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382 results on '"Erdmann, F"'

1. Incidence patterns, survival probabilities, and second primary neoplasms after retinoblastoma among children in Germany, 1981-2018: A nationwide assessment based on data from the German Childhood Cancer Registry

Author

Grabow, D, Ressing, M, Spix, C, Jung, I, Trübenbach, C, Wellbrock, M, Ketteler, P, Eggert, A, Reinhardt, D, Lohmann, D, Bechrakis, N, Biewald, E, Ronckers, CM, Erdmann, F, Grabow, D, Ressing, M, Spix, C, Jung, I, Trübenbach, C, Wellbrock, M, Ketteler, P, Eggert, A, Reinhardt, D, Lohmann, D, Bechrakis, N, Biewald, E, Ronckers, CM, and Erdmann, F

Published
2024

4. Antistaphylococcal evaluation of indole–naphthalene hybrid analogs

Author

Ashraf K, Yasrebi K, Adeniyi ET, Hertlein T, Ohlsen K, Lalk M, Erdmann F, and Hilgeroth A

Subjects
structure-dependent activity, lead structure, antibacterial activity, compound evaluation, MRSA, Therapeutics. Pharmacology, RM1-950
Abstract

Kerolos Ashraf,1 Kaveh Yasrebi,1 Emmanuel Tola Adeniyi,2 Tobias Hertlein,2 Knut Ohlsen,2 Michael Lalk,3 Frank Erdmann,1 Andreas Hilgeroth1 1Institute of Pharmacy, Martin Luther University Halle-Wittenberg, Halle, Germany; 2Institute of Molecular Infection Biology, Julius Maximilians University Würzburg, Würzburg, Germany; 3Institute of Biochemistry, Ernst Moritz Arndt University Greifswald, Greifswald, Germany Abstract: Resistance developments against established antibiotics are an emerging problem for antibacterial therapies. Infections with Staphylococcus aureus and methicillin-resistant S. aureus (MRSA) have become more difficult to treat with standard antibiotics that often fail, especially against MRSA. In consequence, novel antibiotics are urgently needed. Antibiotics from natural sources own complicated structures that cause difficulties for a chemical synthetic production. We developed novel small-molecule antibacterials that are easily accessible in a simple one-pot synthesis. The central indolonaphthalene core is substituted with indole residues at various positions. Both the varied indole substitutions and their positions at the molecular scaffold influence the determined antibacterial activity against the evaluated Staphylococcus strains. Best activities have been found for 5-chloro, -cyano, and -hydroxyl indole substitutions. Therefore, first promising lead compounds could be identified that are nontoxic in human HEK and SH-SY5Y cells and exceed the activity of used standard antibiotics, especially against MRSA. Keywords: structure-dependent activity, lead structure, antibacterial activity, compound evaluation, MRSA

Published
2019

6. Long-term survival and cure fraction estimates for childhood cancer in Europe (EUROCARE-6): results from a population-based study

