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5. α-Particle-induced DNA damage tracks in peripheral blood mononuclear cells of [

Author

S, Schumann, U, Eberlein, C, Lapa, J, Müller, S, Serfling, M, Lassmann, and H, Scherthan

Subjects
Male, Prostate cancer, Biokinetics, Prostatic Neoplasms, Alpha Particles, 53BP1, [223Ra]RaCl2, γ-H2AX, Dosimetry, Nuclear medicine, Leukocytes, Mononuclear, Humans, DNA damage, DNA Breaks, Double-Stranded, Original Article, α-Emitter
Abstract

Purpose One therapy option for prostate cancer patients with bone metastases is the use of [223Ra]RaCl2. The α-emitter 223Ra creates DNA damage tracks along α-particle trajectories (α-tracks) in exposed cells that can be revealed by immunofluorescent staining of γ-H2AX+53BP1 DNA double-strand break markers. We investigated the time- and absorbed dose-dependency of the number of α-tracks in peripheral blood mononuclear cells (PBMCs) of patients undergoing their first therapy with [223Ra]RaCl2. Methods Multiple blood samples from nine prostate cancer patients were collected before and after administration of [223Ra]RaCl2, up to 4 weeks after treatment. γ-H2AX- and 53BP1-positive α-tracks were microscopically quantified in isolated and immuno-stained PBMCs. Results The absorbed doses to the blood were less than 6 mGy up to 4 h after administration and maximally 16 mGy in total. Up to 4 h after administration, the α-track frequency was significantly increased relative to baseline and correlated with the absorbed dose to the blood in the dose range

Published
2020

7. Contents, Vol. 77, 1997

Author

A. Botta, K. Rojas, P. Zaragoza, X.-X. Zhang, M. Pritchard, B.P. Chowdhary, J.P. Park, J.L. Kissil, A. Rocchi, T.K. Watanabe, T. Siddque, N.P. Mertvetsov, W. Engel, A.A. Bosma, C. Rodellar, A. Arai, F. Shimizu, B. Hoebee, K.N. Sastry, R. Houlgatte, P.A. Voûte, N. Guo, U.W. Kenkare, J.-J. Cassiman, J. Guimera, W.R. Harrison, M.Z. Limongi, G. Mirza, A. Fratello, C.H. van Os, T. Ikeuchi, M. Chaffanet, T. Goldammer, M. Mannens, D. Grady, D. Wells, V. Romano, O. Miura, As. Ricco, M. Schwerin, M. Gersh, M.L. Filipenko, S.A. Wilcox, H. Levéziel, S.J. O’Brien, G.F.M. Merkx, C.C. Morton, G. Hardiman, R. Marzella, S. Hirosawa, T.J. Robinson, K.B.M. Reid, C. Elduque, A.S. Hewson, P.M.T. Deen, J.A. Squire, J.A.M. Graves, L. Vatteroni, E. Viegas-Péquignot, K. Yamamoto, M. Carter, L. Frönicke, N.V. Vorobieva, J. Overhauser, N. Ceratto, N.A. de Haan, M. Suzuki, T. Kozaki, M.S. Aly, B. Redeker, S. van Beersum, P.M. Borodin, F.F.B. Elder, A. Kimchi, A.S. Graphodatsky, B. Beatty, J.A. McMahon, M. de Meulemeester, J.B. Searle, I.V. Koroleva, W.Y. Hung, Y. Kuga, M. Jeanpierre, N. Sakuragawa, S. Feo, C. Auffray, M. Ogawa, M. Rocchi, M.P. Hande, C.K. Ullrich, J. Widmer, A. Ponce de León, F.O. Fackelmayer, S. Weremowicz, A. Pizzuti, K. Ohsugi, S. Okuno, R.J.M. Bindels, L.D. Matyakhina, A.P. McMahon, R. Leube, Y. Yang, A. Pandita, M. Lachtermacher, A. Tanzariello, B. Dallapiccola, M.A. Ferguson-Smith, A. Musio, A.F. Davies, D. Patterson, N. Lynch, Y. Nakamura, G. Rainaldi, M. Steenman, S.-T. Lee, H. Hayes, P.C.M. O’Brien, G.G. Karpova, C.H.M. Mellink, E. Jenkins, J.H. Xia, M. Schepens, A.T. Natarajan, B.-L. Lim, R. Meneveri, W.G. Nash, J. Kissing, M. Stacey, T. Fujiwara, M. Schmid, L.A. Witters, C. Zijlstra, L. Viggiano, F. Yang, M. Nagata, W. Bie, H. Scherthan, H. Murer, B. Ghebrehiwet, A. Westerveld, S. Kurata, H.N. Seuánez, M. Lovett, K.-H. Lee, R. Godbout, H.G. Brunner, J.M. Varley, P. Thygesen, R. Slater, S. Ishikawa, S.D. Pack, E. Takahashi, O.V. Cheryaukene, C. Bendixen, F. Ugolini, M. Matsumoto, R.M. Brunner, A. Risch, D. Birnbaum, Y. Takei, C.H. Fan, L.A. James, E.M. Ladenburger, P. Laurent, G. von Beust, T.K. Mohandas, H. Kobayashi, E. Burt, K. Wiesmeijer, M. Kai, A. Baldini, P. Eydoux, F.C. Canavez, F. Pelliccia, A. Geurts van Kessel, Déborah Bourc'his, S.-H. Park, S. Sebastian, C. Dobkin, R. Stanyon, R.A. Kastelein, L. Langbein, R. Toder, K. Okui, O.L. Serov, N. Matas, M.R. Koehler, R. Moyzis, J.F. Bazan, M.A. van Kuijck, A. Simons, P. Miniou, Y. Yokoyama, D. Molina Gomes, L. Xu, M.A.M. Moreira, H. Kim, E. Sim, J. Ragoussis, F. Saito-Ohara, M. Kool, N. Miyasaka, T. Katagiri, P. Bosco, X. Estivill, N. Archidiacono, G. Novelli, R. Knippers, P. Maccarone, J. Wienberg, M.-J. Pébusque, H.S. Tenenhouse, M. Nadal, W. Schwaeble, H. Hameister, H. van Bokhoven, T. Takahashi, E.I.B. Peerschke, V. Jurecic, X.-L. Yao, Y. Hey, P. Riegman, S.N. Malchenko, H.X. Deng, A.B. Spurdle, and N. Hoggard

Subjects
Botany, Genetics, Zoology, Biology, Molecular Biology, Genetics (clinical)
Published
1997
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8. Roles for two RecA homologs in promoting meiotic chromosome synapsis

Author

H Scherthan, G S Roeder, M Sym, and Beth Rockmill

Subjects
Saccharomyces cerevisiae Proteins, Time Factors, Saccharomyces cerevisiae, Cell Cycle Proteins, Haploidy, Fungal Proteins, Meiosis, Genetics, Homologous chromosome, Alleles, Recombination, Genetic, Deoxyribonucleases, Sequence Homology, Amino Acid, biology, Synaptonemal Complex, Genetic Complementation Test, fungi, Synapsis, Nuclear Proteins, Spores, Fungal, biology.organism_classification, Meiotic recombination checkpoint, DNA-Binding Proteins, Rec A Recombinases, Synaptonemal complex, MSH4, Exoribonucleases, Mutation, DMC1, Rad51 Recombinase, Chromosomes, Fungal, Developmental Biology
Abstract

Previous studies have shown that the RAD51 and DMC1 genes of Saccharomyces cerevisiae encode homologs of the Escherichia coli RecA strand exchange enzyme. Results presented here demonstrate that the dmc1 and rad51 mutants undergo nearly complete chromosome synapsis, but synaptonemal complex formation is delayed substantially compared with wild type. In the zip1 mutant, chromosomes are paired homologously, but not synapsed, and the protein backbones (axial elements) of each pair of chromosomes are connected intimately to each other at a few sites referred to herein as axial associations. dmc1 zip1 and rad51 zip1 double mutants assemble axial elements that are not obviously associated, demonstrating that the Dmc1 and Rad51 proteins are required to establish or stabilize axial associations. We propose that axial associations serve to promote meiotic chromosome synapsis and that the absence of these associations accounts for the delayed and inefficient synapsis observed in dmc1 and rad51 strains. During meiosis in haploid yeast, chromosome synapsis takes place between nonhomologous chromosome segments. In a zip1 haploid, axial associations are not apparent, suggesting that these associations depend on interactions between homologous sequences.

