3,382 results on '"Bursch W"'
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2. Hepatocyte apoptosis: Is transforming growth factor-B1 the kiss of death? Oberhammer FA, Pavelka M, Sharma S, Tietenbacher R, Purchio AF, Bursch W, Schulte-Hermann R. Induction of apoptosis in cultured hepatocytes and in regressing liver by transforming growth factor β1. Proc Natl Acad Sci USA 1992;89:5408–5412
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Fausto, N, primary
- Published
- 1993
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3. Hepatocyte apoptosis: Is transforming growth factor-B1 the kiss of death? Oberhammer FA, Pavelka M, Sharma S, Tietenbacher R, Purchio AF, Bursch W, Schulte-Hermann R. Induction of apoptosis in cultured hepatocytes and in regressing liver by transforming growth factor β1. Proc Natl Acad Sci USA 1992;89:5408–5412
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N Fausto
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medicine.medical_specialty ,Endocrinology ,Hepatology ,Chemistry ,Apoptosis ,Internal medicine ,medicine ,Hepatocyte apoptosis ,Molecular biology ,KISS (TNC) ,Transforming growth factor - Published
- 1993
4. Hormone und Krebs
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Grasl-Kraupp, B., Bursch, W., Schulte-Hermann, R., Hiddemann, Wolfgang, Huber, Heinz, and Bartram, Claus R.
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- 2004
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5. Hormonal Regulation of Hepatic Cell Proliferation and Apoptosis: Implications for Carcinogenesis
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Schulte-Hermann, Rolf, Bursch, W., Grasl-Kraupp, B., Müllauer, L., Ochs, H., Parzefall, W., Ruttkay-Nedecky, B., Li, J. Jonathan, editor, Li, Sara Antonia, editor, Gustafsson, Jan-Åke, editor, Nandi, Satyabrata, editor, and Sekely, Lea I., editor
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- 1996
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6. Active Cell Death and Cancer
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Bursch, W., Grasl-Kraupp, B., Ellinger, A., Török, L., Kienzl, H., Müllauer, L., Schulte-Hermann, R., Tenniswood, Martin, editor, and Michna, Horst, editor
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- 1995
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7. Nongenotoxic Carcinogenesis in the Liver
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Schulte-Hermann, R., Bursch, W., Grasl-Kraupp, B., Huber, W., Parzefall, W., Stock, Günter, editor, Habenicht, Ursula-F., editor, Cockburn, Andrew, editor, and Smith, Lewis, editor
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- 1994
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8. Apoptosis and Its Role in Hepatic Carcinogenesis by Non-Genotoxic Agents
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Schulte-Hermann, R., Bursch, W., Grasl-Kraupp, B., Huber, W., Ruttkay-Nedecky, B., Wagner, A., and Skouteris, George G., editor
- Published
- 1994
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9. Induction of Apoptosis in Cultured Hepatocytes and in Regressing Liver by Transforming Growth Factor β1
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Oberhammer, Franziska A., Pavelka, Margit, Sharma, Sushitra, Tiefenbacher, Roman, Purchio, Anthony F., Bursch, W., and Schulte-Hermann, Rolf
- Published
- 1992
10. The Role of Growth of Normal and Preneoplastic Cell Populations for Tumor Promotion in Rat Liver
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Schulte-Hermann, R., Schuppler, J., Timmermann-Trosiener, I., Ohde, G., Bursch, W., and Berger, H.
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- 1983
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11. Apoptosis in the liver and its role in hepatocarcinogenesis
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Schulte-Hermann, R., Bursch, W., Löw-Baselli, A., Wagner, A., and Grasl-Kraupp, B.
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- 1997
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12. Nutrition and Cancer: Glucose and Amino Acids in Apoptosis Control: O8
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Bursch, W., Karwan, A., Mayer, M., Dornetshuber, J., and Schulte-Hermann, R.
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- 2008
13. Expression of clusterin (testosterone-repressed prostate message-2) mRNA during growth and regeneration of rat liver
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Bursch, W., Gleeson, T., Kleine, L., and Tenniswood, M.
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- 1995
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14. Cell Proliferation and Apoptosis in the Liver of Mice with Different Genetic Susceptibility to Tumor Induction and Its Control by Food and TGF-β1
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Chabicovsky, M., primary, Wastl, U., additional, Hufnagl, K., additional, Bursch, W., additional, and Schulte-Hermann, R., additional
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- 2000
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15. Role of apoptosis for mouse liver growth regulation and tumor promotion: comparative analysis of mice with high (C3H/He) and low (C57Bl/6J) cancer susceptibility
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Bursch, W., Grasl-Kraupp, B., Wastl, U., Hufnagl, K., Chabicovsky, M., Taper, H., and Schulte-Hermann, R.
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- 2004
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16. Tumor Promotion
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Schulte-Hermann, R., primary, Marian, B., additional, and Bursch, W., additional
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- 1999
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17. Induction of apoptosis in cultured hepatocytes and in regressing liver by transforming growth factor beta-1
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Oberhammer, Franziska A., Pavelka, Margit, Sharma, Sushitra, Tiefenbacher, Roman, Purchio, Anthony F., Bursch, W., and Schulte-Hermann, Rolf
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Growth factors -- Physiological aspects ,Liver -- Physiological aspects ,Cell death -- Research ,Science and technology - Abstract
Transforming factor beta-1 (TGF-beta-1) is a negative regulator of liver growth. In vitro analyses of the mode of action of TGF-beta-1 showed that apoptosis is the mode of action by which this regulator mediates hepatocyte cell death. In vivo mouse injections of this regulator led to apoptosis of the animal's liver. Tests on the precursor of TGF-beta-1 showed that it could not mediate hepatic apoptosis. These results indicate that TGF-beta-1 is involved in hepatic apoptosis, and acts through its mature form.
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- 1992
18. Programmed Cell Death (PCD): Apoptosis, Autophagic PCD, or Others?
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BURSCH, W., ELLINGER, A., GERNER, CH., FRÖHWEIN, U., and SCHULTE-HERMANN, R.
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- 2000
19. Apoptosis 24.06
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Schulte-Hermann, R., Bursch, W., Marian, B., and Grasl-Kraupp, B.
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- 1997
20. Phenobarbital and other Liver Tumor Promoters
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Schulte-Hermann, R., Schuppler, J., Ohde, G., Bursch, W., Timmermann-Trosiener, I., and Nicolini, Claudio, editor
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- 1982
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21. Cytoprotective Effect of Iloprost Against Liver Cell Death Induced by Carbon Tetrachloride (CCl4) or Bromobenzene
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Bursch, W., Schulte-Hermann, R., Gryglewski, R. J., editor, and Stock, G., editor
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- 1987
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22. Cell Death (Apoptosis) in Normal and Preneoplastic Liver Tissue
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Bursch, W., Schulte-Hermann, R., Roberfroid, M. B., editor, and Préat, V., editor
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- 1988
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23. Hepatocarcinogenesis by Non-Genotoxic Compounds
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Schulte-Hermann, R., Parzefall, W., Bursch, W., Timmermann-Trosiener, I., and Travis, Curtis C., editor
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- 1989
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24. Tumor Development and Apoptosis.
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Schulte-Hermann, R., Grasl-Kraupp, B., and Bursch, W.
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- 1994
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25. Elimination of preneoplastic rat liver cells via induction of apoptosis by transforming growth factor β1
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Grasl-Kraupp, B., Müllauer, L., Ruttkay-Nedecky, B., Bursch, W., and Schulte-Hermann, R.