Author

Botta, L, Gatta, G, Capocaccia, R, Stiller, C, Canete, A, Dal Maso, L, Innos, K, Mihor, A, Erdmann, F, Spix, C, Lacour, B, Marcos-Gragera, R, Murray, D, Rossi, S, Hackl, M, Van Eycken, E, Van Damme, N, Valerianova, Z, Sekerija, M, Scoutellas, V, Demetriou, A, Dusek, L, Krejci, D, Storm, H, Magi, M, Paapsi, K, Malila, N, Pitkaniemi, J, Jooste, V, Clavel, J, Poulalhon, C, Desandes, E, Monnereau, A, Katalinic, A, Petridou, E, Markozannes, G, Garami, M, Birgisson, H, Walsh, P, Mazzoleni, G, Vittadello, F, Cuccaro, F, Galasso, R, Sampietro, G, Rosso, S, Gasparotto, C, Maifredi, G, Ferrante, M, Torrisi, A, Sutera Sardo, A, Gambino, M, Lanzoni, M, Ballotari, P, Giacomazzi, E, Ferretti, S, Caldarella, A, Manneschi, G, Sant, M, Baili, P, Berrino, F, Trama, A, Lillini, R, Bernasconi, A, Bonfarnuzzo, S, Vener, C, Didone, F, Lasalvia, P, Del Monego, G, Buratti, L, Serraino, D, Taborelli, M, De Angelis, R, Demuru, E, Di Benedetto, C, Santaquilani, M, Venanzi, S, Tallon, M, Boni, L, Iacovacci, S, Russo, A, Gervasi, F, Spagnoli, G, Cavalieri d'Oro, L, Fusco, M, Vitale, M, Usala, M, Vitale, F, Michiara, M, Chiranda, G, Sacerdote, C, Maule, M, Cascone, G, Spata, E, Mangone, L, Falcini, F, Cavallo, R, Piras, D, Dinaro, Y, Castaing, M, Fanetti, A, Minerba, S, Candela, G, Scuderi, T, Rizzello, R, Stracci, F, Tagliabue, G, Rugge, M, Brustolin, A, Pildava, S, Smailyte, G, Azzopardi, M, Johannesen, T, Didkowska, J, Wojciechowska, U, Bielska-Lasota, M, Pais, A, Ferreira, A, Bento, M, Miranda, A, Safaei Diba, C, Zadnik, V, Zagar, T, Sanchez-Contador Escudero, C, Franch Sureda, P, Lopez de Munain, A, De-La-Cruz, M, Rojas, M, Aleman, A, Vizcaino, A, Almela, F, Sanvisens, A, Sanchez, M, Chirlaque, M, Sanchez-Gil, A, Guevara, M, Ardanaz, E, Canete-Nieto, A, Peris-Bonet, R, Galceran, J, Carulla, M, Kuehni, C, Redmond, S, Visser, O, Karim-Kos, H, Stevens, S, Gavin, A, Morrison, D, Huws, D, Botta L., Gatta G., Capocaccia R., Stiller C., Canete A., Dal Maso L., Innos K., Mihor A., Erdmann F., Spix C., Lacour B., Marcos-Gragera R., Murray D., Rossi S., Hackl M., Van Eycken E., Van Damme N., Valerianova Z., Sekerija M., Scoutellas V., Demetriou A., Dusek L., Krejci D., Storm H., Magi M., Paapsi K., Malila N., Pitkaniemi J., Jooste V., Clavel J., Poulalhon C., Desandes E., Monnereau A., Katalinic A., Petridou E., Markozannes G., Garami M., Birgisson H., Walsh P. M., Mazzoleni G., Vittadello F., Cuccaro F., Galasso R., Sampietro G., Rosso S., Gasparotto C., Maifredi G., Ferrante M., Torrisi A., Sutera Sardo A., Gambino M. L., Lanzoni M., Ballotari P., Giacomazzi E., Ferretti S., Caldarella A., Manneschi G., Sant M., Baili P., Berrino F., Trama A., Lillini R., Bernasconi A., Bonfarnuzzo S., Vener C., Didone F., Lasalvia P., Del Monego G., Buratti L., Serraino D., Taborelli M., De Angelis R., Demuru E., Di Benedetto C., Santaquilani M., Venanzi S., Tallon M., Boni L., Iacovacci S., Russo A. G., Gervasi F., Spagnoli G., Cavalieri d'Oro L., Fusco M., Vitale M. F., Usala M., Vitale F., Michiara M., Chiranda G., Sacerdote C., Maule M., Cascone G., Spata E., Mangone L., Falcini F., Cavallo R., Piras D., Dinaro Y., Castaing M., Fanetti A. C., Minerba S., Candela G., Scuderi T., Rizzello R. V., Stracci F., Tagliabue G., Rugge M., Brustolin A., Pildava S., Smailyte G., Azzopardi M., Johannesen T. B., Didkowska J., Wojciechowska U., Bielska-Lasota M., Pais A., Ferreira A. M., Bento M. J., Miranda A., Safaei Diba C., Zadnik V., Zagar T., Sanchez-Contador Escudero C., Franch Sureda P., Lopez de Munain A., De-La-Cruz M., Rojas M. D., Aleman A., Vizcaino A., Almela F., Sanvisens A., Sanchez M. J., Chirlaque M. D., Sanchez-Gil A., Guevara M., Ardanaz E., Canete-Nieto A., Peris-Bonet R., Galceran J., Carulla M., Kuehni C., Redmond S., Visser O., Karim-Kos H., Stevens S., Gavin A., Morrison D., Huws D. W., Botta, L, Gatta, G, Capocaccia, R, Stiller, C, Canete, A, Dal Maso, L, Innos, K, Mihor, A, Erdmann, F, Spix, C, Lacour, B, Marcos-Gragera, R, Murray, D, Rossi, S, Hackl, M, Van Eycken, E, Van Damme, N, Valerianova, Z, Sekerija, M, Scoutellas, V, Demetriou, A, Dusek, L, Krejci, D, Storm, H, Magi, M, Paapsi, K, Malila, N, Pitkaniemi, J, Jooste, V, Clavel, J, Poulalhon, C, Desandes, E, Monnereau, A, Katalinic, A, Petridou, E, Markozannes, G, Garami, M, Birgisson, H, Walsh, P, Mazzoleni, G, Vittadello, F, Cuccaro, F, Galasso, R, Sampietro, G, Rosso, S, Gasparotto, C, Maifredi, G, Ferrante, M, Torrisi, A, Sutera Sardo, A, Gambino, M, Lanzoni, M, Ballotari, P, Giacomazzi, E, Ferretti, S, Caldarella, A, Manneschi, G, Sant, M, Baili, P, Berrino, F, Trama, A, Lillini, R, Bernasconi, A, Bonfarnuzzo, S, Vener, C, Didone, F, Lasalvia, P, Del Monego, G, Buratti, L, Serraino, D, Taborelli, M, De Angelis, R, Demuru, E, Di Benedetto, C, Santaquilani, M, Venanzi, S, Tallon, M, Boni, L, Iacovacci, S, Russo, A, Gervasi, F, Spagnoli, G, Cavalieri d'Oro, L, Fusco, M, Vitale, M, Usala, M, Vitale, F, Michiara, M, Chiranda, G, Sacerdote, C, Maule, M, Cascone, G, Spata, E, Mangone, L, Falcini, F, Cavallo, R, Piras, D, Dinaro, Y, Castaing, M, Fanetti, A, Minerba, S, Candela, G, Scuderi, T, Rizzello, R, Stracci, F, Tagliabue, G, Rugge, M, Brustolin, A, Pildava, S, Smailyte, G, Azzopardi, M, Johannesen, T, Didkowska, J, Wojciechowska, U, Bielska-Lasota, M, Pais, A, Ferreira, A, Bento, M, Miranda, A, Safaei Diba, C, Zadnik, V, Zagar, T, Sanchez-Contador Escudero, C, Franch Sureda, P, Lopez de Munain, A, De-La-Cruz, M, Rojas, M, Aleman, A, Vizcaino, A, Almela, F, Sanvisens, A, Sanchez, M, Chirlaque, M, Sanchez-Gil, A, Guevara, M, Ardanaz, E, Canete-Nieto, A, Peris-Bonet, R, Galceran, J, Carulla, M, Kuehni, C, Redmond, S, Visser, O, Karim-Kos, H, Stevens, S, Gavin, A, Morrison, D, Huws, D, Botta L., Gatta G., Capocaccia R., Stiller C., Canete A., Dal Maso L., Innos K., Mihor A., Erdmann F., Spix C., Lacour B., Marcos-Gragera R., Murray D., Rossi S., Hackl M., Van Eycken E., Van Damme N., Valerianova Z., Sekerija M., Scoutellas V., Demetriou A., Dusek L., Krejci D., Storm H., Magi M., Paapsi K., Malila N., Pitkaniemi J., Jooste V., Clavel J., Poulalhon C., Desandes E., Monnereau A., Katalinic A., Petridou E., Markozannes G., Garami M., Birgisson H., Walsh P. M., Mazzoleni G., Vittadello F., Cuccaro F., Galasso R., Sampietro G., Rosso S., Gasparotto C., Maifredi G., Ferrante M., Torrisi A., Sutera Sardo A., Gambino M. L., Lanzoni M., Ballotari P., Giacomazzi E., Ferretti S., Caldarella A., Manneschi G., Sant M., Baili P., Berrino F., Trama A., Lillini R., Bernasconi A., Bonfarnuzzo S., Vener C., Didone F., Lasalvia P., Del Monego G., Buratti L., Serraino D., Taborelli M., De Angelis R., Demuru E., Di Benedetto C., Santaquilani M., Venanzi S., Tallon M., Boni L., Iacovacci S., Russo A. G., Gervasi F., Spagnoli G., Cavalieri d'Oro L., Fusco M., Vitale M. F., Usala M., Vitale F., Michiara M., Chiranda G., Sacerdote C., Maule M., Cascone G., Spata E., Mangone L., Falcini F., Cavallo R., Piras D., Dinaro Y., Castaing M., Fanetti A. C., Minerba S., Candela G., Scuderi T., Rizzello R. V., Stracci F., Tagliabue G., Rugge M., Brustolin A., Pildava S., Smailyte G., Azzopardi M., Johannesen T. B., Didkowska J., Wojciechowska U., Bielska-Lasota M., Pais A., Ferreira A. M., Bento M. J., Miranda A., Safaei Diba C., Zadnik V., Zagar T., Sanchez-Contador Escudero C., Franch Sureda P., Lopez de Munain A., De-La-Cruz M., Rojas M. D., Aleman A., Vizcaino A., Almela F., Sanvisens A., Sanchez M. J., Chirlaque M. D., Sanchez-Gil A., Guevara M., Ardanaz E., Canete-Nieto A., Peris-Bonet R., Galceran J., Carulla M., Kuehni C., Redmond S., Visser O., Karim-Kos H., Stevens S., Gavin A., Morrison D., and Huws D. W.