Published
1995
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9. Heteroduplex DNA formation and homolog pairing in yeast meiotic mutants

Author

B. Rockmill, Jaya Bhargava, D. K. Nag, H. Scherthan, and G. S. Roeder

Subjects
Genetics, Hybridization probe, fungi, Mutant, Nucleic Acid Heteroduplexes, Saccharomyces cerevisiae, Investigations, Biology, Molecular biology, Meiotic recombination checkpoint, Meiosis, Synaptonemal complex, Prophase, Mutation, Chromosomes, Fungal, DNA, Fungal, Homologous recombination, Heteroduplex
Abstract

Previous studies of Saccharomyces cerevisiae have identified several meiosis-specific genes whose products are required for wild-type levels of meiotic recombination and for normal synaptonemal complex (SC) formation. Several of these mutants were examined in a physical assay designed to detect heteroduplex DNA (hDNA) intermediates in meiotic recombination. hDNA was not detected in the rec102, mei4 and hop1 mutants; it was observed at reduced levels in red1, mek1 and mer1 strains and at greater than the wild-type level in zip1. These results indicate that the REC102, MEI4, HOP1, RED1, MEK1 and MER1 gene products act before hDNA formation in the meiotic recombination pathway, whereas ZIP1 acts later. The same mutants assayed for hDNA formation were monitored for meiotic chromosome pairing by in situ hybridization of chromosome-specific DNA probes to spread meiotic nuclei. Homolog pairing occurs at wild-type levels in the zip1 and mek1 mutants, but is substantially reduced in mei4, rec102, hop1, red1 and mer1 strains. Even mutants that fail to recombine or to make any SC or SC precursors undergo a significant amount of meiotic chromosome pairing. The in situ hybridization procedure revealed defects in meiotic chromatin condensation in mer1, red1 and hop1 strains.

Published
1995
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10. Abstracts