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- 1995
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26. Quantitative histological and histochemical studies on the occurrence and stages of controlled cell death (apoptosis) during regression of rat liver hyperplasia
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Bursch, W., Taper, H. S., Lauer, B., and Schulte-Hermann, R.
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- 1986
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27. Growth, regression and cell death in rat liver as related to tissue levels of the hepatomitogen cyproterone acetate
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Bursch, W., Düsterberg, B., and Schulte-Hermann, R.
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- 1986
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28. Guidelines for the use and interpretation of assays for monitoring autophagy
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Klionsky, D.J. Abdalla, F.C. Abeliovich, H. Abraham, R.T. Acevedo-Arozena, A. Adeli, K. Agholme, L. Agnello, M. Agostinis, P. Aguirre-Ghiso, J.A. Ahn, H.J. Ait-Mohamed, O. Ait-Si-Ali, S. Akematsu, T. Akira, S. Al-Younes, H.M. Al-Zeer, M.A. Albert, M.L. Albin, R.L. Alegre-Abarrategui, J. Aleo, M.F. Alirezaei, M. Almasan, A. Almonte-Becerril, M. Amano, A. Amaravadi, R. Amarnath, S. Amer, A.O. Andrieu-Abadie, N. Anantharam, V. Ann, D.K. Anoopkumar-Dukie, S. Aoki, H. Apostolova, N. Arancia, G. Aris, J.P. Asanuma, K. Asare, N.Y.O. Ashida, H. Askanas, V. Askew, D.S. Auberger, P. Baba, M. Backues, S.K. Baehrecke, E.H. Bahr, B.A. Bai, X.-Y. Bailly, Y. Baiocchi, R. Baldini, G. Balduini, W. Ballabio, A. Bamber, B.A. Bampton, E.T.W. Bánhegyi, G. Bartholomew, C.R. Bassham, D.C. Bast Jr., R.C. Batoko, H. Bay, B.-H. Beau, I. Béchet, D.M. Begley, T.J. Behl, C. Behrends, C. Bekri, S. Bellaire, B. Bendall, L.J. Benetti, L. Berliocchi, L. Bernardi, H. Bernassola, F. Besteiro, S. Bhatia-Kissova, I. Bi, X. Biard-Piechaczyk, M. Blum, J.S. Boise, L.H. Bonaldo, P. Boone, D.L. Bornhauser, B.C. Bortoluci, K.R. Bossis, I. Bost, F. Bourquin, J.-P. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N.R. Brancolini, C. Brech, A. Brenman, J.E. Brennand, A. Bresnick, E.H. Brest, P. Bridges, D. Bristol, M.L. Brookes, P.S. Brown, E.J. Brumell, J.H. Brunetti-Pierri, N. Brunk, U.T. Bulman, D.E. Bultman, S.J. Bultynck, G. Burbulla, L.F. Bursch, W. Butchar, J.P. Buzgariu, W. Bydlowski, S.P. Cadwell, K. Cahová, M. Cai, D. Cai, J. Cai, Q. Calabretta, B. Calvo-Garrido, J. Camougrand, N. Campanella, M. Campos-Salinas, J. Candi, E. Cao, L. Caplan, A.B. Carding, S.R. Cardoso, S.M. Carew, J.S. Carlin, C.R. Carmignac, V. Carneiro, L.A.M. Carra, S. Caruso, R.A. Casari, G. Casas, C. Castino, R. Cebollero, E. Cecconi, F. Celli, J. Chaachouay, H. Chae, H.-J. Chai, C.-Y. Chan, D.C. Chan, E.Y. Chang, R.C.-C. Che, C.-M. Chen, C.-C. Chen, G.-C. Chen, G.-Q. Chen, M. Chen, Q. Chen, S.S.-L. Chen, W. Chen, X. Chen, X. Chen, X. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, Y. Cheong, H. Cheong, J.-H. Cherry, S. Chess-Williams, R. Cheung, Z.H. Chevet, E. Chiang, H.-L. Chiarelli, R. Chiba, T. Chin, L.-S. Chiou, S.-H. Chisari, F.V. Cho, C.H. Cho, D.-H. Choi, A.M.K. Choi, D. Choi, K.S. Choi, M.E. Chouaib, S. Choubey, D. Choubey, V. Chu, C.T. Chuang, T.-H. Chueh, S.-H. Chun, T. Chwae, Y.-J. Chye, M.-L. Ciarcia, R. Ciriolo, M.R. Clague, M.J. Clark, R.S.B. Clarke, P.G.H. Clarke, R. Codogno, P. Coller, H.A. Colombo, M.I. Comincini, S. Condello, M. Condorelli, F. Cookson, M.R. Coombs, G.H. Coppens, I. Corbalan, R. Cossart, P. Costelli, P. Costes, S. Coto-Montes, A. Couve, E. Coxon, F.P. Cregg, J.M. Crespo, J.L. Cronjé, M.J. Cuervo, A.M. Cullen, J.J. Czaja, M.J. D'Amelio, M. Darfeuille-Michaud, A. Davids, L.M. Davies, F.E. De Felici, M. De Groot, J.F. De Haan, C.A.M. De Martino, L. De Milito, A. De Tata, V. Debnath, J. Degterev, A. Dehay, B. Delbridge, L.M.D. Demarchi, F. Deng, Y.Z. Dengjel, J. Dent, P. Denton, D. Deretic, V. Desai, S.D. Devenish, R.J. Di Gioacchino, M. Di Paolo, G. Di Pietro, C. Díaz-Araya, G. Díaz-Laviada, I. Diaz-Meco, M.T. Diaz-Nido, J. Dikic, I. Dinesh-Kumar, S.P. Ding, W.-X. Distelhorst, C.W. Diwan, A. Djavaheri-Mergny, M. Dokudovskaya, S. Dong, Z. Dorsey, F.C. Dosenko, V. Dowling, J.J. Doxsey, S. Dreux, M. Drew, M.E. Duan, Q. Duchosal, M.A. Duff, K. Dugail, I. Durbeej, M. Duszenko, M. Edelstein, C.L. Edinger, A.L. Egea, G. Eichinger, L. Eissa, N.T. Ekmekcioglu, S. El-Deiry, W.S. Elazar, Z. Elgendy, M. Ellerby, L.M. Er Eng, K. Engelbrecht, A.-M. Engelender, S. Erenpreisa, J. Escalante, R. Esclatine, A. Eskelinen, E.-L. Espert, L. Espina, V. Fan, H. Fan, J. Fan, Q.-W. Fan, Z. Fang, S. Fang, Y. Fanto, M. Fanzani, A. Farkas, T. Farré, J.-C. Faure, M. Fechheimer, M. Feng, C.G. Feng, J. Feng, Q. Feng, Y. Fésüs, L. Feuer, R. Figueiredo-Pereira, M.E. Fimia, G.M. Fingar, D.C. Finkbeiner, S. Finkel, T. Finley, K.D. Fiorito, F. Fisher, E.A. Fisher, P.B. Flajolet, M. Florez-McClure, M.L. Florio, S. Fon, E.A. Fornai, F. Fortunato, F. Fotedar, R. Fowler, D.H. Fox, H.S. Franco, R. Frankel, L.B. Fransen, M. Fuentes, J.M. Fueyo, J. Fujii, J. Fujisaki, K. Fujita, E. Fukuda, M. Furukawa, R.H. Gaestel, M. Gailly, P. Gajewska, M. Galliot, B. Galy, V. Ganesh, S. Ganetzky, B. Ganley, I.G. Gao, F.