Abstract

Background: The EUROCARE-5 study revealed disparities in childhood cancer survival among European countries, giving rise to important initiatives across Europe to reduce the gap. Extending its representativeness through increased coverage of eastern European countries, the EUROCARE-6 study aimed to update survival progress across countries and years of diagnosis and provide new analytical perspectives on estimates of long-term survival and the cured fraction of patients with childhood cancer. Methods: In this population-based study, we analysed 135 847 children (aged 0–14 years) diagnosed during 2000–13 and followed up to the end of 2014, recruited from 80 population-based cancer registries in 31 European countries. We calculated age-adjusted 5-year survival differences by country and over time using period analysis, for all cancers combined and for major cancer types. We applied a variant of standard mixture cure models for survival data to estimate the cure fraction of patients by childhood cancer and to estimate projected 15-year survival. Findings: 5-year survival for all childhood cancer combined in Europe in 2010–14 was 81% (95% CI 81–82), showing an increase of three percentage points compared with 2004–06. Significant progress over time was observed for almost all cancers. Survival remained stable for osteosarcomas, Ewing sarcoma, Burkitt lymphoma, non-Hodgkin lymphomas, and rhabdomyoscarcomas. For all cancers combined, inequalities still persisted among European countries (with age-adjusted 5-year survival ranging from 71% [95% CI 60–79] to 87% [77–93]). The 15-year survival projection for all patients with childhood cancer diagnosed in 2010–13 was 78%. We estimated the yearly long-term mortality rate due to causes other than the diagnosed cancer to be around 2 per 1000 patients for all childhood cancer combined, but to approach zero for retinoblastoma. The cure fraction for patients with childhood cancer increased over time from 74% (95% CI 73–75) in 1998–

Published
2022

7. RENAL TRANSPLANTATION IN THE INBRED RAT

Author

Suehadeh, I H, Guttmann, R D, Lindquist, R R, and Rodriguez-Erdmann, F

Abstract

Modification of renal allograft rejection in rats was attempted by using drugs presumed to interfere with some secondary tissue damage reactions. Acetylsalicylic acid and sodium salicylate were used to modify platelet behavior, and heparin and bishydroxycoumarin were used to inhibit fibrin deposition. The assay system revealed, significant retention of venal function on the 7th postoperative day following treatment with acetylsalicylic acid or sodium salicylate despite the persistence of platelet aggregates and fibrin deposition m the allograft. Similarly, heparin, but not bishydroxycoumarin, in nearly lethal doses resulted in the modification of the usual pattern of allograft rejection. It is concluded that, while interference with some of the secondary effects involved in allograft rejection may alter the degree of tissue damage, control of rejection requires inhibition of primary immunological events.

Published
2024

9. Age-, sex- and disease subtype–related foetal growth differentials in childhood acute myeloid leukaemia risk: A Childhood Leukemia International Consortium analysis

Author

Karalexi, M.A. Dessypris, N. Ma, X. Spector, L.G. Marcotte, E. Clavel, J. Pombo-de-Oliveira, M.S. Heck, J.E. Roman, E. Mueller, B.A. Hansen, J. Auvinen, A. Lee, P.-C. Schüz, J. Magnani, C. Mora, A.M. Dockerty, J.D. Scheurer, M.E. Wang, R. Bonaventure, A. Kane, E. Doody, D.R. Baka, M. Moschovi, M. Polychronopoulou, S. Kourti, M. Hatzipantelis, E. Pelagiadis, I. Dana, H. Kantzanou, M. Tzanoudaki, M. Anastasiou, T. Grenzelia, M. Gavriilaki, E. Sakellari, I. Anagnostopoulos, A. Kitra, V. Paisiou, A. Bouka, E. Nikkilä, A. Lohi, O. Erdmann, F. Kang, A.Y. Metayer, C. Milne, E. Petridou, E.T. NARECHEM-ST Group FRECCLE Group

Abstract

Aim: Evidence for an association of foetal growth with acute myeloid leukaemia (AML) is inconclusive. AML is a rare childhood cancer, relatively more frequent in girls, with distinct features in infancy. In the context of the Childhood Leukemia International Consortium (CLIC), we examined the hypothesis that the association may vary by age, sex and disease subtype using data from 22 studies and a total of 3564 AML cases. Methods: Pooled estimates by age, sex and overall for harmonised foetal growth markers in association with AML were calculated using the International Fetal and Newborn Growth Consortium for the 21st Century Project for 17 studies contributing individual-level data; meta-analyses were, thereafter, conducted with estimates provided ad hoc by five more studies because of administrative constraints. Subanalyses by AML subtype were also performed. Results: A nearly 50% increased risk was observed among large-for-gestational-age infant boys (odds ratio [OR]: 1.49, 95% confidence interval [CI]: 1.03–2.14), reduced to 34% in boys aged

