Concepts of Cell Death and Application to Carcinogenesis

The occurrence of cell death as a physiologic event in multicellular organisms has been known for more than 150 yr. In 1972, the term apoptosis was introduced on morphological grounds. The hypothesis that all kinds of cell death can be categorized as either "apoptotic" or "necrotic" is not generally confirmed. Cells seem to use different pathways for suicide, as reflected by different morphology: condensation-prominent, Type I or apoptosis; autophagy-prominent, Type II; and so forth. Type II cell death was found in mammary tissue and mammary tumor cells and in a variety of other organs. For unequivocal identification of the various types of cell death, morphological, biochemical, and functional criteria may be used in combination. During tumor development in various organs of animals and humans, not only rates of cell proliferation but also rates of cell death may increase with increasing malignancy. Morphological and functional criteria (antipromotion, withdrawal of survival factors) indicate that cell death in tumors frequently is of an active nature.

[1]  A. Wyllie,et al.  Apoptosis. The role of the endonuclease. , 1990, The American journal of pathology.

[2]  W. Bursch,et al.  Controlled death (apoptosis) of normal and putative preneoplastic cells in rat liver following withdrawal of tumor promoters. , 1984, Carcinogenesis.

[3]  W. Bursch,et al.  DNA synthesis, apoptosis, and phenotypic expression as determinants of growth of altered foci in rat liver during phenobarbital promotion. , 1990, Cancer research.

[4]  B. Ruttkay-Nedecky,et al.  Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression , 1997, Hepatology.

[5]  A. Wyllie,et al.  Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics , 1972, British Journal of Cancer.

[6]  R. Lockshin,et al.  Ultrastructural study of the normal degeneration of the intersegmental muscles of Antheraea polyphemus and Manduca sexta (Insecta, lepidoptera) with particular reference to cellular autophagy , 1977, Journal of morphology.

[7]  H. Greenberg Progress in Liver Disease , 1970 .

[8]  G. M. Ledda-Columbano,et al.  Induction of two different modes of cell death, apoptosis and necrosis, in rat liver after a single dose of thioacetamide. , 1991, The American journal of pathology.

[9]  W. Bursch,et al.  Transforming growth factor-beta 1 as a signal for induction of cell death by apoptosis. , 1993, British Journal of Cancer.

[10]  J. Kerr,et al.  Internucleosomal DNA cleavage should not be the sole criterion for identifying apoptosis. , 1992, International journal of radiation biology.

[11]  A. Wyllie The biology of cell death in tumours. , 1985, Anticancer research.

[12]  Z. Darżynkiewicz,et al.  Assays of cell viability: discrimination of cells dying by apoptosis. , 1994, Methods in cell biology.

[13]  E G Luebeck,et al.  Effects of polychlorinated biphenyls in rat liver: quantitative analysis of enzyme-altered foci. , 1991, Toxicology and applied pharmacology.

[14]  W. Bursch,et al.  Cell death: programmed, apoptosis, necrosis, or other? , 1995, Cell death and differentiation.

[15]  B. Kraupp,et al.  Cell Death by Apoptosis in Normal, Preneoplastic and Neoplastic Tissue , 1988 .

[16]  B. Ruttkay-Nedecky,et al.  Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[17]  P. Walker,et al.  Endonuclease activities associated with high molecular weight and internucleosomal DNA fragmentation in apoptosis. , 1994, Experimental cell research.

[18]  L. M. Schwartz The faces of death. , 1995, Cell death and differentiation.

[19]  R. Schulte‐Hermann,et al.  Response of liver foci in rats to hepatic tumor promoters , 1982, Toxicologic pathology.

[20]  B. Kraupp,et al.  In situ detection of fragmented dna (tunel assay) fails to discriminate among apoptosis, necrosis, and autolytic cell death: A cautionary note , 1995, Hepatology.

[21]  W. H. Butler,et al.  Apoptosis—the mechanism of cell death in dimethylnitrosamine‐induced hepatotoxicity , 1989, The Journal of pathology.

[22]  W. Bursch,et al.  Transforming growth factor β1‐induced cell death in preneoplastic foci of rat liver and sensitization by the antiestrogen tamoxifen , 1996, Hepatology.

[23]  A. Wyllie Apoptosis: cell death under homeostatic control. , 1987, Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement.

[24]  W. Bursch,et al.  Active cell death (apoptosis) in liver biology and disease. , 1995, Progress in liver diseases.

[25]  C. Sarraf,et al.  Kinetic studies on a murine sarcoma and an analysis of apoptosis. , 1986, British Journal of Cancer.

[26]  R. Maronpot,et al.  Importance of and Approaches to Quantification of Hepatocyte Apoptosis , 1996, Toxicologic pathology.

[27]  W. Bursch,et al.  Control of cell death (apoptosis) by diethylstilbestrol in an estrogen-dependent kidney tumor. , 1991, Carcinogenesis.

[28]  B. Kraupp,et al.  In situ detection of fragmented dna (tunel assay) fails to discriminate among apoptosis, necrosis, and autolytic cell death: A cautionary note , 1995, Hepatology.

[29]  H. Merker,et al.  The morphology of various types of cell death in prenatal tissues. , 1973, Teratology.

[30]  E. Cooper,et al.  Cell death in normal and malignant tissues. , 1975, Advances in cancer research.

[31]  M. Lieberman,et al.  Cell Suicide and Cell Death , 1971 .

[32]  W. Bursch,et al.  Active cell death induced by the anti-estrogens tamoxifen and ICI 164 384 in human mammary carcinoma cells (MCF-7) in culture: the role of autophagy. , 1996, Carcinogenesis.

[33]  D L Evans,et al.  Analysis and discrimination of necrosis and apoptosis (programmed cell death) by multiparameter flow cytometry. , 1992, Biochimica et biophysica acta.

[34]  W. Bursch,et al.  Determination of the length of the histological stages of apoptosis in normal liver and in altered hepatic foci of rats. , 1990, Carcinogenesis.