-B. Gao, G.F. Gao, J. Garcia, L. Garcia-Manero, G. Garcia-Marcos, M. Garmyn, M. Gartel, A.L. Gatti, E. Gautel, M. Gawriluk, T.R. Gegg, M.E. Geng, J. Germain, M. Gestwicki, J.E. Gewirtz, D.A. Ghavami, S. Ghosh, P. Giammarioli, A.M. Giatromanolaki, A.N. Gibson, S.B. Gilkerson, R.W. Ginger, M.L. Ginsberg, H.N. Golab, J. Goligorsky, M.S. Golstein, P. Gomez-Manzano, C. Goncu, E. Gongora, C. Gonzalez, C.D. Gonzalez, R. González-Estévez, C. González-Polo, R.A. Gonzalez-Rey, E. Gorbunov, N.V. Gorski, S. Goruppi, S. Gottlieb, R.A. Gozuacik, D. Granato, G.E. Grant, G.D. Green, K.N. Gregorc, A. Gros, F. Grose, C. Grunt, T.W. Gual, P. Guan, J.-L. Guan, K.-L. Guichard, S.M. Gukovskaya, A.S. Gukovsky, I. Gunst, J. Gustafsson, A.B. Halayko, A.J. Hale, A.N. Halonen, S.K. Hamasaki, M. Han, F. Han, T. Hancock, M.K. Hansen, M. Harada, H. Harada, M. Hardt, S.E. Harper, J.W. Harris, A.L. Harris, J. Harris, S.D. Hashimoto, M. Haspel, J.A. Hayashi, S.-I. Hazelhurst, L.A. He, C. He, Y.-W. Hébert, M.-J. Heidenreich, K.A. Helfrich, M.H. Helgason, G.V. Henske, E.P. Herman, B. Herman, P.K. Hetz, C. Hilfiker, S. Hill, J.A. Hocking, L.J. Hofman, P. Hofmann, T.G. Höhfeld, J. Holyoake, T.L. Hong, M.-H. Hood, D.A. Hotamisligil, G.S. Houwerzijl, E.J. Høyer-Hansen, M. Hu, B. Hu, C.-A.A. Hu, H.-M. Hua, Y. Huang, C. Huang, J. Huang, S. Huang, W.-P. Huber, T.B. Huh, W.-K. Hung, T.-H. Hupp, T.R. Hur, G.M. Hurley, J.B. Hussain, S.N.A. Hussey, P.J. Hwang, J.J. Hwang, S. Ichihara, A. Ilkhanizadeh, S. Inoki, K. Into, T. Iovane, V. Iovanna, J.L. Ip, N.Y. Isaka, Y. Ishida, H. Isidoro, C. Isobe, K.-I. Iwasaki, A. Izquierdo, M. Izumi, Y. Jaakkola, P.M. Jäättelä, M. Jackson, G.R. Jackson, W.T. Janji, B. Jendrach, M. Jeon, J.-H. Jeung, E.-B. Jiang, H. Jiang, H. Jiang, J.X. Jiang, M. Jiang, Q. Jiang, X. Jiménez, A. Jin, M. Jin, S. Joe, C.O. Johansen, T. Johnson, D.E. Johnson, G.V.W. Jones, N.L. Joseph, B. Joseph, S.K. Joubert, A.M. Juhász, G. Juillerat-Jeanneret, L. Jung, C.H. Jung, Y.-K. Kaarniranta, K. Kaasik, A. Kabuta, T. Kadowaki, M. Kagedal, K. Kamada, Y. Kaminskyy, V.O. Kampinga, H.H. Kanamori, H. Kang, C. Kang, K.B. Il Kang, K. Kang, R. Kang, Y.-A. Kanki, T. Kanneganti, T.-D. Kanno, H. Kanthasamy, A.G. Kanthasamy, A. Karantza, V. Kaushal, G.P. Kaushik, S. Kawazoe, Y. Ke, P.-Y. Kehrl, J.H. Kelekar, A. Kerkhoff, C. Kessel, D.H. Khalil, H. Kiel, J.A.K.W. Kiger, A.A. Kihara, A. Kim, D.R. Kim, D.-H. Kim, D.-H. Kim, E.-K. Kim, H.-R. Kim, J.-S. Kim, J.H. Kim, J.C. Kim, J.K. Kim, P.K. Kim, S.W. Kim, Y.-S. Kim, Y. Kimchi, A. Kimmelman, A.C. King, J.S. Kinsella, T.J. Kirkin, V. Kirshenbaum, L.A. Kitamoto, K. Kitazato, K. Klein, L. Klimecki, W.T. Klucken, J. Knecht, E. Ko, B.C.B. Koch, J.C. Koga, H. Koh, J.-Y. Koh, Y.H. Koike, M. Komatsu, M. Kominami, E. Kong, H.J. Kong, W.-J. Korolchuk, V.I. Kotake, Y. Koukourakis, M.I. Kouri Flores, J.B. Kovács, A.L. Kraft, C. Krainc, D. Krämer, H. Kretz-Remy, C. Krichevsky, A.M. Kroemer, G. Krüger, R. Krut, O. Ktistakis, N.T. Kuan, C.-Y. Kucharczyk, R. Kumar, A. Kumar, R. Kumar, S. Kundu, M. Kung, H.-J. Kurz, T. Kwon, H.J. La Spada, A.R. Lafont, F. Lamark, T. Landry, J. Lane, J.D. Lapaquette, P. Laporte, J.F. László, L. Lavandero, S. Lavoie, J.N. Layfield, R. Lazo, P.A. Le, W. Le Cam, L. Ledbetter, D.J. Lee, A.J.X. Lee, B.-W. Lee, G.M. Lee, J. Lee, J.-H. Lee, M. Lee, M.-S. Lee, S.H. Leeuwenburgh, C. Legembre, P. Legouis, R. Lehmann, M. Lei, H.-Y. Lei, Q.-Y. Leib, D.A. Leiro, J. Lemasters, J.J. Lemoine, A. Lesniak, M.S. Lev, D. Levenson, V.V. Levine, B. Levy, E. Li, F. Li, J.-L. Li, L. Li, S. Li, W. Li, X.-J. Li, Y.-B. Li, Y.-P. Liang, C. Liang, Q. Liao, Y.-F. Liberski, P.P. Lieberman, A. Lim, H.J. Lim, K.-L. Lim, K. Lin, C.-F. Lin, F.-C. Lin, J. Lin, J.D. Lin, K. Lin, W.-W. Lin, W.-C. Lin, Y.-L. Linden, R. Lingor, P. Lippincott-Schwartz, J. Lisanti, M.P. Liton, P.B. Liu, B. Liu, C.-F. Liu, K. Liu, L. Liu, Q.A. Liu, W. Liu, Y.-C. Liu, Y. Lockshin, R.A. Lok, C.-N. Lonial, S. Loos, B. Lopez-Berestein, G. López-Otín, C. Lossi, L. Lotze, M.T. Lõw, P. Lu, B. Lu, B. Lu, B. Lu, Z. Luciano, F. Lukacs, N.W. Lund, A.H. Lynch-Day, M.A. Ma, Y. Macian, F. MacKeigan, J.P. Macleod, K.F. Madeo, F. Maiuri, L. Maiuri, M.C. Malagoli, D. Malicdan, M.C.V. Malorni, W. Man, N. Mandelkow, E.-M. Manon, S. Manov, I. Mao, K. Mao, X. Mao, Z. Marambaud, P. Marazziti, D. Marcel, Y.L. Marchbank, K. Marchetti, P. Marciniak, S.J. Marcondes, M. Mardi, M. Marfe, G. Mariño, G. Markaki, M. Marten, M.R. Martin, S.J. Martinand-Mari, C. Martinet, W. Martinez-Vicente, M. Masini, M. Matarrese, P. Matsuo, S. Matteoni, R. Mayer, A. Mazure, N.M. McConkey, D.J. McConnell, M.J. McDermott, C. McDonald, C. McInerney, G.M. McKenna, S.L. McLaughlin, B. McLean, P.J. McMaster, C.R. McQuibban, G.A. Meijer, A.J. Meisler, M.H. Meléndez, A. Melia, T.J. Melino, G. Mena, M.A. Menendez, J.A. Menna-Barreto, R.F.S. Menon, M.B. Menzies, F.M. Mercer, C.A. Merighi, A. Merry, D.E. Meschini, S. Meyer, C.G. Meyer, T.F. Miao, C.-Y. Miao, J.-Y. Michels, P.A.M. Michiels, C. Mijaljica, D. Milojkovic, A. Minucci, S. Miracco, C. Miranti, C.K. Mitroulis, I. Miyazawa, K. Mizushima, N. Mograbi, B. Mohseni, S. Molero, X. Mollereau, B. Mollinedo, F. Momoi, T. Monastyrska, I. Monick, M.M. Monteiro, M.J. Moore, M.N. Mora, R. Moreau, K. Moreira, P.I. Moriyasu, Y. Moscat, J. Mostowy, S. Mottram, J.C. Motyl, T. Moussa, C.E.-H. Müller, S. Muller, S. Münger, K. Münz, C. Murphy, L.O. Murphy, M.E. Musarò, A. Mysorekar, I. Nagata, E. Nagata, K. Nahimana, A. Nair, U. Nakagawa, T. Nakahira, K. Nakano, H. Nakatogawa, H. Nanjundan, M. Naqvi, N.I. Narendra, D.P. Narita, M. Navarro, M. Nawrocki, S.T. 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- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field. © 2012 Landes Bioscience.