Author

J. M. Derlon, M. C. Petit-taboué, F. Dauphin, P. Courtheoux, F. Chapon, P. Creissard, F. Darcel, J. P. Houtteville, B. Kaschten, B. Sadzot, A. Stevenaert, Juri G. Tjuvajev, Homer A. Macapinlac, Farhad Daghighian, James Z. Ginos, Ronald D. Finn, M. S. Jiaju Zhang, Bradley Beattie, Martin Graham, Steven M. Larson, Ronald G. Blasberg, M. Levivier, S. Goldman, B. Pirotte, J. M. Brucher, D. Balériaux, A. Luxen, J. Hildebrand, J. Brotchi, K. G. Go, R. L. Kamman, E. L. Mooyaart, M. A. A. M. Heesters, P. E. Sijens, M. Oudksrk, P. van Dijk, P. C. Levendag, Ch. J. Vecht, R. J. Metz, D. N. Kennedy, B. R. Rosen, F. H. Hochberg, A. J. Fishman, P. A. Filipek, V. S. Caviness, M. W. Gross, F. X. Weinzierl, A. E. Trappe, W. E. Goebel, A. M. Frank, Georg Becker, Andreas Krone, Karsten Schmidt, Erich Hofmann, Ulrich Bogdahn, H. Bencsch, S. Fclber, G. Finkenstedt, C. Kremser, G. Sfockhammer, F. Aichner, U. Bogdahn, T. Fröhlich, G. Becker, A. Krone, R. Schlief, J. Schürmann, P. Jachimczak, E. Hofmann, W. Roggendorf, K. Roosen, C. M. Carapella, G. Carpinelli, R. Passalacqua, L. Raus, M. Giannini, R. Mastrostefano, F. Podo, A. Tofani, R. Maslrostefano, M. Mottoles, A. Ferraironi, M. G. Scelsa, P. Oppido, A. Riccio, C. L. Maini, L. Collombier, L. Taillandier, M. Dcbouverie, M. H. Laurens, P. Thouvenot, M. Weber, A. Bertrand, G. S. Cruickshank, J. Patterson, D. Hadley, Olivier De Witte, Jerzy Hildebrand, André Luxen, Serge Goldman, R. -I. Ernestus, K. Bockhorst, M. Eis, T. Els, M. Hoehn-Berlage, M. Gliese, R. Fründ, A. Geissler, C. Woertgen, M. Holzschuh, O. Hausmann, A. Merlo, E. Jerrnann, J. Uirich, R. Chiquet-Ehrismann, J. Müller, H. Mäcke, O. Gratzl, K. Herholz, M. Ghaemi, M. Würker, U. Pietrzyk, W. -D. Heiss, K. Kotitschke, M. Brandl, J. C. Tonn, A. Haase, S. Muigg, S. Felber, M. Woydt, Heinrich Lanfermann, Walter Heindel, Harald Kugel, Ralf -Ingo Erneslus, Gabricle Röhn, Klaus Lackner, F. S. Pardo, S. Kutke, A. G. Sorensen, L. L. Mechtler, S. Withiam-Lench, K. Shin, W. R. Klnkel, M. Patel, B. Truax, P. Kinkel, L. Mechtler, M. Ricci, P. Pantano, A. Maleci, S. Pierallini, D. Di Stefano, L. Bozzao, G. P. Cantore, Gabriele Röhn, R. Schröder, R. Ruda, C. Mocellini, R. Soffietti, M. Campana, R. Ropolo, A. Riva, P. G. de Filippi, D. Schiffer, D. Salgado, M. Rodrigues, L. Salgado, A. T. Fonseca, M. R. Vieira, J. M. Bravo Marques, H. Satoh, T. Uozumi, K. Kiya, K. Kurisu, K. Arita, M. Sumida, F. Ikawa, Tz. Tzuk-Shina, J. M. Gomori, R. Rubinstein, A. Lossos, T. Siegal, W. Vaalburg, A. M. J. Paans, A. T. M. Willemsen, A. van Waarde, J. Pruim, G. M. Visser, S. Valentini, Y. L. T. Ting, R. De Rose, G. Chidichimo, G. Corricro, Karin van Lcycn-Pilgram, Ralf -Ingo Erncslus, Norfried Klug, K. van Leyen-Pilgram, N. Klug, U. Neumann, Karl H. Plate, Georg Breier, Birgit Millaucr, Herbert A. Weich, Axel Ullrich, Werner Risau, N. Roosen, R. K. Chopra, T. Mikkelsen, S. D. Rosenblum, P. S. Yan, R. Knight, J. Windham, M. L. Rosenblum, A. Attanasio, P. Cavalla, A. Chio, M. T. Giordana, A. Migheli, V. Amberger, T. Hensel, M. E. Schwab, Luigi Cervoni, Paolo Celli, Roberto Tarantino, C. Huettner, U. Berweiler, I. Salmon, S. Rorive, K. Rombaut, J. Haot, R. Kiss, C. Maugard-Louboutin, J. Charrier, G. Fayet, C. Sagan, P. Cuillioere, G. Ricolleau, S. Martin, D. Menegalli-Bogeelli, Y. Lajat, F. Resche, Péter Molnàr, Helga Bárdos, Róza Ádány, J. P. Rogers, G. J. Pilkington, B. Pollo, G. Giaccone, A. Allegranza, O. Bugiani, J. Prim, J. Badia, E. Ribas, F. Coello, E. Shezen, O. Abramsky, M. Scerrati, R. Roselli, M. Iacoangeli, A. Pompucci, G. F. Rossi, Saleh M. Al. Deeb, Osama Koreich, Basim Yaqub, Khalaf R. Al. Moutaery, S. Marino, M. C. Vigliani, V. Deburghgraeve, D. Gedouin, M. Ben Hassel, Y. Guegan, B. Jeremic, D. Grujicic, V. Antunovic, M. Matovic, Y. Shibamoto, Merja Kallio, Helena Huhmar, Ch. Kudoh, A. Detta, K. Sugiura, E. R. Hitchcock, R. Di Russo, M. Cipriani§, E. M. Occhipinti, E. M. S. Conti, A. Clowegeser, M. Ortler, M. Seiwald, H. Kostron, B. Rajan, G. Ross, C. Lim, S. Ashlcy, D. Goode, D. Traish, M. Brada, G. A. C. vd Sanden, L. J. Schouten, J. W. W. Coebergh, P. P. A. Razenberg, A. Twijnstra, A. Snilders-Keilholz, J. H. C. Voormolen, J. Hermans, J. W. H. Leer, F. Baylac, M. Dcbouvcrie, R. Anxionnal, S. Bracard, J. M. Vignand, A. Duprcz, M. Winking, D. K. Böker, T. Simmet, David Rothbart, John Strugar, Jeroen Balledux, Gregory R. Criscuolo, Piotr Jachimczak, Armin Blesch, Birgit Heβdörfer, Ralf -Ingo Ernestus, Roland Schröder, Norfrid Klug, H. G. J. Krouwer, S. G. v. Duinen, A. Algra, J. Zentner, H. K. Wolf, B. Ostertun, A. Hufnagel, M. G. Campos, L. Solymosi, J. Schramm, E. S. Newlands, S. M. O'Reilly, M. Brampton, R. Sciolla, D. Seliak, R. Henriksson, A. T. Bergenheim, P. Björk, P. -O. Gunnarsson, Ml. Hariz, R. Grant, D. Collie, A. Gregor, K. P. Ebmeier, G. Jarvis, F. Lander, A. Cull, R. Sellar, C. Thomas, S. Elyan, F. Hines, S. Ashley, S. Stenning, J. J. Bernstein, W. J. Goldberg, U. Roelcke, K. Von Ammon, E. W. Radu, D. Kaech, K. L. Leenders, M. M. Fitzek, J. Efird Aronen, F. Hochberg, M. Gruber, E. Schmidt, B. Rosen, A. Flschman, P. Pardo, U. M. U. Afra, L. Sipos, F. Slouik, A. Boiardi, A. Salmaggi, A. Pozzi, L. Farinotti, L. Fariselli, A. Silvani, A. Brandes, E. Scelzi, A. Rigon, P. Zampieri, M. Pignataro, P. D'. Amanzo, P. Amista, A. Rotilio, M. V. Fiorentino, R. Thomas, L. Brazil, A. M. O'Connor, Maurizio Salvati, Fabrizio Puzzilli, Michele Raguso, R. Duckworth, R. Rumpling, M. Rottuci, G. Broggi, N. G. Plrint, E. Sabattini, V. Manetto, H. Gambacorta, S. Poggi, S. Pileri, R. Ferracini, D. V. Plev, N. J. Hopf, E. Knosp, J. Bohl, A. Perncczky, I. Catnby, O. Dewitte, J. L. Pasteels, I. Camby, F. Darro, A. Danguy, M. C. Kiu, G. M. Lai, T. S. Yang, K. T. Ng, J. S. Chen, C. N. Chang, W. M. Leung, Y. S. Ho, M. Deblec Rychter, A. Klimek, P. P. Liberski, A. Karpinaka, P. Krauseneck, V. Schöffel, B. Müller, F. W. Kreth, M. Faist, P. C. Warnke, C. B. Ostertag, K. M. B. v. Nielen, M. C. Visscr, C. Lebrun, M. Lonjon, T. Desjardin, J. F. Michiels, Sa. Lagrange J. L. Chanalet, J. L. Roche, M. Chatel, L. Mastronardi, F. Puzzilli, Farah J. Osman, P. Lunardi, M. Matsutani, Y. Ushio, K. Takakura, Johan Menten, Han Hamers, Jacques Ribot, René Dom, Hans Tcepen, N. Weidner, G. Naujocks, D. van Roost, O. D. Wiestler, A. Kuncz, C. Nieder, M. Setzel-Sesterhein, M. Niewald, I. Schnabel, K. S. O'Neill, N. D. Kitchen, P. R. Wilkins, H. T. Marsh, E. Pierce, R. Doshi, R. Deane, S. Previtali, A. Quattrini, R. Nemni, A. Ducati, L. Wrabetz, N. Canal, C. J. A. Punt, L. Stamatakis, B. Giroux, E. Rutten, Matthew R. Quigley, P. A. -C. Beth Sargent, Nicholas Flores, Sheryl Simon, Joseph C. Maroon, A. A. Rocca, C. Gervasoni, A. Castagna, P. Picozzi, E. Giugni, G. P. Tonnarelli, F. Mangili, G. Truci, M. Giovanelli, W. Sachsenheimer, T. Bimmler, H. Rhomberg W. Eiter, A. Obwegesser, H. Steilen, W. Henn, J. R. Moringlane, H. Kolles, W. Feiden, K. D. Zang, W. I. Sleudel, Andreas Steinbrecher, Martin Schabet, Clemens Heb, Michael Bamberg, Johannes Dichgans, G. Stragliotto, J. Y. Delattre, M. Poisson, L. Tosatto, P. D'Amanzo, N. Menicucci, S. Mingrino, W. I. Steudel, R. Feld, J. Ph. Maire, M. Caudry, J. Guerin, D. Celerier, N. Salem, H. Demeaux, J. F. Fahregat, M. E. Kusak, A. Bucno, J. Albisua, P. Jerez, J. L. Sarasa, R. Garefa, J. M. de Campos, A. Bueno, R. García-Delgado, R. García-Sola, A. A. Lantsov, T. I. Shustova, D. Lcnartz, R. Wellenreuther, A. von Deirnling, W. Köning, J. Menzel, S. Scarpa, A. Manna, M. G. Reale, P. A. Oppido, L. Frati, C. A. Valery, M. Ichen, J. P. Foncin, C. Soubrane, D. Khayat, J. Philippon, R. Vaz, C. Cruz, S. Weis, D. Protopapa, R. März, P. A. Winkler, H. J. Reulen, K. Bise, E. Beuls, J. Berg, W. Deinsberger, M. Samii, V. Darrouzet, J. Guérin, R. Trouette, N. Causse, J. P. Bébéar, F. Parker, J. N. Vallee, R. Carlier, M. Zerah, C. Lacroix-Jousselin, Joseph M. Piepmeier, John Kveton, Agnes Czibulka, G. S. Tigliev, M. P. Chernov, L. N. Maslova, José M. Valdueza, Werner Jänisch, Alexander Bock, Lutz Harms, E. M. Bessell, F. Graus, J. Punt, J. Firth, T. Hope, Osama