Published
2020

13. Abstracts

Author

Kaatsch, Hans-Jürgen, Püschel, K., Heinemann, A., Klaas, Jakob, Graß, Hildegard, Staak, Michael, Benthaus, S., Vock, R., Brinkmann, B., Temme, O., Daldrup, T., Dilger, M., Fink, T., Rittner, Ch., Thali, Michael J., Braun, M., Brueschweiler, W., Kneubuehl, B. P., Vock, P., Wirth, J., Dirnhofer, R., Bohnert, M., Berger, H., Buck, U., Pollak, S., Gotta, J. C., Erdmann, F., Riße, M., Schütz, H., Weiler, G., Pragst, F., Auwärter, V., Sporkcrt, F., Roewer, L., Willuweit, S., Kayser, M., Nagy, M., de Knijff, P., Geserick, G., Augustin, C., Betz, A., Carracedo, A., Corach, D., Dupuy, B. M., Gusmaõ, L., Henke, L., Hidding, M., Kärgel, H. J., Lessig, R., Liebeherr, E., Parson, W., Pascali, V. L., Rolf, B., Schneider, P. M., Dobosz, T., Teifel-Greding, J., Krawczak, M., Bauer, M., Patzelt, D., Kuznik, J., Bondy, B., Eisenmenger, W., Möller, H. -J., Zehner, R., Niess, C., Amendt, J., Krettek, R., Weinmann, W., Görner, M., Goerke, R., Mahler, H., Fowinkel, C., Haarhoff, K., Schmidt, P., Schmolke, C., Mußhoff, F., Menzen, M., Prohaska, C., Madea, B., Kauert, G., Gleicher, S., Drasch, G., von Meyer, L., Roider, G., Quitterer, D., Kröner, L., Toennes, S. W., Jurowich, S., Käferstein, H., Sticht, G., Gilg, T., Priemer, F., Jocham, N., Fechner, G., Ortmann, Ch., Schulte, T., Nieschalk, M., Weirich, V., Rummel, J., Rentsch, D., Wegener, R., Berehaus, G., Graß, H., Grellner, W., Rettig-Stürmer, A., Kühn-Becker, H., Georg, T., Möller, M., Wilske, J., Kemmerling, R., Sachs, H., Menting, T., Musshoff, F., Schoenemeier, S., Bürrig, K. -F., Jacob, B., Bonte, W., Maeda, H., Zhu, B. -L., Fujita, M. Q., Quan, L., Ishida, K., Taniguchi, M., Böhme, B., Rauch, E., Penning, R., Amberg, R., Blackwell, C. C., Pelz, K., Meier, V., Saternus, K. -S., Gessler, F., Böhnel, H., Bouska, I., Toupalík, P., Klir, P., Kleemann, W. J., Ast, F., Beck, U., Debertin, S., Giebe, B., Heide, S., Sperhake, J., Poets, C. F., Weis, C., Schlaud, M., Bajanowski, T., Wedekind, H., Breithardt, G., Debertin, A. S., Tönjes, H., Tschernig, T., Pabst, R., Tröger, H. D., Krill, A., Hame, M., Bouška, I., Ježková, J., Kernbach-Wighton, G., Wense, A. v. d., Kijewski, H., Goeke, M., Weber, B., Staak, M., Dettmeyer, R., Driever, F., Becker, A., Wiestler, O. D., Verhoff, M. A., Woenckhaus, J., Hauri-Bionda, R., Strehler, M., Bär, W., Ohshima, T., Takayasu, T., Kondo, T., Sato, Y., Tarbah, Fuad A., Mahler, Hellmut, Temme, Oliver, Daldrup, Thomas, Pötsch, Lucia, Emmerich, Patricia, Skopp, Gisela, Andresen, H., Schmoldt, A., Thurau, K., Vogt, S., Große-Perdekamp, M., Pufal, E., Sykutera, M., Rochholz, G., Lis, G., Sliwka, K., Zörntlein, S., Röhrich, J., Pötsch, L., Becker, J., Mattern, Rainer, Yamamoto, Yoshiko, Hayase, Tamaki, Yamamoto, Keiichi, Piette, Michel H. A., De Letter, Els A., Cordonnier, Jan, Schultes, A., Pluisch, F., Darok, M., Kollroser, M., Mannweiler, S., Babel, B., Magerl, H., Mahfoud, B., Stein, S., Iwersen-Bergmann, S., Risser, D., Hönigschnabl, S., Stichenwirth, M., Sebald, D., Kaff, A., Schneider, B., Vycudilik, W., Bauer, G., Reitz, E., Kimont, H. -G., Molnár, A., Jeszenszky, E., Benkó, A., Száz, E., Varga, T., Mayr, N. P., Schmidbauer, S., Hallfeldt, K., Bank, A., Iffland, R., Schuff, A., Fischer, T., Weingarten, Y., Alt, A., Janda, I., Wurst, F. M., Seidl, S., Seitler, C., Haag-Dawoud, Munira, Beike, J., Vennemann, B., Köhler, H., Hendreich, F. -I., Giebe, W., Reimann, I., Werner, R., Klein, A., Schulz, K., Feischer, D., Erfurt, Ch., Arnold, R., Winnefeld, K., Riepert, T., Iffland, R., Longauer, F., Kardošovå, V., Anders, S., Hildebrand, E., Schulz, F., Möbus, U., Jaroß, W., Wittig, H., Schmidt, U., Hauptmann, K., Krause, D., Prudlow, B., Rohner, T., Molz, G., Früchtnicht, W., Hoppe, B., Henßge, C., Althaus, L., Herbst, J., Preiß, U., Stein, C., Glenewinkel, F., Leinzinger, E. P., Lászik, A., Soós, M., Hubay, M., Sótonyi, P., Schliff, A., Gatternig, R., Hering, S., Edelmann, J., Plate, I., Michael, M., Kuhlisch, E., Szibor, R., von Wurmb, N., Hammer, U., Meissner, D., Kirches, E., Dietzmann, K., Pfeiffer, H., Ortmann, C., Meißner, C., Mohamed, S. A., Warnk, H., Gehlsen-Lorenzen, A., Oehmichen, M., Heidorn, F., Henkel, R., Schulz, M. M., Reichert, W., Mattern, R., Baasner, A., Banaschak, S., Schäfer, C., Benecke, M., Reibe, S., Barksdale, Larry, Sundermeier, Jon, Ratcliffe, Brett C., Lutz, S., Hohoff, C., Schürenkamp, M., Kahle, C., Fieguth, A., Ritz-Timme, S., Laumeier, I., Schütz, H. W., Schulte-Mönting, J., Chaudri, S., Welti, M., Dittmann, V., Olze, A., Schmeling, A., Reisinger, W., Klotzbach, H., Gabriel, P., Demir, T., Huckenbeck, W., Reuhl, J., Schuster, R., Maxeiner, H., Bockholdt, B., Jachau, K., Kuchheuser, W., Försterling, T., Ehrlich, E., Besselmann, M., Du Chesne, A., Albrecht, U. -V., Guan, D. W., Dreßler, J., Voigtmann, K., Müller, E., Vieler, S., Kirchner, A., Humpert, M., Breitmeier, D., Mansouri, F., Wyler, D., Marty, W., Sigrist, Th., Zollinger, U., Meyer, U., Allmen, G. v., Karger, B., Hoekstra, A., Stehmann, B., Schmidt, P. F., Peschel, O., Vollmar, C., Szeimies, U., Rothschild, M. A., Kegel, D., Klatt, A., Klatt, C., Briese, B. -H., Schyma, C., Schyma, P., Angetter, Daniela, Perdekamp, M. Große, Sun, Y., Guttenberge, R., Riede, U. -N., Poetsch, M., Seefeldt, S., Maschke, M., Lignitz, E., Zeller, M., Wehner, H. -D., Czarnetzki, A., Blin, N., Bender, K., Emmerich, P., Pádár, Zs., Egyed, B., Kemény, G., Woller, J., Füredi, S., Balogh, I., Cremer, U., Scheil, H. -G., Schiwy-Bochat, K. -H., Althoff, H., Immel, U. -D., Tatschner, Th., Lang, C., Versmold, D., Reineke, Th., Mall, G., Dahlmann, F., Büttner, A., Hubig, M., Rötzscher, K., Grundmann, C., Oritani, S., Peter, J., Popov, V., Olejnik, V., Khokhlov, V. D., Stiller, D., Romanowski, U., Kleiber, M., Klupp, N., Mortinger, H., Chadová, L., Bouška, I., Toupalik, P., Schnabel, A., Lutz, F. -U., Crivellaro, A., Strauch, H., Dan, Dermengiu, Silvia, Dermengiu, Buda, Octavian, Kandolf, R., Kaiser, R., Eis-Hübinger, A. M., Kobek, M., Jankowski, Z., Rygol, K., Kulikowska, J., Martin, H., Kolbow, K., Keil, W., Wang, Huijun, Ding, Yanqing, Huang, Guangzhao, Wu, Zhongbi, Wehner, F., Subke, J., Zdravkovic, M., Otasevic, V., Rostov, M., Karadzic, R., Kildüschov, E. M., Buromski, I. W., Plaksin, W. O., Wendland, A., Spiridonow, W. A., Sabusow, J. G., Kalinin, J. P., Heide, S., Schmidt, V., Wiegand, P., Kleiber, M., Demmler, G., Zack, F., Reischle, S., Schönpflug, M., Beier, G., Berchtenbreiter, C., Lackner, K., Jendrusch, B., Wolf, H., Buhmann, D., Summa, H., Matschke, J., Stürenburg, H. J., Junge, M., Wischhusen, F., Müldner, C., Schröder, A., Kaiser, E., Lasczkowski, G., Hofbauer, V., Eberl, N., Thomson, H., Tatschner, T., Milz, S., Gazov, E., Trübner, K., Brenner, M., Tsokos, M., Anders, S., Paulsen, F., Reith, K., Bratzke, H., Schapfeld, R., Graefe-Kirci, U., Stiller, D., Trübner, K., and Schäfer, A. Th.