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- 2012
29. Nicht-gentoxische Kanzerogene
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Schulte-Hermann, R., primary, Parzefall, W., additional, Bursch, W., additional, Ochs, H., additional, and Kraupp, B., additional
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- 1989
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30. Transforming growth factor-β 1 as a signal for induction of cell death by apoptosis.
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Bursch, W, Oberhammer, F, Jirtle, RL, Askari, M, Sedivy, R, Grasl-Kraupp, B, Purchio, AF, and Schulte-Hermann, R
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- 1993
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31. Guidelines for the use and interpretation of assays for monitoring autophagy.
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Harris, J, Harris, Sd, Hashimoto, M, Haspel, Ja, Hayashi, S, Hazelhurst, La, He, C, He, Yw, Hébert, Mj, Heidenreich, Ka, Helfrich, Mh, Helgason, Gv, Henske, Ep, Herman, B, Herman, Pk, Hetz, C, Hilfiker, S, Hill, Ja, Hocking, Lj, Hofman, P, Hofmann, Tg, Höhfeld, J, Holyoake, Tl, Hong, Mh, Hood, Da, Hotamisligil, G, Houwerzijl, Ej, Høyer-Hansen, M, Hu, B, Hu, Ca, Hu, Hm, Hua, Y, Huang, C, Huang, J, Huang, S, Huang, Wp, Huber, Tb, Huh, Wk, Hung, Th, Hupp, Tr, Hur, Gm, Hurley, Jb, Hussain, Sn, Hussey, Pj, Hwang, Jj, Hwang, S, Ichihara, A, Ilkhanizadeh, S, Inoki, K, Into, T, Iovane, V, Iovanna, Jl, Ip, Ny, Isaka, Y, Ishida, H, Isidoro, C, Isobe, K, Iwasaki, A, Izquierdo, M, Izumi, Y, Jaakkola, Pm, Jäättelä, M, Jackson, Gr, Jackson, Wt, Janji, B, Jendrach, M, Jeon, Jh, Jeung, Eb, Jiang, H, Jiang, Jx, Jiang, M, Jiang, Q, Jiang, X, Jiménez, A, Jin, M, Jin, S, Joe, Co, Johansen, T, Johnson, De, Johnson, Gv, Jones, Nl, Joseph, B, Joseph, Sk, Joubert, Am, Juhász, G, Juillerat-Jeanneret, L, Jung, 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Kurz, T, Kwon, Hj, La Spada, Ar, Lafont, F, Lamark, T, Landry, J, Lane, Jd, Lapaquette, P, Laporte, Jf, László, L, Lavandero, S, Lavoie, Jn, Layfield, R, Lazo, Pa, Le, W, Le Cam, L, Ledbetter, Dj, Lee, Aj, Lee, Bw, Lee, Gm, Lee, J, Lee, Jh, Lee, M, Lee, Sh, Leeuwenburgh, C, Legembre, P, Legouis, R, Lehmann, M, Lei, Hy, Lei, Qy, Leib, Da, Leiro, J, Lemasters, Jj, Lemoine, A, Lesniak, M, Lev, D, Levenson, Vv, Levine, B, Levy, E, Li, F, Li, Jl, Li, L, Li, S, Li, W, Li, Xj, Li, Yb, Li, Yp, Liang, C, Liang, Q, Liao, Yf, Liberski, Pp, Lieberman, A, Lim, Hj, Lim, Kl, Lim, K, Lin, Cf, Lin, Fc, Lin, J, Lin, Jd, Lin, K, Lin, Ww, Lin, Wc, Lin, Yl, Linden, R, Lingor, P, Lippincott-Schwartz, J, Lisanti, Mp, Liton, Pb, Liu, B, Liu, Cf, Liu, K, Liu, L, Liu, Qa, Liu, W, Liu, Yc, Liu, Y, Lockshin, Ra, Lok, Cn, Lonial, S, Loos, B, Lopez-Berestein, G, López-Otín, C, Lossi, L, Lotze, Mt, Lőw, P, Lu, B, Lu, Z, Luciano, F, Lukacs, Nw, Lund, Ah, Lynch-Day, Ma, Ma, Y, Macian, F, Mackeigan, Jp, Macleod, Kf, Madeo, F, Maiuri, L, Maiuri, Mc, Malagoli, D, Malicdan, Mc, Malorni, W, Man, N, Mandelkow, Em, Manon, S, Manov, I, Mao, K, Mao, X, Mao, Z, Marambaud, P, Marazziti, D, Marcel, Yl, Marchbank, K, Marchetti, P, Marciniak, Sj, Marcondes, M, Mardi, M, Marfe, G, Mariño, G, Markaki, M, Marten, Mr, Martin, Sj, Martinand-Mari, C, Martinet, W, Martinez-Vicente, M, Masini, M, Matarrese, P, Matsuo, S, Matteoni, R, Mayer, A, Mazure, Nm, Mcconkey, Dj, Mcconnell, Mj, Mcdermott, C, Mcdonald, C, Mcinerney, Gm, Mckenna, Sl, Mclaughlin, B, Mclean, Pj, Mcmaster, Cr, Mcquibban, Ga, Meijer, Aj, Meisler, Mh, Meléndez, A, Melia, Tj, Melino, G, Mena, Ma, Menendez, Ja, Menna-Barreto, Rf, Menon, Mb, Menzies, Fm, Mercer, Ca, Merighi, A, Merry, De, Meschini, S, Meyer, Cg, Meyer, Tf, Miao, Cy, Miao, Jy, Michels, Pa, Michiels, C, Mijaljica, D, Milojkovic, A, Minucci, S, Miracco, C, Miranti, Ck, Mitroulis, I, Miyazawa, K, Mizushima, N, Mograbi, B, Mohseni, S, Molero, X, Mollereau, B, Mollinedo, F, Momoi, T, Monastyrska, I, Monick, Mm, Monteiro, Mj, Moore, Mn, Mora, R, Moreau, K, Moreira, Pi, Moriyasu, Y, Moscat, J, Mostowy, S, Mottram, Jc, Motyl, T, Moussa, Ce, Müller, S, Muller, S, Münger, K, Münz, C, Murphy, Lo, Murphy, Me, Musarò, A, Mysorekar, I, Nagata, E, Nagata, K, Nahimana, A, Nair, U, Nakagawa, T, Nakahira, K, Nakano, H, Nakatogawa, H, Nanjundan, M, Naqvi, Ni, Narendra, Dp, Narita, M, Navarro, M, Nawrocki, St, Nazarko, Ty, Nemchenko, A, Netea, Mg, Neufeld, Tp, Ney, Pa, Nezis, Ip, Nguyen, Hp, Nie, D, Nishino, I, Nislow, C, Nixon, Ra, Noda, T, Noegel, Aa, Nogalska, A, Noguchi, S, Notterpek, L, Novak, I, Nozaki, T, Nukina, N, Nürnberger, T, Nyfeler, B, Obara, K, Oberley, Td, Oddo, S, Ogawa, M, Ohashi, T, Okamoto, K, Oleinick, Nl, Oliver, Fj, Olsen, Lj, Olsson, S, Opota, O, Osborne, Tf, Ostrander, Gk, Otsu, K, Ou, Jh, Ouimet, M, Overholtzer, M, Ozpolat, B, Paganetti, P, Pagnini, U, Pallet, N, Palmer, Ge, Palumbo, C, Pan, T, Panaretakis, T, Pandey, Ub, Papackova, Z, Papassideri, I, Paris, I, Park, J, Park, Ok, Parys, Jb, Parzych, Kr, Patschan, S, Patterson, C, Pattingre, S, Pawelek, Jm, Peng, J, Perlmutter, Dh, Perrotta, I, Perry, G, Pervaiz, S, Peter, M, Peters, Gj, Petersen, M, Petrovski, G, Phang, Jm, Piacentini, M, Pierre, P, Pierrefite-Carle, V, Pierron, G, Pinkas-Kramarski, R, Piras, A, Piri, N, Platanias, Lc, Pöggeler, S, Poirot, M, Poletti, A, Poüs, C, Pozuelo-Rubio, M, Prætorius-Ibba, M, Prasad, A, Prescott, M, Priault, M, Produit-Zengaffinen, N, Progulske-Fox, A, Proikas-Cezanne, T, Przedborski, S, Przyklenk, K, Puertollano, R, Puyal, J, Qian, Sb, Qin, L, Qin, Zh, Quaggin, Se, Raben, N, Rabinowich, H, Rabkin, Sw, Rahman, I, Rami, A, Ramm, G, Randall, G, Randow, F, Rao, Va, Rathmell, Jc, Ravikumar, B, Ray, Sk, Reed, Bh, Reed, Jc, Reggiori, F, Régnier-Vigouroux, A, Reichert, A, Reiners