Koriech, Saleh Al Deeb, Khalaf Al Moutaery, B. Yaqub, A. Franzini, R. Goldbrunner, M. Warmuth-Metz, W. Paulus, J. -Ch. Tonn, I. I. Strik, C. Markert, K. -W. Pflughaupt, B. P. O'Neill, R. P. Dinapoli, J. Voges, V. Sturm, U. Deuß, C. Traud, H. Treuer, R. Lehrke, D. G. Kim, R. P. Müller, Yu. S. Alexandrov, K. Moutaery, M. Aabed, O. Koreich, G. M. Ross, D. Ford, I. L. O. Schmeets, J. J. Jager, M. A. G. Pannebakker, J. M. A. de Jong, E. van Lindert, K. Kitz, S. Blond, F. Dubois, R. Assaker, M. C. Baranzelli, M. Sleiman, J. P. Pruvo, B. Coche-Dequeant, K. Sano, G. PetriČ-Grabnar, B. Jereb, N. Župančič, M. Koršič, N. G. Rainov, W. Burkert, Yukitaka Ushio, Masato Kochi, Youichi Itoyama, R. García, L. Ferrando, K. Hoang-Xuan, M. Sanson, P. Merel, O. Delattre, G. Thomas, D. Haritz, B. Obersen, F. Grochulla, D. Gabel, K. Haselsberger, H. Radner, G. Pendl, R. W. Laing, A. P. Warrington, P. J. C. M. Nowak, I. K. K. Kolkman-Deurloo, A. G. Visser, Hv. d. Berge, C. G. J. H. Niël, P. Bergström, M. Hariz, P. -O. Löfroth, T. Bergenheim, C. Cortet-rudelli, D. Dewailly, B. Coche-dequeant, B. Castelain, R. Dinapoli, E. Shaw, R. Coffey, J. Earle, R. Foote, P. Schomberg, D. Gorman, N. Girard, M. N. Courel, B. Delpech, G. M. Friehs, O. Schröttner, R. Pötter, R. hawliczek, P. Sperveslage, F. J. Prott, S. Wachter, K. Dieckmann, B. Bauer, R. Jund, F. Zimmermann, H. J. Feldmann, P. Kneschaurek, M. Molls, G. Lederman, J. Lowry, S. Wertheim, L. Voulsinas, M. Fine, I. Voutsinas, G. Qian, H. Rashid, P. Montemaggi, R. Trignani, C. West, W. Grand, C. Sibata, D. Guerrero, N. James, R. Bramer, H. Pahlke, N. Banik, M. Hövels, H. J. J. A. Bernsen, P. F. J. W. Rijken, B. P. J. Van der Sanden, N. E. M. Hagemeier, A. J. Van der Kogel, P. J. Koehler, H. Verbiest, J. Jager, A. McIlwrath, R. Brown, C. Mottolesb, A. Pierre'Kahn, M. Croux, J. Marchai, P. Delhemes, M. Tremoulet, B. Stilhart, J. Chazai, P. Caillaud, R. Ravon, J. Passacha, E. Bouffet, C. M. F. Dirven, J. J. A. Mooy, W. M. Molenaar, G. M. Lewandowicz, N. Grant, W. Harkness, R. Hayward, D. G. T. Thomas, J. L. Darling, N. Delepine, I. I. Subovici, B. Cornille, S. Markowska, JC. Desbois Alkallaf, J. KühI, D. Niethammer, H. J. Spaar, A. Gnekow, W. Havers, F. Berthold, N. Graf, F. Lampert, E. Maass, R. Mertens, V. Schöck, A. Aguzzi, A. Boukhny, S. Smirtukov, A. Prityko, B. Hoiodov, O. Geludkova, A. Nikanorov, P. Levin, B. D'haen, F. Van Calenbergh, P. Casaer, R. Dom, J. Menten, J. Goffin, C. Plets, A. Hertel, P. Hernaiz, C. Seipp, K. Siegler, R. P. Baum, F. D. Maul, D. Schwabe, G. Jacobi, B. Kornhuber, G. Hör, A. Merzak, H. K. Rooprai, P. Bullock, P. H. M. F. van Domburg, P. Wesseling, H. O. M. Thijssen, J. E. A. Wolff, J. Boos, K. H. Krähling, V. Gressner-Brocks, H. Jürgens, J. Schlegel, H. Scherthan, N. Arens, Gabi Stumm, Marika Kiessling, S. Koochekpour, G. Reifenberger, J. Reifenberger, L. Liu, C. D. James, W. Wechsler, V. P. Collins, Klaus Fabel-Schulte, Plotr Jachimczak, Birgitt Heßdörfer, Inge Baur, Karl -Hermann Schlingensiepen, Wolgang Brysch, A. Blesch, A. K. Bosserhoff, R. Apfel, F. Lottspeich, R. Büttner, R. Cece, I. Barajon, S. Tazzari, G. Cavaletti, L. Torri-Tarelli, G. Tredici, B. Hecht, C. Turc-Carel, R. Atllas, P. Gaudray, J. Gioanni, F. Hecht, J. A. Rey, M. J. Bello, M. Parent, P. Gosselin, J. L. Christiaens, J. R. Schaudies, M. Janka, U. Fischer, E. Meese, M. Remmelink, P. Cras, R. J. Bensadoun, M. Frenay, J. L. Formento, G. Milano, J. L. Lagrange, P. Grellier, J. -Y. Lee, H. -H. Riese, J. Cervós-Navarro, W. Reutter, B. Lippitz, C. Scheitinger, M. Scholz, J. Weis, J. M. Gilsbach, L. Füzesi, Y. J. Li, R. Hamelin, Erik Van de Kelft, Erna Dams, Jean -Jacques Martin, Patrick Willems, J. Erdmann, R. E. Wurm, S. Sardell, J. D. Graham, Jun -ichi Kuratsu, M. Aichholzer, K. Rössler, F. Alesch, A. Ertl, P. S. Sorensen, S. Helweg-Larsen, H. Mourldsen, H. H. Hansen, S. Y. El Sharoum, M. W. Berfelo, P. H. M. H. Theunissen, I. Fedorcsák, I. Nyáry, É. Osztie, Á. Horvath, G. Kontra, J. Burgoni-chuzel, P. Paquis, SW. Hansen, PS. Sørensen, M. Morche, F. J. Lagerwaard, W. M. H. Eijkenboom, P. I. M. Schmilz, S. Lentzsch, F. Weber, J. Franke, B. Dörken, G. Schettini, R. Qasho, D. Garabello, S. Sales, R. De Lucchi, E. Vasario, X. Muracciole, J. Régis, L. Manera, J. C. Peragut, P. Juin, R. Sedan, K. Walter, K. Schnabel, N. Niewald, U. Nestle, W. Berberich, P. Oschmann, R. D. Theißen, K. H. Reuner, M. Kaps, W. Dorndorf, K. K. Martin, J. Akinwunmi, A. Kennedy, A. Linke, N. Ognjenovic, A. I. Svadovsky, V. V. Peresedov, A. A. Bulakov, M. Y. Butyalko, I. G. Zhirnova, D. A. Labunsky, V. V. Gnazdizky, I. V. Gannushkina, M. J. B. Taphoorn, R. Potman, F. Barkhof, J. G. Weerts, A. B. M. F. Karim, J. J. Heimans, M. van de Pol, V. C. van Aalst, J. T. Wilmink, J. J. van der Sande, W. Boogerd, R. Kröger, A. Jäger, C. Wismeth, A. Dekant, W. Brysch, K. H. Schlingensiepen, B. Pirolte, V. Cool, C. Gérard, J. L. Dargent, T. Velu, U. Herrlinger, M. Schabet, P. Ohneseit, R. Buchholz, Jianhong Zhu, Regina Reszka, Friedrich Weber, Wolfgang Walther, L. I. Zhang, Mario Brock, J. P. Rock, H. Zeng, J. Feng, J. D. Fenstermacher, A. Gabizon, M. Beljanski, S. Crochet, B. Zackrisson, J. Elfverson, G. Butti, R. Baetta, L. Magrassi, M. R. De Renzis, M. R. Soma, C. Davegna, S. Pezzotta, R. Paoletti, R. Fumagalli, L. Infuso, A. A. Sankar, G. -L. Defer, P. Brugières, F. Gray, C. Chomienne, J. Poirier, L. Degos, J. D. Degos, Bruno M. Colombo, Stefano DiDonato, Gaetano Finocchiaro, K. M. Hebeda, H. J. C. M. Sterenborg, A. E. Saarnak, J. G. Wolbers, M. J. C. van Gemert, P. Kaaijk, D. Troost, S. Leenstra, P. K. Das, D. A. Bosch, B. W. Hochleitner, A. Obwegeser, W. Vooys, G. C. de Gast, J. J. M. Marx, T. Menovsky, J. F. Beek, V. Schirrmacher, A. Schmitz, A. M. Eis-Hübinger, p. h. Piepmeier, Patricia Pedersen, Charles Greer, Tommy Shih, Amr Elrifal, William Rothfus, L. Rohertson, R. Rampling, T. L. Whoteley, J. A. Piumb, D. J. Kerr, P. A. Falina, I. M. Crossan, K. L. Ho, M. M. Ruchoux, S. Vincent, F. Jonca, J. Plouet, M. Lecomte, D. Samid, A. Thibault, Z. Ram, E. H. Oldfield, C. E. Myers, E. Reed, Y. Shoshan, Tz. Siegal, G. Stockhammer, M. Rosenblum, F. Lieberman, A. J. A. Terzis, R. Bjerkvig, O. D. Laerum, H. Arnold, W. D. Figg, G. Flux, S. Chittenden, P. Doshi, D. Bignor, M. Zalutsky, Juri Tjuvajev, Michael Kaplitt, Revathi Desai, M. S. Bradley, B. S. Bettie, Bernd Gansbacher, Ronald Blasberg, H. K. Haugland, J. Saraste, K. Rooseni, A. J. P. E. Vincent, C. J. J. Avezaat, A. Bout, J. L. Noteboom, C. h. Vecht, D. Valerio, P. M. Hoogerbrugge, R. Reszka, J. Zhu, W. Walther, J. List, W. Schulz, I. I. J. C. M. Sterenborg, W. Kamphorst, H. A. M. van Alplien, P. Salander, R. Laing, B. Schmidt, G. Grau, T. Bohnstedt, A. Frydrych, K. Franz, R. Lorenz, F. Berti, A. Paccagnella, P. L. van Deventer, P. L. I. Dellemijn, M. J. van den Bent, P. J. Kansen, N. G. Petruccioli, E. Cavalletti, B. Kiburg, L. J. Müller, C. M. Moorer-van Delft, H. H. Boer, A. Pace, L. Bove, A. Pietrangeli, P. Innocenti, A. Aloe, M. Nardi, B. Jandolo, S. J. Kellie, S. S. N. De Graaf, H. Bloemhof, D. Roebuck, Pozza L. Dalla, D. D. R. Uges, I. Johnston, M. Besser, R. A. Chaseling, S. Koeppen, S. Gründemann, M. Nitschke, P. Vieregge, E. Reusche, P. Rob, D. Kömpf, T. J. Postma, J. B. Vermorken, R. P. Rampling, D. J. Dunlop, M. S. Steward, S. M. Campbell, S. Roy, P. H. E. Hilkens, J. Verweij, W. L. J. van Putten, J. W. B. Moll, M. E. L. van der Burg, A. S. T. Planting, E. Wondrusch, U. Zifko, M. Drlicek, U. Liszka, W. Grisold, B. Fazeny, Ch. Dittrich, Jan J. Verschuuren, Patricio I. Meneses, Myrna R. Rosenfeld, Michael G. Kaplitt, Jerome B. Posner, Josep Dalmau, P. A. E. Sillevis Smitt, G. Manley, J. B. Posner, G. Bogliun, L. Margorati, G. Bianchi, U. Liska, B. Casati, C. Kolig, H. Grisold, R. Reñe, M. Uchuya, F. Valldeoriola, C. Benedetti de Cosentiro, D. Ortale, R. Martinez, J. Lambre, S. Cagnolati, C. Vinai, M. G. Forno, R. Luksch, P. Confalonieri, J. Scholz, G. Pfeiffer, J. Netzer, Ch. Hansen, Ch. Eggers, Ch. Hagel, K. Kunze, Marc K. Rosenblum, and Frank S. Lieberman

