Apoptosis and cancer risk assessment

被引:73
作者
Goldsworthy, TL
Conolly, RB
FranssonSteen, R
机构
[1] Chem. Indust. Inst. of Toxicology, Res. Triangle Park, NC 27709-2137, 6 Davis Drive
来源
MUTATION RESEARCH-REVIEWS IN GENETIC TOXICOLOGY | 1996年 / 365卷 / 1-3期
关键词
cancer model; proliferation; hepatocarcinogenesis;
D O I
10.1016/S0165-1110(96)90013-5
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Apoptosis is one form of physiological or active cell death. The balance between cell proliferation and cell death or apoptosis not only effects organ growth but also has a profound impact on the net increase and growth of initiated cells and preneoplastic and tumor cell populations. With respect to cancer development apoptosis is becoming widely recognized as being an innate tissue defense against carcinogens by inhibiting survival and controlling growth of precancerous cell populations and tumors at different stages of carcinogenesis, Experimental data on cell birth and cell. death rates help identify the mode of action of a chemical and can be incorporated into biologically based cancer models. This article describes the quantitation and regulation of apoptosis in rodent liver and how loss of regulation can have a role in hepatocarcinogenesis. A biologically-based mouse liver cancer model is presented and utilized to describe how treatment related growth effects affect the process of carcinogenesis, Advantages acid limitations of biologically based cancer models in cancer research and risk assessment are discussed.
引用
收藏
页码:71 / 90
页数:20
相关论文
共 95 条
[21]   LIMITATIONS OF BIOLOGICAL MODELS OF CARCINOGENESIS FOR LOW-DOSE EXTRAPOLATION [J].
CRUMP, KS .
RISK ANALYSIS, 1994, 14 (06) :883-886
[22]  
CRUMP KS, 1977, BIOMETRICS, V33, P437, DOI 10.2307/2529358
[23]   RELATIONSHIP OF HEPATOCARCINOGENICITY AND HEPATOCELLULAR PROLIFERATION INDUCED BY MUTAGENIC NONCARCINOGENS VS CARCINOGENS .2. 1-NITROPROPANE VS 2-NITROPROPANE [J].
CUNNINGHAM, ML ;
MATTHEWS, HB .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1991, 110 (03) :505-513
[24]   FEATURES OF APOPTOTIC CELLS MEASURED BY FLOW-CYTOMETRY [J].
DARZYNKIEWICZ, Z ;
BRUNO, S ;
DELBINO, G ;
GORCZYCA, W ;
HOTZ, MA ;
LASSOTA, P ;
TRAGANOS, F .
CYTOMETRY, 1992, 13 (08) :795-808
[25]   A STOCHASTIC 2-STAGE MODEL FOR CANCER RISK ASSESSMENT .2. THE NUMBER AND SIZE OF PREMALIGNANT CLONES [J].
DEWANJI, A ;
VENZON, DJ ;
MOOLGAVKAR, SH .
RISK ANALYSIS, 1989, 9 (02) :179-187
[26]  
DRAGAN YP, 1993, P SOC EXP BIOL MED, V202, P16
[27]   APOPTOSIS - A PRODUCT OF PROGRAMMED AND UNPROGRAMMED CELL-DEATH [J].
EASTMAN, A .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1993, 121 (01) :160-164
[28]   SURVIVAL FACTORS, INTRACELLULAR SIGNAL-TRANSDUCTION, AND THE ACTIVATION OF ENDONUCLEASES IN APOPTOSIS [J].
EASTMAN, A .
SEMINARS IN CANCER BIOLOGY, 1995, 6 (01) :45-52
[29]   A CELLULAR-DYNAMICS MODEL OF EXPERIMENTAL BLADDER-CANCER - ANALYSIS OF THE EFFECT OF SODIUM SACCHARIN IN THE RAT [J].
ELLWEIN, LB ;
COHEN, SM .
RISK ANALYSIS, 1988, 8 (02) :215-221
[30]  
FISHER JC, 1951, CANCER, V4, P916, DOI 10.1002/1097-0142(195109)4:5<916::AID-CNCR2820040504>3.0.CO