Published
2000
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14. The impact of childhood cancer on parents' socio-economic situation-A systematic review

Author

Roser, K., Erdmann, F., Michel, G., Winther, J.F., and Mader, L.

Abstract

OBJECTIVE: Taking care of children diagnosed with cancer may have considerable consequences on parents' socio-economic situation. Our systematic review aimed to evaluate and synthesise the evidence on the impact of childhood cancer on parents' socio-economic situation. METHODS: Systematic literature searches for articles published between January 2000 and January 2019 were performed in PubMed, Scopus, and PsycINFO. Findings of eligible articles were narratively synthesised and quality appraised. RESULTS: Our systematic review included 35 eligible articles. Childhood cancer had a substantial impact on parents' socio-economic situation across all studies. This impact varied largely by geographical region. We observed a high prevalence of disruptions in parental employment such as job quitting or job loss, particularly among mothers. The associated income losses further contributed to families' perceived financial burden in addition to increased cancer-related expenses. Adverse socio-economic consequences were most pronounced shortly after diagnosis, however, persisted into early survivorship for certain groups of parents. We identified families of children diagnosed with haematological cancers, younger age at diagnosis, and lower parental socio-economic position to be at particular risk for adverse socio-economic consequences. CONCLUSIONS: Following the child's cancer diagnosis, parents experience a broad range of adverse socio-economic consequences. Further effort is needed to systematically implement an assessment of financial hardship in paediatric oncology together with appropriate support services along the cancer trajectory.

Published
2019

15. Coffee and tea consumption during pregnancy and risk of childhood acute myeloid leukemia: A Childhood Leukemia International Consortium (CLIC) study

Author

Karalexi, M.A. Dessypris, N. Clavel, J. Metayer, C. Erdmann, F. Orsi, L. Kang, A.Y. Schüz, J. Bonaventure, A. Greenop, K.R. Milne, E. Petridou, E.T.

Abstract

Background: Dietary habits during pregnancy have been inconsistently linked to childhood acute myeloid leukemia (AML), given the putative intrauterine onset of the disease as a result of triggering events during the critical period of fetal hematopoiesis. We investigated the potential association of maternal coffee and tea consumption during pregnancy with childhood AML risk, pooling primary data from eight case-control studies participating in the Childhood Leukemia International Consortium. Methods: Information on coffee and/or tea consumption was available for 444 cases and 1255 age- and sex-matched controls, on coffee consumption for 318 cases and 971 controls and on tea consumption for 388 cases and 932 controls. Categories for cups of daily coffee/tea consumption were created in order to explore potential dose-response associations. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression. Results: Associations were found neither in the analysis on coffee or tea nor in the analysis on coffee only consumption (any versus no). A positive association with increasing coffee intake was observed (>1 cup per day; OR: 1.40, 95% CI: 1.03–1.92, increment of one cup per day; OR: 1.18, 95% CI: 1.01–1.39). No associations were observed with tea consumption. Interaction analyses showed non-significant associations between coffee/tea and smoking. Hyperdiploidy was inversely associated with tea consumption, with other cytogenetic markers having no association with coffee/tea. Conclusion: Given the widespread consumption of caffeinated beverages among pregnant women, our finding is of important public health relevance, suggesting adverse effects of maternal coffee consumption during pregnancy in the offspring. © 2019

Published
2019

16. Parental occupational exposure to low-frequency magnetic fields and risk of leukaemia in the offspring: Findings from the Childhood Leukaemia International Consortium (CLIC)

Author

Talibov, M. Olsson, A. Bailey, H. Erdmann, F. Metayer, C. Magnani, C. Petridou, E. Auvinen, A. Spector, L. Clavel, J. Roman, E. Dockerty, J. Nikkilä, A. Lohi, O. Kang, A. Psaltopoulou, T. Miligi, L. Vila, J. Cardis, E. Schüz, J.

Abstract

Objectives Previously published studies on parental occupational exposure to extremely low-frequency magnetic fields (ELF-MF) and risk of acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML) in their offspring were inconsistent. We therefore evaluated this question within the Childhood Leukemia International Consortium. Methods We pooled 11 case-control studies including 9723 childhood leukaemia cases and 17 099 controls. Parental occupational ELF-MF exposure was estimated by linking jobs to an ELF-MF job-exposure matrix (JEM). Logistic regression models were used to estimate ORs and 95% CIs in pooled analyses and meta-analyses. Results ORs from pooled analyses for paternal ELF-MF exposure >0.2 microtesla (μT) at conception were 1.04 (95% CI 0.95 to 1.13) for ALL and 1.06 (95% CI 0.87 to 1.29) for AML, compared with ≤0.2 μT. Corresponding ORs for maternal ELF-MF exposure during pregnancy were 1.00 (95% CI 0.89 to 1.12) for ALL and 0.85 (95% CI 0.61 to 1.16) for AML. No trends of increasing ORs with increasing exposure level were evident. Furthermore, no associations were observed in the meta-analyses. Conclusions In this large international dataset applying a comprehensive quantitative JEM, we did not find any associations between parental occupational ELF-MF exposure and childhood leukaemia. © © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

Published
2019

17. Parental age and the risk of childhood acute myeloid leukemia: results from the Childhood Leukemia International Consortium

Author

Panagopoulou, P. Skalkidou, A. Marcotte, E. Erdmann, F. Ma, X. Heck, J.E. Auvinen, A. Mueller, B.A. Spector, L.G. Roman, E. Metayer, C. Magnani, C. Pombo-de-Oliveira, M.S. Scheurer, M.E. Mora, A.-M. Dockerty, J.D. Hansen, J. Kang, A.Y. Wang, R. Doody, D.R. Kane, E. Schüz, J. Christodoulakis, C. Ntzani, E. Petridou, E.T. FRECCLE group NARECHEM-ST group

Abstract

Background: Parental age has been associated with several childhood cancers, albeit the evidence is still inconsistent. Aim: To examine the associations of parental age at birth with acute myeloid leukemia (AML) among children aged 0–14 years using individual-level data from the Childhood Leukemia International Consortium (CLIC) and non-CLIC studies. Material/methods: We analyzed data of 3182 incident AML cases and 8377 controls from 17 studies [seven registry-based case-control (RCC) studies and ten questionnaire-based case-control (QCC) studies]. AML risk in association with parental age was calculated using multiple logistic regression, meta-analyses, and pooled-effect estimates. Models were stratified by age at diagnosis (infants

Published
2019

20. Advanced parental age as risk factor for childhood acute lymphoblastic leukemia: results from studies of the Childhood Leukemia International Consortium

Author

Petridou, E.T. Georgakis, M.K. Erdmann, F. Ma, X. Heck, J.E. Auvinen, A. Mueller, B.A. Spector, L.G. Roman, E. Metayer, C. Magnani, C. Pombo-de-Oliveira, M.S. Ezzat, S. Scheurer, M.E. Mora, A.M. Dockerty, J.D. Hansen, J. Kang, A.Y. Wang, R. Doody, D.R. Kane, E. Rashed, W.M. Dessypris, N. Schüz, J. Infante-Rivard, C. Skalkidou, A.