Subjects
Cancer Research, Neurology, Oncology, Neurology (clinical)
Published
1994
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11. Contents Vol. 93, 2001

Author

T. Brueckmann, W. Brenner, M. Steinemann, W. Vogel, S. Schlaubitz, C. Zühlke, M. Lombard, F. Boán, K. Benirschke, S. Naumann, S.W. Bremer, C. Steinlein, S. Steinemann, F. Richard, P.D. Thomsen, M. Yerle, K.D. Zang, Z. Docherty, C. Amid, K. Mrasek, I. Schubert, M. Mende, I. Nanda, T. Paiss, C. Genêt, L.J. Peelman, I. Chudoba, M. Hughes, R.-D. Wegner, U. Claussen, L. Sánchez, B. Seipel, F. Grützner, F.J. García-Cozar, D. Prawitt, B.U. Zabel, J.L. Wright, A. Van Zeveren, K. Stout, V. Kalscheuer, M. Stumm, R.V. Rambau, N. Reissmann, D.S. Gallagher, B. Zabel, A. Ishikawa, C. Messaoudi, A.T. Kumamoto, E.C. Akeson, A. Mujica, A. Dalski, P. Kaiser, T. Liehr, J.G. Scammell, S. Bremer, C. Pfeifer, S. Munsche, M.M. Valdivia, M. Van Poucke, M. Schmid, C.M. Tuck-Muller, H. Starke, F. Domínguez, Y. Matsuda, S. Störkel, C.G. Mathew, F.F.B. Elder, S. Narayanswami, H. Scherthan, J. Decker, E. Schwinger, A. Niveleau, V. Trifonov, H. Mayrhofer, J. Gómez-Márquez, J.P. Lambert, S.-E. Bikar, E. Zend-Ajusch, L.J. Bechtel, T. Haaf, Y.A. Wang, A. Viñas, C. Iglesias, C. Mackie Ogilvie, A. Bahr, T. Nagase, A. Dufke, H.H.Q. Heng, A. Winterpacht, W. Lu, T.J. Robinson, C. Maier, K. Matsubara, A. Heller, A. Kuroiwa, M. Rocchi, B. Dutrillaux, C.J. Ye, N. Nomura, N. Rubtsov, E.R. Schmidt, T. Namikawa, M.T. Davisson, C. Tuggle, K. Gardiner, H. Enders, G. Liu, M. Buceta, H. Hanson, H. Hauser, N. Sampson, H. Neitzel, P.D. Waters, T. Hankeln, H. Tönnies, C. Pendón, J. Bolívar, M.L. Houck, D. Reutzel, M. Leipoldt, A. Cichutek, P. Moens, J.A.M. Graves, P.J. Kirby, B. Maurer, A. Astola, S.A. Krawetz, and F. Piumi

Subjects
Botany, Genetics, Biology, Molecular Biology, Genetics (clinical)
Published
2001
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12. Scientific Proceedings Second International Symposium on Cytostatic Drug Resistance