JJ, Jr, Reiter, Rj, Ren, J, Revuelta, Jl, Rhodes, Cj, Ritis, K, Rizzo, E, Robbins, J, Roberge, M, Roca, H, Roccheri, Mc, Rocchi, S, Rodemann, Hp, Rodríguez de Córdoba, S, Rohrer, B, Roninson, Ib, Rosen, K, Rost-Roszkowska, Mm, Rouis, M, Rouschop, Km, Rovetta, F, Rubin, Bp, Rubinsztein, Dc, Ruckdeschel, K, Rucker EB, 3rd, Rudich, A, Rudolf, E, Ruiz-Opazo, N, Russo, R, Rusten, Te, Ryan, Km, Ryter, Sw, Sabatini, Dm, Sadoshima, J, Saha, T, Saitoh, T, Sakagami, H, Sakai, Y, Salekdeh, Gh, Salomoni, P, Salvaterra, Pm, Salvesen, G, Salvioli, R, Sanchez, Am, Sánchez-Alcázar, Ja, Sánchez-Prieto, R, Sandri, M, Sankar, U, Sansanwal, P, Santambrogio, L, Saran, S, Sarkar, S, Sarwal, M, Sasakawa, C, Sasnauskiene, A, Sass, M, Sato, K, Sato, M, Schapira, Ah, Scharl, M, Schätzl, Hm, Scheper, W, Schiaffino, S, Schneider, C, Schneider, Me, Schneider-Stock, R, Schoenlein, Pv, Schorderet, Df, Schüller, C, Schwartz, Gk, Scorrano, L, Sealy, L, Seglen, Po, Segura-Aguilar, J, Seiliez, I, Seleverstov, O, Sell, C, Seo, Jb, Separovic, D, Setaluri, V, Setoguchi, T, Settembre, C, Shacka, Jj, Shanmugam, M, Shapiro, Im, Shaulian, E, Shaw, Rj, Shelhamer, Jh, Shen, Hm, Shen, Wc, Sheng, Zh, Shi, Y, Shibuya, K, Shidoji, Y, Shieh, Jj, Shih, Cm, Shimada, Y, Shimizu, S, Shintani, T, Shirihai, O, Shore, Gc, Sibirny, Aa, Sidhu, Sb, Sikorska, B, Silva-Zacarin, Ec, Simmons, A, Simon, Ak, Simon, Hu, Simone, C, Simonsen, A, Sinclair, Da, Singh, R, Sinha, D, Sinicrope, Fa, Sirko, A, Siu, Pm, Sivridis, E, Skop, V, Skulachev, Vp, Slack, R, Smaili, S, Smith, Dr, Soengas, M, Soldati, T, Song, X, Sood, Ak, Soong, Tw, Sotgia, F, Spector, Sa, Spies, Cd, Springer, W, Srinivasula, Sm, Stefanis, L, Steffan, J, Stendel, R, Stenmark, H, Stephanou, A, Stern, St, Sternberg, C, Stork, B, Strålfors, P, Subauste, C, Sui, X, Sulzer, D, Sun, J, Sun, Sy, Sun, Zj, Sung, Jj, Suzuki, K, Suzuki, T, Swanson, M, Swanton, C, Sweeney, St, Sy, Lk, Szabadkai, G, Tabas, I, Taegtmeyer, H, Tafani, M, Takács-Vellai, K, Takano, Y, Takegawa, K, Takemura, G, Takeshita, F, Talbot, Nj, Tan, K, Tanaka, K, Tang, D, Tanida, I, Tannous, Ba, Tavernarakis, N, Taylor, G, Taylor, Ga, Taylor, Jp, Terada, L, Terman, A, Tettamanti, G, Thevissen, K, Thompson, Cb, Thorburn, A, Thumm, M, Tian, F, Tian, Y, Tocchini-Valentini, G, Tolkovsky, Am, Tomino, Y, Tönges, L, Tooze, Sa, Tournier, C, Tower, J, Towns, R, Trajkovic, V, Travassos, Lh, Tsai, Tf, Tschan, Mp, Tsubata, T, Tsung, A, Turk, B, Turner, L, Tyagi, Sc, Uchiyama, Y, Ueno, T, Umekawa, M, Umemiya-Shirafuji, R, Unni, Vk, Vaccaro, Mi, Valente, Em, Van den Berghe, G, van der Klei, Ij, van Doorn, W, van Dyk, Lf, van Egmond, M, van Grunsven, La, Vandenabeele, P, Vandenberghe, Wp, Vanhorebeek, I, Vaquero, Ec, Velasco, G, Vellai, T, Vicencio, Jm, Vierstra, Rd, Vila, M, Vindis, C, Viola, G, Viscomi, Maria Teresa, Voitsekhovskaja, Ov, von Haefen, C, Votruba, M, Wada, K, Wade-Martins, R, Walker, Cl, Walsh, Cm, Walter, J, Wan, Xb, Wang, A, Wang, C, Wang, D, Wang, F, Wang, G, Wang, H, Wang, Hg, Wang, Hd, Wang, J, Wang, K, Wang, M, Wang, Rc, Wang, X, Wang, Yj, Wang, Y, Wang, Z, Wang, Zc, Wansink, Dg, Ward, Dm, Watada, H, Waters, Sl, Webster, P, Wei, L, Weihl, Cc, Weiss, Wa, Welford, Sm, Wen, Lp, Whitehouse, Ca, Whitton, Jl, Whitworth, Aj, Wileman, T, Wiley, Jw, Wilkinson, S, Willbold, D, Williams, Rl, Williamson, Pr, Wouters, Bg, Wu, C, Wu, Dc, Wu, Wk, Wyttenbach, A, Xavier, Rj, Xi, Z, Xia, P, Xiao, G, Xie, Z, Xu, Dz, Xu, J, Xu, L, Xu, X, Yamamoto, A, Yamashina, S, Yamashita, M, Yan, X, Yanagida, M, Yang, D, Yang, E, Yang, Jm, Yang, Sy, Yang, W, Yang, Wy, Yang, Z, Yao, Mc, Yao, Tp, Yeganeh, B, Yen, Wl, Yin, Jj, Yin, Xm, Yoo, Oj, Yoon, G, Yoon, Sy, Yorimitsu, T, Yoshikawa, Y, Yoshimori, T, Yoshimoto, K, You, Hj, Youle, Rj, Younes, A, Yu, L, Yu, Sw, Yu, Wh, Yuan, Zm, Yue, Z, Yun, Ch, Yuzaki, M, Zabirnyk, O, Silva-Zacarin, E, Zacks, D, Zacksenhaus, E, Zaffaroni, N, Zakeri, Z, Zeh HJ, 3rd, Zeitlin, So, Zhang, H, Zhang, Hl, Zhang, J, Zhang, Jp, Zhang, L, Zhang, My, Zhang, Xd, Zhao, M, Zhao, Yf, Zhao, Y, Zhao, Zj, Zheng, X, Zhivotovsky, B, Zhong, Q, Zhou, Cz, Zhu, C, Zhu, Wg, Zhu, Xf, Zhu, X, Zhu, Y, Zoladek, T, Zong, Wx, Zorzano, A, Zschocke, J, Zuckerbraun, B., and Viscomi M. T. (ORCID:0000-0002-9096-4967)
- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused o
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- 2012
32. A cell's agony of choice: how to cross the Styx? : From morphological to molecular approaches to disclose its decision.
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Bursch W
- Subjects
- Apoptosis, Cell Line, Tumor, Homeostasis physiology, Humans, Necrosis, Nuclear Proteins, Autophagy, Intracellular Signaling Peptides and Proteins, Phagocytosis physiology