Abstract

Advanced parental age has been associated with adverse health effects in the offspring including childhood (0–14 years) acute lymphoblastic leukemia (ALL), as reported in our meta-analysis of published studies. We aimed to further explore the association using primary data from 16 studies participating in the Childhood Leukemia International Consortium. Data were contributed by 11 case–control (CC) studies (7919 cases and 12,942 controls recruited via interviews) and five nested case–control (NCC) studies (8801 cases and 29,690 controls identified through record linkage of population-based health registries) with variable enrollment periods (1968–2015). Five-year paternal and maternal age increments were introduced in two meta-analyses by study design using adjusted odds ratios (OR) derived from each study. Increased paternal age was associated with greater ALL risk in the offspring (OR CC 1.05, 95% CI 1.00–1.11; OR NCC 1.04, 95% CI 1.01–1.07). A similar positive association with advanced maternal age was observed only in the NCC results (OR CC 0.99, 95% CI 0.91–1.07, heterogeneity I 2 = 58%, p = 0.002; OR NCC 1.05, 95% CI 1.01–1.08). The positive association between parental age and risk of ALL was most marked among children aged 1–5 years and remained unchanged following mutual adjustment for the collinear effect of the paternal and maternal age variables; analyses of the relatively small numbers of discordant paternal-maternal age pairs were not fully enlightening. Our results strengthen the evidence that advanced parental age is associated with increased childhood ALL risk; collinearity of maternal with paternal age complicates causal interpretation. Employing datasets with cytogenetic information may further elucidate involvement of each parental component and clarify underlying mechanisms. © 2018, Springer Science+Business Media B.V., part of Springer Nature.

Published
2018

28. PO-124 Childhood Leukemia International Consortium (CLIC) Studies Report Diffrential Associations of Advanced Parental Age with Childhood Acute Lymphoblastic Leukemia

Author

Petridou, E., Georgakis, M., Erdmann, F., Ezzat, S., Mora, A.M., Dessypris, N., Schüz, J., Infante-Rivard, C., Skalkidou, Alkistis, C.S.G. CLIC Studies Group,, Petridou, E., Georgakis, M., Erdmann, F., Ezzat, S., Mora, A.M., Dessypris, N., Schüz, J., Infante-Rivard, C., Skalkidou, Alkistis, and C.S.G. CLIC Studies Group,

Abstract

Background/Objectives:Advanced parental age has beenassociated with adverse health effects in the offspring includ-ing childhood (0-14 years) acute lymphoblastic leukemia(ALL), as reported in our meta-analysis of published stud-ies. Primary data from 16 studies participating in theChildhood Leukemia International Consortium provide aunique methodological opportunity to further explore thisassociation.Design/Methods:Data from 11 case-control (CC) studies(7919 cases; 12942 interviewed controls) and five nested case-control (NCC) studies (8801 cases; 29690 controls recordlinked via population-based registries) with enrollment peri-ods ranging from 1968 to 2015 were used. Adjusted oddsratios (OR) were derived from each study using five-yearpaternal and maternal age increments and introduded in twometa-analyses by CC or NCC study design.Results:Advancement of paternal age was associated withstatistically significant higher risk for ALL in the off-spring (ORCC:1.05; ORNCC:1.04) and advanced mater-nal age only in the NCC (ORNCC:1.05). By contrast, theresults were heterogeneous in CC studies (ORCC:0.99, 95%CI:0.91-1.07, heterogeneityI2=58%,p=0.002). The positive association between parental age and risk of ALL was moreevident in the age group among 1-5 years and remainedunchanged after mutual adjustment for the collinear effect ofthe paternal and maternal age variables. We further performedanalyses of the relatively small numbers of discordant pater-nal and maternal age pairs to explore the collinear effect ofparental age but the results were not fully enlightening.Conclusions:The results of this larger ever dataset of primarydata allowing for separate analysis by study design and bettercontrol of selection bias in CC studies strengthen the evidencethat advanced parental age is associated with increased child-hood ALL risk. The observational study design and ollinear-ity of maternal with paternal age complicate causal interpre-tation. Employing datasets with cytogenetic inf

Published
2018
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30. Caesarean delivery and risk of childhood leukaemia: A pooled analysis from the Childhood Leukemia International Consortium (CLIC)

Author

Marcotte, E.L. Thomopoulos, T.P. Infante-Rivard, C. Clavel, J. Petridou, E.T. Schüz, J. Ezzat, S. Dockerty, J.D. Metayer, C. Magnani, C. Scheurer, M.E. Mueller, B.A. Mora, A.M. Wesseling, C. Skalkidou, A. Rashed, W.M. Francis, S.S. Ajrouche, R. Erdmann, F. Orsi, L. Spector, L.G.

Subjects
reproductive and urinary physiology
Abstract

Background: Results from case-control studies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children born by caesarean delivery, and prelabour caesarean delivery in particular; however, an association of method of delivery with childhood leukaemia subtypes has yet to be established. We therefore did a pooled analysis of data to investigate the association between childhood leukaemia and caesarean delivery. Methods: We pooled data from 13 case-control studies from the Childhood Leukemia International Consortium done in nine countries (Canada, Costa Rica, Egypt, France, Germany, Greece, Italy, New Zealand, and the USA) for births from 1970-2013. We analysed caesarean delivery overall and by indications that probably resulted in prelabour caesarean delivery or emergency caesarean delivery. We used multivariable logistic regression models, adjusted for child's birthweight, sex, age, ethnic origin, parental education, maternal age, and study, to estimate odds ratios (ORs) and 95% CIs for the risk of ALL and acute myeloid leukaemia (AML) in children aged 0-14 years at diagnosis. Findings: The studies provided data for 8780 ALL cases, 1332 AML cases, and 23 459 controls, of which the birth delivery method was known for 8655 (99%) ALL cases, 1292 (97%) AML cases, and 23 351 (>99%) controls. Indications for caesarean delivery were available in four studies (there were caesarean deliveries for 1061 of 4313 ALL cases, 138 of 664 AML cases, and 1401 of 5884 controls). The OR for all indications of caesarean delivery and ALL was 1·06 (95% CI 0·99-1·13), and was significant for prelabour caesarean delivery and ALL (1·23 [1·04-1·47]; p=0·018). Emergency caesarean delivery was not associated with ALL (OR 1·02 [95% CI 0·81-1·30]). AML was not associated with caesarean delivery (all indications OR 0·99 [95% CI 0·84-1·17]; prelabour caesarean delivery 0·83 [0·54-1·26]; and emergency caesarean delivery 1·05 [0·63-1·77]). Interpretation: Our results suggest an increased risk of childhood ALL after prelabour caesarean delivery. If this association is causal, maladaptive immune activation due to an absence of stress response before birth in children born by prelabour caesarean delivery could be considered as a potential mechanism. Funding: National Cancer Institute. © 2016 Elsevier Ltd.