Author

Bridget T. Hill, L. K. Hosking, S. McClean, S. A. Shellard, W. C. M. Dempke, R. D. H. Whelan, M. Sehested, E. Friche, E. J. F. Demant, P. B. Jensen, B. P. Kopnin, B. Wolf, A. Seidel, M. Nickelsen, I. Brandt, G. Heinemann, M. Dietel, S. Bremer, T. Hoof, B. Tümmler, H. J. Broxterman, C. H. M. Versantvoort, C. M. Kuiper, N. Feller, G. J. Schuurhuis, J. Lankelma, S. Gupta, T. Tsuruo, C. Kim, S. Gollapudi, A. Bittl, M. Nap, W. Jäger, B. Lathan, N. Lang, N. T. Raikhlin, A. G. Perevozchikov, J. L. Volodina, T. Licht, H. H. Fiebig, K. J. Bross, F. Herrmann, R. Mertelsmann, I. Bashir, K. Sikora, C. S. Foster, M. Castagna, P. Viacava, M. Cianfrigliao, A. Favati, P. Collecchi, M. A. Caligo, G. Cipollini, G. Bevilacqua, D. Schrenk, T. W. Gant, J. A. Silverman, S. S. Thorgeirsson, A. Harstrick, Z. G. Zhang, H. J. Schmoll, Y. Rustum, M. Mitze, T. Beck, W. Weikel, C. Brumm, P. G. Knapstein, T. McDonald, P. Gardner, N. Kang, S. A. M. van der Heyden, H. J. Elst, U. Stein, B. Jandrig, H. Krause, P. Schmidt-Peter, J. Frege, V. Wunderlich, E. Boven, C. K. van Kalken, H. M. Pinedo, W. Gebauer, E. Fallgren-Gebauer, M. Diete, T. Wagner, M. R. Müller, K. Lennartz, H. R. Nowrousian, S. Seeber, A. A. Shtil, A. R. Kazarov, A. V. Gudkov, A. A. Stavrovskaya, F. H. Djuraeva, T. P. Stromskaya, A. Noller, G. Frese, M. Neumann, A. Wilisch, H. Probst, V. Gekeler, R. Handgretinger, H. Schmidt, C. P. Muller, R. Dopfer, T. Klingebiel, D. Niethammer, S. Weger, H. Diddens, E. Daumiller, A. Bunge, R. Lilischkis, A. Salmassi, M. Kopun, H. Scherthan, C. Granzow, I. Leuschner, D. Schmidt, H. Hoffmann, D. Harms, G. V. Scagliotli, E. Leonardo, S. Cappia, G. Esposito, M. Tombesi, M. Cianfriglia, G. V. Esposito, N. Merendino, M. Viora, M. Caserta, E. Tritarelli, E. Rocca, G. Boccoli, P. Samoggia, C. Fossati, U. Testa, C. Peschle, J. L. Darling, S. M. Ashmore, D. C. Peterson, D. G. T. Thomas, R. A. Kramer, R. Stanlunas, T. Summerhayes, T. Lion, R. H. Shoemaker, L. Wu, A. Smythe, M. R. Boyd, W. T. Beck, M. K. Danks, J. S. Wolverton, M. Chen, B. Y. Bugg, D. P. Suttle, C. V. Catapano, D. J. Fernandes, F. Gieseler, F. Boege, R. Erttmann, H. Arps, L. Zwelling, K. Wilms, H. Biersack, G. J. L. Kaspers, R. Pieters, E. Klumper, F. C. de Waal, E. R. van Wering, A. J. P. Veerman, C. A. Schmidt, F. Lorenz, A. Schäfer, A. Kirsch, W. Siegert, D. Huhn, W. E. Simon, G. Siebert, M. Schneider, M. Oettling, A. Reymann, R. Entmann, S. Schmidt, C. Woermann, C. Windmeier, I. Herzig, B. Schaefer, H. J. Heidebrecht, H. H. Wacker, H. Künnemann, Th. H. M. van Heijningen, M. L. Slovak, J. P. A. Baak, K. Steidtmann, A. -M. J. Fichtinger-Schepman, B. I. Hill, K. J. Scanlon, W. J. Zeller, G. Chen, J. A. Gietema, E. G. E de Vries, D.Th Sleijfer, P. H. B. Willemse, H. J. Guchelaar, D. R. A. Uges, P. Aulenbacher, R. Voegeli, N. H. Mulder, C. Skrezek, H. Bertermann, H. Eichholtz-Wirth, R. Born, H. Bier, M. Koch, G. Bernhardt, K. Hählen, H. Reile, C. H. van Zantwijk, T. Görögh, B. Lippert, J. A. Werner, J. E. Eickbohm, G. H. Mickiseh, M. M. Gottesman, I. Pastan, J. Hofmann, A. Wolf, M. Spitaler, G. Bock, H. Grunicke, H. Ponstingl, I. Roth, C. Dörner, G. Looft, G. J. Ossenkoppele, G. L. Scheffer, G. Atassi, A. Pierre, L. Kraus, S. Leonce, G. Regnier, A. Dhainaut, M. Stöhr, C. Rohlff, R. I. Glazer, Y. S. Cho-Chung, V. Höllt, M. Kouba, G. Vogt, H. Allmeier, N. I. Nissen, S. Cros, N. Guilbaud, T. Dunn, M. Berlion, J. P. Bizzari, A. M. Messing, A. Matuschek, I. Mutter, J. C. W. Kiwit, L. Bastian, P. E. Goretzki, A. Frilling, D. Simon, H. D. Röher, A. Reichle, F. Altmayr, J. Rastetter, C. Erbil, G. Jaques, M. Maasberg, K. Havemann, K. Häußermann, H. -J. Heidebrecht, W. Van de Vrie, E. E. O. Gheuens, N. M. C. Durante, E. A. De Bruijn, R. L. Marquet, A. T. Van Oosterom, A. M. M. Eggermont, M. W. Stow, S. E. Vickers, J. R. Warr, E. Roller, M. Eichelbaum, B. Klumpp, J. Krause, K. Schumacher, S. Hörner, A. Laßmann, U. Traugott, E. Schlick, D. Bürkle, BW Futscher, AF List, WS Dalton, E. Ladda, K. Bühl, A. Weimer, C. Eser, K. Hamprecht, K. P. Schalk, C. Jackisch, B. Brandt, M. Blum, F. Louwen, K. Schulz, J. P. Hanker, U. Rüther, A. Schmidt, H. A. G. Müller, C. Nunnensiek, H. Bader, F. Eisenberger, P. Jipp, B. Niethammer, C. Muller, V. Ling, F. Joncourt, S. Redmond, K. Buser, M. Fey, A. Tobler, K. Brunner, A. Gratwohl, T. Cerrry, V. Nuessler, R. Pelka-Fleischer, C. Nerl, B. Beckert, W. Wilmanns, S. Hegewisch-Becker, M. Fliegner, A. Zander, D. K. Hossfeld, J. Blanz, K. Mewes, G. Ehninger, K. -P. Zeller, H. Schuldes, G. Herrmann, W. Boeckmann, R. Schroeder, D. Jonas, K. -H. Zurborn, H. D. Bruhn, L. Uharek, B. Glass, W. Gassmann, H. Loeffler, W. Mueller-Ruohholtz, W. Mueller-Ruchholtz, K. Jaquet, H. Kreipe, J. Felgner, H. J. Radzun, M. R. Parwaresch, EA Kogan, NN Mazurenko, SM Sekamova, H. Wolf, K. Röhe, K. Wilkens, M. Clausen, E. Henze, J. van der Bosch, S. Rüller, M. Schlaak, U. Köhl, D. Schwabe, E. Rohrbach, E. Montag, S. Bauer, J. Cinatl, I. Cinatl, M. Mainke, H. Geiss, B. Kornhuber, H. Juhl, H. Stritzel, H. Kalhoff, W. Schniegel, T. Menke, B. Pröbsting, P. Schulze-Westhoff, J. Boos, J. Weidner, N. Wedemeyer, K. Wiedorn, Y. Ueda, S. Blasius, P. Wuisman, W. Böcker, A. Roessner, B. Dockhorn-Dworniczak, D. Ramm, J. Knebel, W. Sass, M. Aufderheide, and J. Seifert

Subjects
Cancer Research, medicine.medical_specialty, Oncology, business.industry, medicine, General Medicine, Drug resistance, Pharmacology, Intensive care medicine, business
Published
1991
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13. Telomere attachment and clustering during meiosis

Author

H, Scherthan

Subjects
Meiosis, Chromosomal Proteins, Non-Histone, Nuclear Envelope, Chromosome Segregation, Heterochromatin, Nuclear Proteins, Cell Cycle Proteins, Spindle Apparatus, Telomere, Models, Biological, Actins
Abstract

Telomeres are important segments of chromosomes that protect chromosome ends from nucleolytic degradation and fusion. At meiosis telomeres display an unprecedented behavior which involves their attachment and motility along the nuclear envelope. The movements become restricted to a limited nuclear sector during the so-called bouquet stage, which is widely conserved among species. Recent observations suggest that telomere clustering involves actin and/or microtubules, and is altered in the presence of impaired recombinogenic and chromosome related functions. This review aims to provide an overview of what is currently known about meiotic telomere attachment, dynamics and regulation in synaptic meiosis.

Published
2007

16. Genomic structure, conservation and FISH mapping of the Rattus norvegicus Adprt gene

Author

S, Beneke, R, Kappler, A, Bürkle, and H, Scherthan

Subjects
ADP Ribose Transferases, Genome, Chromosome Mapping, Exons, Cell Line, Rats, Mice, Animals, Humans, Cattle, Amino Acid Sequence, Conserved Sequence, In Situ Hybridization, Fluorescence, Phylogeny
Abstract

Poly(ADP-ribose) polymerase 1 (PARP-1) lies at the basis of a DNA-interacting protein family that maintains genome integrity. Here we describe the genomic organisation of rat PARP-1 gene (Adprt), refine its assignment to rat chromosome (RNO) 13q25--q26 by FISH and compare its genomic organisation between rat, mouse and human. It appears that in human, mouse and rat Adprt consists of 23 similar-sized exons with well-conserved intron and exon borders. Adprt orthologs map to homologous chromosome regions at the termini of the q-arms of human and mouse chromosomes 1 and rat 13, with gene order being conserved between the rodents. Kimura protein distance comparison with human PARP-1 as reference revealed the bovine protein to be the least conserved with 10.3 substitutions per 100 amino acids, followed by rat (8.6) and mouse (8.4).

Published
2003

18. Asynchronous chromosome pairing in male meiosis of the rat (Rattus norvegicus)

Author

H, Scherthan and I, Schönborn

Subjects
DNA-Binding Proteins, Male, Meiosis, Microscopy, Fluorescence, Synaptonemal Complex, Testis, Animals, Nuclear Proteins, Rats, Wistar, Spermatogenesis, Chromosomes, In Situ Hybridization, Fluorescence, Rats
Abstract

Premeiotic and meiotic chromosome distribution was studied in rat testes suspensions by a triple-color fluorescent staining protocol which allows simultaneous visual inspection of two chromosomal targets highlighted by FISH together with immunostained SCP3 synaptonemal complex (SC) proteins which are marked by a third, composite color. Triple labeling with rat chromosome (RNO) 4q and 19p specific probes and SCP3 staining disclosed that homologs are separated in premeiotic and leptotene nuclei. Pairing of homologous chromosome regions commenced during early zygotene, with pairing of the small metacentric chromosomes 19 preceding that of the distal region of the long arm of RNO4. Our results show that homolog association occurs during zygotene of rat spermatogenesis, with small and large chromosomes showing a considerable asynchrony. Comparison with pairing progression in meiosis of other mammals suggests that asynchronous chromosome pairing reflects size differences within a complement.