- Abstract
The original "apoptosis-necrosis" concept was based on morphology and (patho)physiological conditions of the occurrence of cell death: (1) apoptosis, with nuclear and cytoplasmic condensation/fragmentation prominent, exclusion of autolysis, considered to result from coordinated self-destruction of a cell; (2) necrosis, with cell lysis prominent, caused by violent environmental perturbation leading to collapse of internal homeostasis. This suggestion initiated a controversial discussion within the scientific community and it soon became clear that the "apoptosis-necrosis dichotomy" was not generally applicable. Nowadays, there is sufficient evidence that cells may activate diverse suicide pathways, thereby allowing a flexible response to environmental changes, either physiological or pathological. The present paper commemorates electron microscopic and cytochemical studies on cell death of cultured human mammary carcinoma cells performed by Adi Ellinger, adding a significant contribution to recognize that autophagy can be involved in regulated cell death, thereby challenging the apoptosis-necrosis dichotomy still predominant in the 1990s.
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- 2018
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33. Clearance of dying autophagic cells of different origin by professional and non-professional phagocytes.
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Petrovski, G., Zahuczky, G., Katona, K., Vereb, G., Martinet, W., Nemes, Z., Bursch, W., and Fésüs, L.
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KILLER cells ,CELLULAR mechanics ,TAMOXIFEN ,PHAGOCYTES ,AUTOPHAGY ,ANTINEOPLASTIC agents ,ESTROGEN antagonists ,CANCER treatment - Abstract
MCF-7 cells undergo autophagic death upon tamoxifen treatment. Plated on non-adhesive substratum these cells died by anoikis while inducing autophagy as revealed by monodansylcadaverine staining, elevated light-chain-3 expression and electron microscopy. Both de novo and anoikis-derived autophagic dying cells were engulfed by human macrophages and MCF-7 cells. Inhibition of autophagy by 3-methyladenine abolished engulfment of cells dying through de novo autophagy, but not those dying through anoikis. Blocking exposure of phosphatidylserine (PS) on both dying cell types inhibited phagocytosis by MCF-7 but not by macrophages. Gene expression profiling showed that though both types of phagocytes expressed full repertoire of the PS recognition and signaling pathway, macrophages could evolve during engulfment of de novo autophagic cells the potential of calreticulin-mediated processes as well. Our data suggest that cells dying through autophagy and those committing anoikis with autophagy may engage in overlapping but distinct sets of clearance mechanisms in professional and non-professional phagocytes.Cell Death and Differentiation (2007) 14, 1117–1128. doi:10.1038/sj.cdd.4402112; published online 16 March 2007 [ABSTRACT FROM AUTHOR]
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- 2007
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34. The autophagosomal–lysosomal compartment in programmed cell death.
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Bursch, W
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CELL death ,PROTEOLYTIC enzymes - Abstract
In the last decade a tremendous progress has been achieved in understanding the control of apoptosis by survival and death factors as well as the molecular mechanisms of preparation and execution of the cell's suicide. However, accumulating evidence suggests that programmed cell death (PCD) is not confined to apoptosis but that cells use different pathways for active self-destruction as reflected by different morphology: condensation prominent, type I or apoptosis; autophagy prominent, type II; etc. Autophagic PCD appears to be a phylogenetically old phenomenon, it may occur in physiological and disease states. Recently, distinct biochemical and molecular features have been be assigned to this type of PCD. However, autophagic and apoptotic PCD should not be considered as mutually exclusive phenomena. Rather, they appear to reflect a high degree of flexibility in a cell's response to changes of environmental conditions, both physiological or pathological. Furthermore, recent data suggest that diverse or relatively unspecific signals such as photodamage or lysosomotropic agents may be mediatd by lysosomal cysteine proteases (cathepsins) to caspases and thus, apoptosis. The present paper reviews morphological, functional and biochemical/molecular data suggesting the participation of the autophagosomal-lysosomal compartment in programmed cell death. [ABSTRACT FROM AUTHOR]
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- 2001
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35. Active cell death induced by the antiestrogens Tamoxifen and ICI 164 384 in juman mammary carcinoma cells (MCF-7) in culture
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Bursch, W., Ellinger, A., Kienzl, H., Torok, L., Pandey, S., Walker, P., Sikorska, Marianna, and Schulte-Hermann, R.
