Preneoplastic lesions as end points in carcinogenicity testing. I. Hepatic preneoplasia.

Preneoplastic lesions as end points in carcinogenicity testing. I. Hepatic preneoplasia.
复制标题

癌前病变作为致癌性测试的终点。

DOI:
--
复制
发表时间:
1986
期刊:
影响因子:
4.7
通讯作者:
P. Bannasch
P. Bannasch
中科院分区:
医学2区
文献类型:
--
作者:
P. Bannasch

文献摘要

参考文献

被引文献

相似文献

The evaluation of the carcinogenic risk deriving from chemical compounds depends mainly on conventional histopathology up to the present. The accepted end point in carcinogenicity testing is the tumor as defined histologically. A great disadvantage of this approach is the long lag period in the development of tumors induced by chemicals. In order to overcome this drawback, many efforts have been made to detect early biological or morphological lesions which might be specific for carcinogens. A great number of short-term tests carried out in vitro provided valuable information about the reactions of cellular constituents and biological macromolecules to the chemicals tested, but they did not allow an unequivocal prediction of the carcinogenic potential of the respective compounds in whole animals, not to mention man. The introduction of modern micromorphological methods such as electron microscopy and cytochemistry in the evaluation of whole-animal studies also revealed many new aspects on carcinogen-induced cellular and subcellular alterations which appeared to be unreliable as indicators of the carcinogenic risk of chemicals. However, during the past two decades a number of characteristic cellular changes has been detected in various tissues, especially in the liver. These changes regularly precede the development of certain tumor types, and are regarded as preneoplastic lesions (1,2). The altered cell populations usually form well-defined foci. They appear prior to the development of tumors in the target tissue of the carcinogen, and should be duly considered in the evaluation of the carcinogenic risk from chemicals in bioassays.
DOI: --
发表时间: 1983-09
期刊: Cancer research
影响因子: 11.2
作者:
S. Vesselinovitch;N. Mihailovich
通讯作者: S. Vesselinovitch;N. Mihailovich
苯巴比妥和二乙基亚硝胺给药后大鼠肝脏酶改变病灶的自然史和剂量反应特征。
DOI: 10.1093/carcin/5.1.67
发表时间: 1984
期刊: Carcinogenesis
影响因子: 4.7
作者:
Goldsworthy,T;Campbell,HA;Pitot,HC
通讯作者: Pitot,HC
部分肝切除术在 Fischer 344 和 Wistar-Furth 大鼠再生和移植肝细胞中诱导 γ-谷氨酰转肽酶的能力。
DOI: --
发表时间: 1985
期刊: Cancer research
影响因子: 11.2
作者:
Bone3rd,SN;Michalopoulos,G;Jirtle,RL
通讯作者: Jirtle,RL
DOI: 10.1016/0304-419x(83)90002-1
发表时间: 1984
期刊: Biochimica et biophysica acta
影响因子: --
作者:
Emmanuel Farber
通讯作者: Emmanuel Farber
婴儿小鼠单一二乙基亚硝胺治疗诱导的局灶性肝损伤的组织化学特征。
DOI: --
发表时间: 1985
期刊: Cancer research
影响因子: 11.2
作者:
Vesselinovitch,SD;Hacker,HJ;Bannasch,P
通讯作者: Bannasch,P