Published
2016

33. Mupirocin-Empfindlichkeit klinischer Staphylokokkenisolate in Deutschland

Author

Strommenger, B, Layer, F, Ziegler, S, Erdmann, F, Klare, I, and Werner, G

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Mupirocin ist ein topisches Antibiotikum, das vorwiegend für die MRSA-Sanierung bei kolonisierten Patienten und medizinischem Personal eingesetzt wird. Seine antibakterielle Wirkung ist auf die Hemmung der bakteriellen Isoleucyl-fRNA-synthetase (IleRS) mit Inhibierung der Proteinsynthese zurückzuführen.[for full text, please go to the a.m. URL], Bad Honnef-Symposium 2015

Published
2015
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36. European Code against Cancer 4th edition: Ultraviolet radiation and cancer

Author

Greinert, R. (Rüdiger), Vries, E. (Esther) de, Erdmann, F. (Friederike), Espina, C. (Carolina), Auvinen, A. (Anssi), Kesminiene, A. (Ausrele), Schüz, J. (Joachim), Greinert, R. (Rüdiger), Vries, E. (Esther) de, Erdmann, F. (Friederike), Espina, C. (Carolina), Auvinen, A. (Anssi), Kesminiene, A. (Ausrele), and Schüz, J. (Joachim)

Abstract

Ultraviolet radiation (UVR) is part of the electromagnetic spectrum emitted naturally from the sun or from artificial sources such as tanning devices. Acute skin reactions induced by UVR exposure are erythema (skin reddening), or sunburn, and the acquisition of a suntan triggered by UVR-induced DNA damage. UVR exposure is the main cause of skin cancer, including cutaneous malignant melanoma, basal-cell carcinoma, and squamous-cell carcinoma. Skin cancer is the most common cancer in fair-skinned populations, and its incidence has increased steeply over recent decades. According to estimates for 2012, about 100,000 new cases of cutaneous melanoma and about 22,000 deaths from it occurred in Europe. The main mechanisms by which UVR causes cancer are well understood. Exposure during childhood appears to be particularly harmful. Exposure to UVR is a risk factor modifiable by individuals' behaviour. Excessive exposure from natural sources can be avoided by seeking shade when the sun is strongest, by wearing appropriate clothing, and by appropriately applying sunscreens if direct sunlight is unavoidable. Exposure from artificial sources can be completely avoided by not using sunbeds. Beneficial effects of sun or UVR exposure, such as for vitamin D production, can be fully achieved while still avoiding too much sun exposure and the use of sunbeds. Taking all the scientific evidence together, the recommendation of the 4th edition of the European Code Against Cancer for ultraviolet radiation is: "Avoid too much sun, especially for children. Use sun protection. Do not use sunbeds.".

Published
2015
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37. European Code against Cancer 4th Edition: Ionising and non-ionising radiation and cancer

Author

McColl, N. (Neil), Auvinen, A. (Anssi), Kesminiene, A. (Ausrele), Espina, C. (Carolina), Erdmann, F. (Friederike), Vries, E. (Esther) de, Greinert, R. (Rüdiger), Harrison, J. (John), Schüz, J. (Joachim), McColl, N. (Neil), Auvinen, A. (Anssi), Kesminiene, A. (Ausrele), Espina, C. (Carolina), Erdmann, F. (Friederike), Vries, E. (Esther) de, Greinert, R. (Rüdiger), Harrison, J. (John), and Schüz, J. (Joachim)

Abstract

Ionising radiation can transfer sufficient energy to ionise molecules, and this can lead to chemical changes, including DNA damage in cells. Key evidence for the carcinogenicity of ionising radiation comes from: follow-up studies of the survivors of the atomic bombings in Japan; other epidemiological studies of groups that have been exposed to radiation from medical, occupational or environmental sources; experimental animal studies; and studies of cellular responses to radiation. Considering exposure to environmental ionising radiation, inhalation of naturally occurring radon is the major source of radiation in the population - in doses orders of magnitude higher than those from nuclear power production or nuclear fallout. Indoor exposure to radon and its decay products is an important cause of lung cancer; radon may cause approximately one in ten lung cancers in Europe. Exposures to radon in buildings can be reduced via a three-step process of identifying those with potentially elevated radon levels, measuring radon levels, and reducing exposure by installation of remediation systems. In the 4th Edition of the European Code against Cancer it is therefore recommended to: "Find out if you are exposed to radiation from naturally high radon levels in your home. Take action to reduce high radon levels". Non-ionising types of radiation (those with insufficient energy to ionise molecules) - including extremely low-frequency electric and magnetic fields as well as radiofrequency electromagnetic fields - are not an established cause of cancer and are therefore not addressed in the recommendations to reduce cancer risk.

Published
2015
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38. European Code against Cancer 4th Edition: Ionising and non-ionising radiation and cancer

Author

McColl, N, Auvinen, A, Kesminiene, A, Espina, C, Erdmann, F, Vries, Esther, Greinert, R, Harrison, J, Schuz, J, McColl, N, Auvinen, A, Kesminiene, A, Espina, C, Erdmann, F, Vries, Esther, Greinert, R, Harrison, J, and Schuz, J

Abstract

Ionising radiation can transfer sufficient energy to ionise molecules, and this can lead to chemical changes, including DNA damage in cells. Key evidence for the carcinogenicity of ionising radiation comes from: follow-up studies of the survivors of the atomic bombings in Japan; other epidemiological studies of groups that have been exposed to radiation from medical, occupational or environmental sources; experimental animal studies; and studies of cellular responses to radiation. Considering exposure to environmental ionising radiation, inhalation of naturally occurring radon is the major source of radiation in the population - in doses orders of magnitude higher than those from nuclear power production or nuclear fallout. Indoor exposure to radon and its decay products is an important cause of lung cancer; radon may cause approximately one in ten lung cancers in Europe. Exposures to radon in buildings can be reduced via a three step process of identifying those with potentially elevated radon levels, measuring radon levels, and reducing exposure by installation of remediation systems. In the 4th Edition of the European Code against Cancer it is therefore recommended to: "Find out if you are exposed to radiation from naturally high radon levels in your home. Take action to reduce high radon levels". Non-ionising types of radiation (those with insufficient energy to ionise molecules)-including extremely low-frequency electric and magnetic fields as well as radiofrequency electromagnetic fields - are not an established cause of cancer and are therefore not addressed in the recommendations to reduce cancer risk. (C) 2015 International Agency for Research on Cancer; Licensee ELSEVIER Ltd