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- 1996
36. Apoptosis in stages of mouse hepatocarcinogenesis: Failure to counterbalance cell proliferation and to account for strain differences in tumor susceptibility
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UCL - Autre, Bursch, W., Chabicovsky, M, Wastl, U, Grasl-Kraupp, B, Bukowska, K, Taper, Henryk, Schulte-Hermann, R, 41st Congress of the European-Societies-of-Toxicology, UCL - Autre, Bursch, W., Chabicovsky, M, Wastl, U, Grasl-Kraupp, B, Bukowska, K, Taper, Henryk, Schulte-Hermann, R, and 41st Congress of the European-Societies-of-Toxicology
- Abstract
C3H/He and B6C3F1 show much higher liver cancer susceptibility than C57BL/6J mice. We studied the hypothesis that this difference might result from failure of apoptosis. Hepatocarcinogenesis was induced by a single dose of N-nitrosodiethylamine (NDEA), followed by phenobarbital (PB) for up to 90 weeks. We observed (1) earlier appearance of putative preneoplastic foci (PPF), hepatocellular adenoma (HCA), and carcinoma (HCC) in C3H/He than in C57Bl/6J mice and (2) an increase of hepatocellular DNA synthesis in C3H/He and C57Bl/6J mice, compared to normal liver, via PPF and HCA to HCC. PB enhanced DNA synthesis and growth of PPF, in the C3H/He strain only, and of HCA and HCC of both strains. Apoptoses were rare in unaltered livers as well as in preneoplastic lesions, but tended to increase in HCA and HCC of both strains. PB lowered apoptotic activity in PPF of C3H/He mice, but enhanced it in HCA and HCC of C57Bl/6J mice at late stages. In conclusion, the strain difference in growth rates of PPF and tumors is largely determined by higher rates of cell proliferation in C3H/He mice, with and without promotion by PB. Moreover, in C57Bl/6J mice the promoting effect of PB was restricted to HCA and HCC and was not seen in PPF. Apoptosis was generally low and was not a major cause of the strain difference in tumor susceptibility. In contrast with rat liver, inhibition of apoptosis appears to be a minor determinant of tumor promotion in mice.
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- 2005
37. Role of apoptosis for mouse liver growth regulation and tumor promotion: comparative analysis of mice with high (C3H/He) and low (C57Bl/6J) cancer susceptibility
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UCL - Autre, Bursch, W., Grasl-Kraupp, B., Wastl, U., Hufnagl, K., Chabicovsky, M., Taper, Henryk, Schulte-Hermann, R., UCL - Autre, Bursch, W., Grasl-Kraupp, B., Wastl, U., Hufnagl, K., Chabicovsky, M., Taper, Henryk, and Schulte-Hermann, R.
- Abstract
Apoptosis constitutes one of the organisms defense lines against cancer. We investigated whether failure of apoptosis may be concurrently causative for the high cancer Susceptibility in C3H/He as compared to C57BL/6J mice (low cancer susceptibility). First, in short-term in vivo experiments (7-21 days), mouse liver growth (C3H/He, C57BL/6J) was induced by administration of phenobarbital (PB; 2 days 500 ppm + 5 days 750 ppm via the food) or nafenopin (NAF; 7 days 500 ppm via the food), cessation of PB or NAF treatment served to initiate liver involution. Liver weight, DNA content, hepatocyte ploidy and apoptotic activity were studied as endpoints. Secondly, in a long-term study liver carcinogenesis was initiated by a single dose of N-nitrosodiethylamine (NDEA, 90 mg/kg b.w.) to 5-weeks-old C57B1/6J and C3H/He mice. After 2 weeks, mice received either standard diet or a diet containing phenobarbital (PB, 90 mg/kg b.w.) for up to 90 weeks. Cell proliferation and apoptosis in normal liver tissue and (pre)neoplastic tissue was quantitatively analysed by histological means. The short term studies revealed that PB and NAF-induced mouse liver growth is essentially due to cell enlargement (hypertrophy). A moderate increase of liver DNA content was brought about by hepatocellular polyploidization; C3H/He mice exhibited the most pronounced ploidy shift, corresponding to their high cancer susceptibility. Upon cessation of PB or NAF treatment, regression of liver mass was neither associated with a loss of DNA nor an increase in apoptoses in the liver of C3H/He and C57B1/6J mice; food restriction did not enforce the occurrence of apoptosis. Thus, the mouse strains did not differ with respect to the occurrence of apoptosis. In the long-term study, PB promoted liver tumor formation in all strains, exhibiting quantitative differences in growth kinetics of preneoplasia rather than a specific biological quality. Quantitative analysis of apoptosis in normal and (pre)neoplastic liver ti
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- 2004
38. EFSA'S risk assessment of bisphenol A in food
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Castoldi, A.F., primary, Bursch, W., additional, Husoy, T., additional, Mennes, W., additional, Pratt, I., additional, Reuter, U., additional, Testai, E., additional, and Woelfle, D., additional
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- 2011
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39. Induction of apoptosis in mouse liver adenoma and carcinoma in vivo by transforming growth factor-beta 1
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UCL, Chabicovsky, M, Wastl, U, Taper, Henryk, Grasl-Kraupp, B, Schulte-Hermann, R, Bursch, W., UCL, Chabicovsky, M, Wastl, U, Taper, Henryk, Grasl-Kraupp, B, Schulte-Hermann, R, and Bursch, W.
- Abstract
Purpose. In the liver, transforming growth factor beta-1 (TGF-beta1) constitutes a major negative growth regulating factor involved in the control of cell numbers; failure of this control mechanism has been associated with the development of liver cancer. Since no reports on the in vivo effects of exogenously administered TGF-beta1 on apoptosis in liver tumors have been published yet, we studied hepatocyte sensitivity to the proapoptotic action of TGF-beta1 in stages of chemically induced mouse liver carcinogenesis. Methods. Mouse liver carcinogenesis was initiated by a single dose of N-nitrosodiethylamine (NDEA, 90 mg/kg b.w., i.p.) to 5-week-old B6C3F1 mice. After 2 weeks, mice received either standard diet or a diet containing phenobarbital (PB, 90 mg/kg b.w) for 85 weeks. Four hours before being killed mice received a single dose of TGF-beta1 (56 mug or 200 mug TGF-beta1/kg of b.w., injected into the tail vein). Quantitative histological analysis of mitosis and apoptosis in normal liver tissue (NL), putative preneoplastic foci (PPF), hepatocellular adenoma (HCA), and hepatocellular carcinoma (HCC) was performed on H&E-stained liver sections. Results. In NDEA and NDEA + PB-treated mice, NL exhibited a very low incidence of apoptosis and mitosis, which increased in HCA and HCC. In the lesions apoptoses ranged between 0.03 and 0.6%. Two hundred micrograms of TGF-beta1/kg stimulated apoptoses in NL as well as in neoplastic lesions (significant increase in NL, HCA, and HCC); the most pronounced proapoptotic action of TGF-ss1 was observed in lesions of NDEA+PB pretreated mice (about 1.7%). Fifty-six mug TGF-beta1/kg had no detectable effect on apoptosis. Conclusion. These observations indicate that during chemically induced liver carcinogenesis in B6C3F1 mice basal rates of apoptoses in adenoma and carcinoma are higher than in normal liver and can be further increased by a proapoptotic cytokine.