Published
2001

19. Double minutes and c-MYC amplification in acute myelogenous leukemia: Are they prognostic factors?

Author

P, Bruckert, R, Kappler, H, Scherthan, H, Link, F, Hagmann, and H, Zankl

Subjects
Adult, X Chromosome, Extrachromosomal Inheritance, Gene Amplification, Genes, myc, Prognosis, Proto-Oncogene Mas, Leukemia, Myeloid, Acute, Karyotyping, Humans, Female, Chromosome Deletion, In Situ Hybridization, In Situ Hybridization, Fluorescence
Abstract

A case of acute myelogenous leukemia (AML) with double minutes (dmin) and X chromosome loss is presented. Using comparative genomic hybridization (CGH), a region of high-level DNA amplification was detected at 8q24, the locus of the c-MYC proto-oncogene. Fluorescence in situ hybridization (FISH) with a DNA probe specific for the human c-MYC gene confirmed the extrachromosomal amplification of this proto-oncogene in the dmin of the leukemic cells. During the course of the disease, three relapses occurred; two complete remissions could be achieved by treatment with various chemotherapy regimens. The patient's survival time of 25 months was considerably longer than in most reported cases of AML with extrachromosomal c-MYC amplification. Therefore, the present case challenges the view that the occurrence of dmin in AML is generally an indication of poor prognosis.

Published
2000

20. The p16/Cdkn2a/Ink4a gene is frequently deleted in nitrosourea-induced rat glial tumors

Author

J, Schlegel, G, Piontek, M, Kersting, M, Schuermann, R, Kappler, H, Scherthan, C, Weghorst, G, Buzard, and H, Mennel

Subjects
Reverse Transcriptase Polymerase Chain Reaction, Genes, p16, Homozygote, Nervous System Neoplasms, Glioma, Neoplasms, Experimental, Fibroblasts, Chromosomes, Nitrosourea Compounds, Rats, Inbred F344, Rats, Tumor Cells, Cultured, Animals, RNA, Neoplasm, Cell Division, Gene Deletion, DNA Primers
Abstract

The present study investigates nitrosourea-induced rat (Rattus norvegicus) glioma cell lines for the functional status of the p16/Cdkn2a/Ink4a gene, which encodes the p16 cdk4 inhibitor and the alternative reading frame protein, p19ARF. We detected homozygous deletions of the p16/Cdkn2a/Ink4a gene locus in 4 of 5 glioma cell lines (C6, F98, RG2, and RGL.3), but not in the 9L gliosarcoma cell line or in a rat primary fibroblast cell line. RT-PCR demonstrated expression of the p16 and p19ARF mRNAs only in 9L cells and in rat fibroblasts. Comparative genomic in situ hybridization showed that the copy number of rat chromosome RNO5 was not altered in any of the glioma cell lines investigated, indicating that the deletions result from a discrete loss in the region of the p16/Cdkn2a/Ink4a locus. This is the first report of p16/Cdkn2a/Ink4a deletions present in nitrosourea-induced rat glioma cell lines. Since this genetic alteration is also commonly observed in human malignant glial tumors, our results validate the use of chemically induced rat glioma cell lines as an experimental model in the development of gene therapy strategies.

Published
2000

21. Segmental homology among cattle (Bos taurus), Indian muntjac (Muntiacus muntjak vaginalis), and Chinese muntjac (M. reevesi) karyotypes

Author

L, Frönicke, B P, Chowdhary, and H, Scherthan

Subjects
Muntjacs, Species Specificity, Karyotyping, Animals, Chromosome Mapping, Cattle, Female, Cosmids, In Situ Hybridization, Fluorescence, Chromosome Banding
Abstract

In an attempt to examine homologies between Indian and Chinese muntjac karyotypes at a subchromosomal level, five bovine cosmids were comparatively mapped by heterologous fluorescence in situ hybridization (FISH). In the Indian muntjac (2n = 6) all cosmids mapped to chromosome 1, whereas in the Chinese muntjac (2n = 46) two cosmids mapped to chromosome 3 and one cosmid each mapped to chromosomes 1, 7, and 17. These markers have maintained their intrachromosomal position relative to a centromere/telomere axis in cattle and in Chinese and Indian muntjac chromosomal arms. Our results corroborate the tandem-fusion hypothesis for muntjac karyotypic evolution and establish orientational homology between the involved Chinese muntjac chromosomes and the discrete segments on Indian muntjac chromosome 1. Furthermore, our data disclose regional homologies between cattle and muntjac genomes and demonstrate the validity of intergeneric cosmid-FISH for investigations on karyotype evolution.

Published
1997

22. Chromosome behaviour in earliest meiotic prophase

Author

H. Scherthan

Subjects
Synaptonemal complex, Meiotic Prophase I, Prophase, Meiosis, Homologous chromosome, Sister chromatids, Chromatid, Biology, Chiasma, Cell biology
Abstract

The formation of haploid gametes in sexually reproducing organisms is dependent on the pairing and recombination of homologous chromosomes (homologues) during meiotic prophase I. This ensures the faithful segregation of homologues at Metaphase I. Chromatids are separated at metaphase II (Hawley, 1988). At the onset of prophase I, sister chromatids of meiotic chromosomes become connected by axial elements (cores) which run along their entire length. Axial elements are called lateral elements, when they become interconnected by transverse filaments to result in the well known tripartite synaptonemal complex (SC) structure (reviewed by Moses, 1968; von Wettstein et al.,, 1984, Giroux, 1988). While chromosome pairing and meiotic recombination can apparently occur without SC formation (Roeder, 1990; Padmore et al., 1991, Hawley and Arbel, 1993; Loidl et al., 1994, Scherthan et al., 1994; Weiner and Kleckner, 1994, Nag et al., 1995), tripartite SC assembly seems to be a prerequisite for proper chiasma distribution, i.e. chiasma interference (Sym and Roeder, 1994).

Published
1997
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23. Comparative genomic hybridization (CGH) discloses chromosomal and subchromosomal copy number changes in Merkel cell carcinomas

Author

Tilman Schulz, Ingrid Moll, H. Scherthan, M. Härle, Walter Back, and N. Arens

Subjects
In situ, Male, medicine.medical_specialty, Pathology, Histology, Skin Neoplasms, Dermatology, Biology, Pathology and Forensic Medicine, chemistry.chemical_compound, Cytogenetics, medicine, Humans, Gene, Aged, medicine.diagnostic_test, Chromosome, Nucleic Acid Hybridization, Middle Aged, Aneuploidy, Carcinoma, Merkel Cell, medicine.anatomical_structure, chemistry, Female, Merkel cell, DNA, Comparative genomic hybridization, Fluorescence in situ hybridization
Abstract

We analyzed three Merkel cell carcinomas (MCC), applying comparative genomic hybridization (CGH) with DNA from paraffin-embedded and cultured tumor material as the probes. By this method, numerous changes in chromosome copy numbers were observed in each tumor investigated. Recurrent gains of chromosomes 1, 6, 18q and 20 were detected in two tumors. A third tumor showed complex chromosomal copy number changes, including gain of chromosome 8 and 9. These gains, as well as gain of chromosome 1 in the first two tumors, were confirmed by fluorescence in situ hybridization to paraffin tissue sections. Our results support the view that important genes for MCC development may be located on chromosomes 1, 6, 18q and 20.

