期刊文献+

六价铬致表观遗传学改变的研究进展 被引量:1

原文传递
导出
摘要 六价铬为铬(chromium,Cr)在自然界中存在的主要形式之一,非职业暴露主要通过摄人六价铬污染的水和食物、皮肤接触含铬产品及吸入汽车尾气中六价铬颗粒物,职业暴露主要来自含铬金属的焊接、电镀、皮革、印染、生产和使用含铬产品如色素、染料、催化剂等[1]。流行病学调查及动物实验研究结果均表明,六价铬暴露可增加肿瘤的发病率[2]。国际癌症研究机构(IARC)已将六价铬列为确认的人类致癌物[3],
作者 王禹 楼建林
出处 《中华劳动卫生职业病杂志》 CAS CSCD 北大核心 2013年第4期309-311,共3页 Chinese Journal of Industrial Hygiene and Occupational Diseases
基金 国家自然科学基金资助项目(81001242) 浙江省自然科学基金资助项目(Y2100687) 浙江省医药卫生骨干人才计划(2011RCA001) 浙江省科技计划项目(2011F10016)
  • 相关文献

参考文献25

  • 1ATSDR. Toxicological Profile for Chromium: Agency for Toxic Substances and Disease Registry, 2008: 367-382.
  • 2Salnikow K, Zhitkovich A. Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium. Chem Res Toxicol, 2008, 21: 28-44.
  • 3IARC. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Chromium, Nickel and Welding Lyon, France: International Agency for Research on Cancer, 1990: 1-648.
  • 4Holmes AL, Wise SS,Wise JP Sr. Carcinogenicity of hexavalent chromium. Indian J Med Res, 2008, 128: 353-372.
  • 5王震凯,汪芳裕.DNA甲基化与肿瘤[J].医学研究生学报,2011,24(6):641-645. 被引量:15
  • 6Cerda S, Weitzman SA. Influence of oxygen radical injury on DNA methylation. Mutat Res, 1997, 386: 141-152.
  • 7Govindarajan B, Klafter R, Miller MS, et al. Reactive oxygen- induced carcinogenesis causes hypermethylation of pl6(Ink4a) and activation of MAP kinase. Mol Med, 2002, 8: 1-8.
  • 8Kondo K, Takahashi Y, Hirose Y, et al. The reduced expression and aberrant methylation of pl6(INK4a) in chromate workers with lungcancer. Lung Cancer, 2006, 53: 295-302.
  • 9Takahashi Y, Kondo K, Hirose T, et al. Microsatellite instability and protein expression of the DNA mismatch repair gene, hMLH1, of lung cancer in chromate-exposed workers. Mol Carcinog, 2005, 42: 150-158.
  • 10Ali AH, Kondo K, Namura T, et al. Aberrant DNA methylation of some tumor suppressor genes in lung cancers from workers with chromate exposure. Mol Carcinog, 2011, 50: 89-99.

二级参考文献33

  • 1彭正良,曹仁贤.甲状腺肿瘤相关基因甲基化研究进展[J].国外医学(生理病理科学与临床分册),2005,25(2):126-129. 被引量:3
  • 2Squatrito M,Gorrini C,Arnati B. Tip60 in DNA damage response and growth control:many tricks in one HAT[J]. Trends Cell Bi-ol,2006,16(9):433-442.
  • 3Avvakumov N,C6t6 J. The MYST family of histone acetyltrans ferases and their intimate links to cancer[J]. Oncogene, 2007,26 (37) : 5395-5407.
  • 4Gorrini C,Squatrito M,Luise C,et al. Tip60 is a haplo-insufficient tumour suppressor required for an oncogene-induced DNA dam- age response[J]. Nature,2007,448(7157) :1063-1067.
  • 5Chan EM,Chan R J, Comer EM, et al. MOZ and MOZ-CBP coop- erate with NF-kappaB to activate transcription from NF-kappaB- dependent promoters[J].Exp Hematol,2007,35(12) :1782-1792.
  • 6Liang J,Prouty L,Williams BJ,et al. Acute mixed lineage leuke- mia with an inv(8)(pllq13) resulting in fusion of the genes for MOZ and TIF2[J].Blood,1998,92(6) :2118-2122.
  • 7Glozak MA, Seto E. Histone deacetylases and cancer[J]. Onco- gene, 2007,26 (37) : 5420-5432.
  • 8Weichert W,R6ske A,Niesporek S, et aI. Class I histone deacety- lase expression has independent prognostic impact in human colo- rectal cancer: specific role of class I histone deacetylases in vitro and in vivo[J].Clin Cancer Res,2008,14(6) :1669-1677.
  • 9Wilson AJ, Byun DS, Popova N, et al. Histone deaeetylase 3 (HDAC3)and other class I HDACs regulate colon cell matura- tion and p21 expression and are deregulated in human colon canc- er[J]. J Biol Chem,2006,281(19) : 13548-13558.
  • 10Bhaskara S, Chyla BJ, Amann JM, et al. Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control[J]. Mol Ce11,2008,30(1) :61-72.

共引文献17

同被引文献4

引证文献1

二级引证文献5

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