Published
2015

39. European Code against Cancer 4th Edition: Ultraviolet radiation and cancer

Author

Greinert, R, Vries, Esther, Erdmann, F, Espina, C, Auvinen, A, Kesminiene, A, Schuz, J, Greinert, R, Vries, Esther, Erdmann, F, Espina, C, Auvinen, A, Kesminiene, A, and Schuz, J

Abstract

Ultraviolet radiation (UVR) is part of the electromagnetic spectrum emitted naturally from the sun or from artificial sources such as tanning devices. Acute skin reactions induced by UVR exposure are erythema (skin reddening), or sunburn, and the acquisition of a suntan triggered by UVR-induced DNA damage. UVR exposure is the main cause of skin cancer, including cutaneous malignant melanoma, basal-cell carcinoma, and squamous-cell carcinoma. Skin cancer is the most common cancer in fair-skinned populations, and its incidence has increased steeply over recent decades. According to estimates for 2012, about 100,000 new cases of cutaneous melanoma and about 22,000 deaths from it occurred in Europe. The main mechanisms by which UVR causes cancer are well understood. Exposure during childhood appears to be particularly harmful. Exposure to UVR is a risk factor modifiable by individuals' behaviour. Excessive exposure from natural sources can be avoided by seeking shade when the sun is strongest, by wearing appropriate clothing, and by appropriately applying sunscreens if direct sunlight is unavoidable. Exposure from artificial sources can be completely avoided by not using sunbeds. Beneficial effects of sun or UVR exposure, such as for vitamin D production, can be fully achieved while still avoiding too much sun exposure and the use of sunbeds. Taking all the scientific evidence together, the recommendation of the 4th edition of the European Code Against Cancer for ultraviolet radiation is: "Avoid too much sun, especially for children. Use sun protection. Do not use sunbeds." (C) 2015 International Agency for Research on Cancer; Licensee ELSEVIER Ltd

Published
2015

40. European code against cancer 4th edition: 12 ways to reduce your cancer risk

Author

Schüz, J., Espina, C., Villain, P., Herrero, R., Leon, M., Minozzi, S., Romieu, I., Segnan, N., Wardle, J., Wiseman, M., Belardelli, F., Bettcher, D., Cavalli, F., Galea, G., Lenoir, G., Martin-Moreno, J., Nicula, F., Olsen, J., Patnick, J., Primic-Zakelj, M., Puska, P., Van Leeuwen, F., Wiestler, O., Zatonski, W., Guha, N., Kralikova, E., McNeill, A., Peruga, A., Anderson, A., Berrino, F., Boutron-Ruault, M., Cecchini, M., Key, T., Leitzmann, M., Norat, T., Powers, H., Scoccianti, C., Auvinen, A., de Vries, E., Erdmann, F., Greinert, R., Harrison, J., Kesminiene, A., McColl, N., Friis, S., Kogevinas, M., Saracci, R., Straif, K., Vainio, H., Almonte, M., Anttila, A., De Vuyst, H., Dillner, J., Franceschi, S., Gonzalez, P., Hall, A., Park, J., Armaroli, P., Atkin, W., Dean, P., de Koning, H., Dillner, L., Kuipers, E., Lansdorp_Vogelaar, Iris, Paci, E., Regula, J., Suonio, E., Törnberg, S., Wood, L., Gaudin, N., Frie, K., Terrasse, V., Winstanley, K., Bellisario, C., Biagioli, E., Cinquini, M., Gianola, S., Lorenzo, M., von Karsa, L., Lignini, T., Schüz, J., Espina, C., Villain, P., Herrero, R., Leon, M., Minozzi, S., Romieu, I., Segnan, N., Wardle, J., Wiseman, M., Belardelli, F., Bettcher, D., Cavalli, F., Galea, G., Lenoir, G., Martin-Moreno, J., Nicula, F., Olsen, J., Patnick, J., Primic-Zakelj, M., Puska, P., Van Leeuwen, F., Wiestler, O., Zatonski, W., Guha, N., Kralikova, E., McNeill, A., Peruga, A., Anderson, A., Berrino, F., Boutron-Ruault, M., Cecchini, M., Key, T., Leitzmann, M., Norat, T., Powers, H., Scoccianti, C., Auvinen, A., de Vries, E., Erdmann, F., Greinert, R., Harrison, J., Kesminiene, A., McColl, N., Friis, S., Kogevinas, M., Saracci, R., Straif, K., Vainio, H., Almonte, M., Anttila, A., De Vuyst, H., Dillner, J., Franceschi, S., Gonzalez, P., Hall, A., Park, J., Armaroli, P., Atkin, W., Dean, P., de Koning, H., Dillner, L., Kuipers, E., Lansdorp_Vogelaar, Iris, Paci, E., Regula, J., Suonio, E., Törnberg, S., Wood, L., Gaudin, N., Frie, K., Terrasse, V., Winstanley, K., Bellisario, C., Biagioli, E., Cinquini, M., Gianola, S., Lorenzo, M., von Karsa, L., and Lignini, T.

Abstract

This overview describes the principles of the 4th edition of the European Code against Cancer and provides an introduction to the 12 recommendations to reduce cancer risk. Among the 504.6 million inhabitants of the member states of the European Union (EU28), there are annually 2.64 million new cancer cases and 1.28 million deaths from cancer. It is estimated that this cancer burden could be reduced by up to one half if scientific knowledge on causes of cancer could be translated into successful prevention. The Code is a preventive tool aimed to reduce the cancer burden by informing people how to avoid or reduce carcinogenic exposures, adopt behaviours to reduce the cancer risk, or to participate in organised intervention programmes. The Code should also form a base to guide national health policies in cancer prevention. The 12 recommendations are: not smoking or using other tobacco products; avoiding second-hand smoke; being a healthy body weight; encouraging physical activity; having a healthy diet; limiting alcohol consumption, with not drinking alcohol being better for cancer prevention; avoiding too much exposure to ultraviolet radiation; avoiding cancer-causing agents at the workplace; reducing exposure to high levels of radon; encouraging breastfeeding; limiting the use of hormone replacement therapy; participating in organised vaccination programmes against hepatitis B for newborns and human papillomavirus for girls; and participating in organised screening programmes for bowel cancer, breast cancer, and cervical cancer.

Published
2015

50. Freiraum und Naturschutz

Author

Baier, H., Erdmann, F., Holz, R., Waterstraat, A., Klenke, Reinhard, Handy, J., Menk, M., Baier, H., Erdmann, F., Holz, R., Waterstraat, A., Klenke, Reinhard, Handy, J., and Menk, M.

Published
2006

Catalog

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