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肿瘤抗异常转录治疗研究进展 被引量:1

Progress in antineoplastic therapy against abnormal transcription
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摘要 肿瘤的发生、发展与转录水平的基因表达调控失常密切相关。对急性早幼粒细胞白血病(APL)发病机制的研究较清晰地阐述了基因转录异常导致肿瘤的机制。抗异常转录治疗即是基于此的一个非常具有吸引力的肿瘤治疗策略,并且其有效性不断被实验研究及临床实践所证明。
出处 《国外医学(肿瘤学分册)》 2005年第6期420-423,共4页 Foreign Medical Sciences (Cancer Section)
基金 上海市科技发展基金资助项目(03ZR14118)
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  • 1Di Gennaro E,Bruzzese F,Caraglia M,et al. Acetylation of proteins as novel target for antitumor therapy. Amino Acids,2004,26(4) :435-441.
  • 2Moe behrens GH, Pandolfi PP. Targeting aberrant transcriptional repression in acute myeloid leukemia. Rev Clin Exp Hematol, 2003,7(2) :139-159.
  • 3Okuno M, Kojima S, Akita K, et al. Retinoids in liver fibrosis and cancer. Front Biosci ,2002,7 :d204-218.
  • 4Gu BW,Xiong H,Zhou Y ,et al. Variant-type PML-RAR(alpha) fusion transcript in acute promyelocytic leukemia:use of a cryptic coding sequence from intron 2 of the RAR(alpha) gene and identification of a new clinical subtype resistant to retinoic acid therapy. Proc Natl Acad Sci USA,2002,99( 11 ):7640-7645.
  • 5Wang ZY. Mechanism of action of all-trans retinoic acid and arsenic trioxide in the treatment of acute promyelocytic leukemia. Gan to Kagaku Ryoho,2002,29 ( Suppl 1 ) :214-218.
  • 6Vigushin DM, Coombes RC. Targeted histone deacetylase inhibition for cancer therapy. Curt Cancer Drug Targets,2004,4(2):205-218.
  • 7Cote S, Rosenauer A, Bianchina A, et al. Response to histone deacetylase inhibition of novel PML/RARalpha mutants detected in retinoic acid-resistant APL cells. Blood ,2002,100 (7) :2586-2596.
  • 8He LZ,Tolentino T, Grayson P, et al. Histone deacetylase inhibitors induce remission in transgenic modds of therapy-resistant acute promyelocytic leukemia.J Clin Invest.2001.108(9):1321-1330.
  • 9Lase A,Carnicer MJ,Aventin A,et al. MEIS 1 expression is downregulated through promoter hypermethylation in AML1-ETO acute myeloid leukemias. Leukemia,2004,18 (7) : 1231-1237.
  • 10Oligny LL. Cancer and epigenesis:a developmental perspective. Adv Pediatr, 2003,50:59-80.

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