1/CDK4I is altered in cell lines derived from primary and metastatic oral squamous cell carcinoma. Carcinogenesis, 1994; 5(12):2883.
  • 9[9]James WR, Daqing Li, Willam HL, et al. p16INK4A Adenovirus-mediated gene therapy for human head and neck squamous cell cancer. Clinical Cancer Res, 1998; 4:1697.
  • 10Li J H,Int J Radiat Oncol Biol Phys,1999年,43卷,3期,607页

共引文献16

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