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- 2003
40. Monitoring, removal and risk assessment of cytostatic drugs in hospital wastewater
- Author
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Lenz, K., primary, Mahnik, S.N., primary, Weissenbacher, N., primary, Mader, R.M., primary, Krenn, P., primary, Hann, S., primary, Koellensperger, G., primary, Uhl, M., primary, Knasmüller, S., primary, Ferk, F., primary, Bursch, W., primary, and Fuerhacker, M., primary
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- 2007
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41. Programmed Cell Death (PCD): Apoptosis, Autophagic PCD, or Others?
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BURSCH, W., primary, ELLINGER, A., additional, GERNER, CH., additional, FRÖHWEIN, U., additional, and SCHULTE-HERMANN, R., additional
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- 2006
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42. Multiple cell death programs: Charon’s lifts to Hades
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BURSCH, W, primary
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- 2004
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43. Endocrine disrupters in the aquatic environment: the Austrian approach - ARCEM
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Bursch, W., primary, Fuerhacker, M., primary, Gemeiner, M., primary, Grillitsch, B., primary, Jungbauer, A., primary, Kreuzinger, N., primary, Moestl, E., primary, Scharf, S., primary, Schmid, E., primary, Skutan, S., primary, and Walter, I., primary
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- 2004
- Full Text
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44. Expression of cytochrome P450 2A5 in preneoplastic and neoplastic mouseliver lesions.
- Author
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Wastl, UM, Rossmanith, W, Lang, MA, Camus-Randon, AM, Grasl-Kraupp, B, Bursch, W, Schulte-Hermann, R, Wastl, UM, Rossmanith, W, Lang, MA, Camus-Randon, AM, Grasl-Kraupp, B, Bursch, W, and Schulte-Hermann, R
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- 1998
45. Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression
- Author
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UCL, GraslKraupp, B, RuttkayNedecky, B, Mullauer, L, Taper, Henryk, Huber, Winfrid, Bursch, W., Schultehermann, R., UCL, GraslKraupp, B, RuttkayNedecky, B, Mullauer, L, Taper, Henryk, Huber, Winfrid, Bursch, W., and Schultehermann, R.
- Abstract
We quantitatively assessed rates of cell replication and of apoptosis during the development and regression of liver cancer. In rats, apoptotic activity gradually increased from normal liver to putative preneoplastic foci (PPF), to hepatocellular adenoma (HCA), and to hepatocellular carcinoma (HCC). At all stages, rates of cell replication were higher than of apoptosis, allowing a preferential net gain of (pre)neoplastic cells. As in rats, in human HCC, birth and death rates were increased manifold, indicating a species independent phenomenon. Implications of the increasing cell turnover were studied in rats using the administration and withdrawal of nafenopin (NAF), a liver mitogen and nongenotoxic carcinogen. Prolonged NAF treatment enhanced cell number in normal liver by 25%, while PPF and liver tumors were amplified at least 100-fold. After stopping NAF treatment, cell replication ceased, while cell elimination by apoptosis was increased in normal and (pre)neoplastic liver. HCA and HCC showed the most pronounced shifts from replication toward apoptosis. As a result, 5 weeks after halting NAF, 20% of cells in normal liver, but about 85% of (pre)neoplastic lesions including HCC, were eliminated. The implications of these findings include that nongenotoxic carcinogens can act as survival factors even for malignant cells. Furthermore, tumor cells not only exhibit excessive proliferation, but also undergo apoptosis at rates that far exceed those in normal tissue. Therefore, inhibition of cell death by the survival activity of nongenotoxic carcinogens results in selective growth of (pre)neoplastic lesions. On the other hand, blockade of survival effects leads to excessive apoptosis in (pre)neoplasia and seems promising as a therapeutic concept for the selective elimination of (liver) cancer.
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- 1997
46. Effects of Non-Genotoxic Hepatocarcinogens Phenobarbital and Nafenopin on Phenotype and Growth of Different Populations of Altered Foci in Rat Liver.
- Author
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Schulte-Hermann, R., Kraupp-Grasl, B., Bursch, W., Gerbracht, U., and Timmermann-Trosiener, I.
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- 1989
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47. Apoptosis in human colorectal tumours: ultrastructure and quantitative studies on tissue localization and association with bak expression.
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Partik, Gerda, Kahl-Rainer, Patrizia, Sedivy, Roland, Ellinger, Adolf, Bursch, Wilfried, Marian, B., Partik, G, Kahl-Rainer, P, Sedivy, R, Ellinger, A, and Bursch, W
- Abstract
Apoptotic cell death in human tumours has been demonstrated by electron and light microscopy. In adenomas, fragmented and apoptotic nuclei and signs of phagocytosis have been observed close to the basement membrane. In carcinomas the characteristic structures were apoptotic bodies with small fragments of chromatin. DNA fragmentation was shown by in situ end-labelling. Quantitative assessment of apoptosis and proliferation revealed a high apoptotic index (AI) in all types of adenoma (tubular: 1.77+/-0.35%, tubulovillous: 2.38+/-0.41%; villous: 3.3+/-0.39%) as well as loss of compartmentalization of proliferating and dying cells. In carcinomas a shift towards proliferation was evident, as shown by lower AIs than in adenomas (0.9+/-0.68% and 1.1+/-0.12% for moderately and poorly differentiated tumours), higher Ki67 indices (38.32+/-2.23% and 57+/-3.89%, respectively) and higher mitosis (0.9+/-0.56% and 1.21+/-0.17%, respectively). However, apoptosis was observed in all tumours and is available as a target for therapeutic intervention. Expression of the apoptosis related proteins bcl-2 and bak also reflected loss of compartmentalization. While bcl-2 did not show a consistent relationship to AI in tumour specimens, bak was positively correlated with apoptosis in 4 of 8 adenomas and 4 of 7 carcinomas, suggesting a role for this protein in the induction of apoptosis in a subset of tumours. [ABSTRACT FROM AUTHOR]
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- 1998
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48. Apoptosis and Hepatocarcinogenesis.
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Schulte-Hermann, R., Hufnagl, K., Löw-Baselli, A., Rossmanith, W., Wagner, A., Ruttkay-Nedecky, B., Bursch, W., Müllauer, L., Parzefall, W., and Grasl-Kraupp, B.
- Subjects
LIVER cancer ,APOPTOSIS ,CELL death ,PRECANCEROUS conditions ,LIVER diseases - Abstract
Cells may die by active mechanisms (cellular suicide). The concept of active cell death goes back to the 19th and early 20th century [1]. Active or programmed cell death serves to eliminate excessive cells, e.g. from hyperplastic organs, or cells damaged by moderate injury. Morphologically and biochemically, mechanisms of active cell death may be diVerent in diVerent organs and in different physiological states. Apoptosis (type I) is characterized by cytoplasmic and nuclear condensation, fragmentation, and heterophagy [2]; in type II cell death autophagic/lysosomal processes are prominent which produce cytoplasmic degradation well before nuclear alterations [3, 4]. [ABSTRACT FROM AUTHOR]
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- 1998
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49. 9th Euroconference on Apoptosis
- Author
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Bursch, W, primary and Fesus, L, additional
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- 2002
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50. Autophagic and apoptotic types of programmed cell death exhibit different fates of cytoskeletal filaments
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Bursch, W., primary, Hochegger, K., additional, Torok, L., additional, Marian, B., additional, Ellinger, A., additional, and Hermann, R.S., additional
- Published
- 2000
- Full Text
- View/download PDF
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