Published
1996

24. The yeast MER2 gene is required for chromosome synapsis and the initiation of meiotic recombination

Author

Beth Rockmill, G S Roeder, J Loidl, H Scherthan, and JoAnne Engebrecht

Subjects
Genetics, Recombination, Genetic, Mitotic crossover, Saccharomyces cerevisiae Proteins, Mutant, Genes, Fungal, Synapsis, Saccharomyces cerevisiae, Biology, Investigations, Genetic recombination, Chromosomal crossover, Fungal Proteins, Synaptonemal complex, Meiosis, Mutation, Gene conversion, Chromosomes, Fungal, Homologous recombination
Abstract

Mutation of the MER2 gene of Saccharomyces cerevisiae confers meiotic lethality. To gain insight into the function of the Mer2 protein, we have carried out a detailed characterization of the mer2 null mutant. Genetic analysis indicates that mer2 completely eliminates meiotic interchromosomal gene conversion and crossing over. In addition, mer2 abolishes intrachromosomal meiotic recombination, both in the ribosomal DNA array and in an artificial duplication. The results of a physical assay demonstrate that the mer2 mutation prevents the formation of meiosis-specific, double-strand breaks, indicating that the Mer2 protein acts at or before the initiation of meiotic recombination. Electron microscopic analysis reveals that the mer2 mutant makes axial elements, which are precursors to the synaptonemal complex, but homologous chromosomes fail to synapse. Fluorescence in situ hybridization of chromosome-specific DNA probes to spread meiotic chromosomes demonstrates that homolog alignment is also significantly reduced in the mer2 mutant. Although the MER2 gene is transcribed during vegetative growth, deletion or overexpression of the MER2 gene has no apparent effect on mitotic recombination or DNA damage repair. We suggest that the primary defect in the mer2 mutant is in the initiation of meiotic genetic exchange.

Published
1995

25. Analysis of sex chromosome distribution in the gonadal tissue of a 45,X/47,XYY mosaic by fluorescence in situ hybridization

Author

S, Ragg, M, Härle, and H, Scherthan

Subjects
Chromosome Aberrations, Male, X Chromosome, Mosaicism, Gonadal Dysgenesis, Chromosomes, Human, Pair 1, Child, Preschool, Y Chromosome, Testis, XYY Karyotype, Humans, DNA Probes, In Situ Hybridization, Fluorescence, Fluorescent Dyes
Abstract

45,X/47,XYY mosaicism is a rare condition with scarce information on the tissue-specific distribution of the different cell lines. Fluorescence in situ hybridization with repetitive, chromosome-specific DNA probes was applied to gain insight into the tissue-specific distribution of the two cell lines in biopsies of the streak gonad and dysgenetic testis of a 2-year-old individual exhibiting 45,X/47,XYY mosaicism. The distribution of the 45,X/47,XYY cells within different tissues was found to be nonrandom. The coelomic epithelium, the vascular endothelium, and the prepuberal germ cells exhibited predominantly a 47,XYY karyotype. In contrast, Sertoli cells exhibited both karyotypes, and the remaining tissue was predominantly composed of 45,X cells. The contribution of the two cell lines to gonadal development is discussed.

Published
1995

26. Suppression of tumorigenicity of breast cancer cells by transfer of human chromosome 17 does not require transferred BRCA1 and p53 genes

Author

M, Theile, S, Hartmann, H, Scherthan, W, Arnold, W, Deppert, R, Frege, F, Glaab, W, Haensch, and S, Scherneck

Subjects
Base Sequence, BRCA1 Protein, Molecular Sequence Data, Gene Transfer Techniques, Breast Neoplasms, DNA, Satellite, Hybrid Cells, Genes, p53, Chromosome Banding, Neoplasm Proteins, Mice, Tumor Cells, Cultured, Animals, Humans, Cell Division, In Situ Hybridization, Fluorescence, Neoplasm Transplantation, Chromosomes, Human, Pair 17, Transcription Factors
Abstract

A number of candidate tumor suppressor genes located on the human chromosome 17 are thought to have a role to play in the development of breast cancer. In addition to the p53 gene on 17p13.1 and the BRCA1 gene mapped to 17q12-21, other chromosomal regions for tumor suppressor genes have been suggested to exist on 17p13.3 and both the central and the distal parts of 17q, although definitive functional proof of their involvement in breast cancer tumorigenesis is still lacking. In this report we show that microcell transfer of a human chromosome 17 into wild-type p53 breast cancer cells CAL51 results in loss of tumorigenicity and anchorage-independent growth, changes in cell morphology and a reduction of cell growth rates of the neo-selected microcell hybrids. In the hybrid cells, which express the p53 wild-type protein, only the p- and the distal parts of the q arm of donor chromosome 17 are transferred. Thus, our results provide functional evidence for the presence of one or more tumor suppressor gene(s) on chromosome 17, which are distinct from the p53 and the BRCA1 genes.

Published
1995

27. Mapping of the murine nuclear factor I/X gene (Nfix) to mouse chromosome 8 C1-2 by FISH

Author

H, Scherthan, C, Seisenberger, K, Greulich, and E L, Winnacker

Subjects
Chromosome Mapping, Nuclear Proteins, Regulatory Factor X Transcription Factors, DNA-Binding Proteins, Mice, NFI Transcription Factors, Species Specificity, CCAAT-Enhancer-Binding Proteins, Animals, Humans, Y-Box-Binding Protein 1, Chromosomes, Human, Pair 19, In Situ Hybridization, Fluorescence, Transcription Factors
Published
1994

28. Contents Vol. 98, 2002

Author

G. Vonghia, Y. Matsuda, P. Laurent, A. Perucatti, P.M. Galetti, S. Holguin, E. Olmo, Q.X. Yu, N. Saïdi-Mehtar, B. Moore, D. Di Berardino, H. Scherthan, C. André, J.M. Pagnozzi, A. Geisinger, A. Splendiani, M. Serrano, S. Rak, P. Quignon, M. Tsudzuki, T. O’Sickey, Hélène Hayes, G.P. Di Meo, M. Heinrich, E. Owens, R. Wettstein, T. Hardt, W. Reardon, Pilar Zaragoza, T.-I. Gan, T. Capriglione, T. Laulhere, J. J. Jurado, André Eggen, L. Iannuzzi, Luca Ferretti, P. Hu, T. Leeb, M. Smith, M. Liebers, T. Palomeque, J. Martinez, A. Dos Santos, A. Caputi Jambrenghi, R. Nesbitt, D.Q. Wang, C. Modahl, A. Woodroffe, G. Odierna, E. Petitpierre, James E. Womack, F. Henrique-Silva, Manfred Schwerin, H. Kuiper, P.A. Filipek, Tom Goldammer, D. Incarnato, I. Garnería, A. Beattie, S. Beneke, J.A. Carrillo, J.D. Liu, P. Lorite, F. Hinrichs, G. Zhao, P. Nisi Cerioni, K. Yamada, P.J. Kirby, R. Smith, H. Wu, M.S. Yi, I. Grandy, M. Gautier, M.E. Bocian, M. Schmid, S.R. Kata, K. Mennicke, P. Flodman, E. Schwinger, U.-J. Kim, C. Rodellar, R. Johannisson, A. Kispert, A.D. Ditchfield, S. Al-Hasani, E. Leuschner, C. Drögemüller, M. Bina, J.A.M. Graves, T. Haaf, R. Roy, A. Bürkle, Y. Yonenaga-Yassuda, L. Rowen, M.A. Spence, M. Shibusawa, R.M. Brunner, R. Benavente, L. Fröhlich Archangelo, R. Kappler, Daniel Vaiman, J.H. Calvo, L. Mays, M. Hüppe, J. Kohlhase, V. Caputo, T. Hatanaka, K. Diedrich, P.D. Waters, B.A. Roe, F. Zhou, O. Distl, and Z. Yao

Subjects
Botany, Genetics, Zoology, Biology, Molecular Biology, Genetics (clinical)
Published
2002
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29. Subject Index Vol. 98, 2002

Author

J.H. Calvo, V. Caputo, T. Hatanaka, R. Johannisson, S. Rak, P.M. Galetti, A. Kispert, P. Quignon, James E. Womack, H. Scherthan, A. Bürkle, T. Leeb, N. Saïdi-Mehtar, F. Hinrichs, Y. Matsuda, E. Olmo, B. Moore, P. Lorite, P.A. Filipek, Hélène Hayes, H. Kuiper, M. Hüppe, R. Smith, J.A. Carrillo, H. Wu, L. Rowen, P.J. Kirby, D. Incarnato, R. Wettstein, M.E. Bocian, M.S. Yi, M. Shibusawa, A. Caputi Jambrenghi, P. Laurent, M. Gautier, R.M. Brunner, R. Benavente, J. Kohlhase, M. Tsudzuki, W. Reardon, S. Beneke, G. Zhao, S.R. Kata, A. Perucatti, T. Laulhere, J. J. Jurado, M. Liebers, K. Yamada, André Eggen, M.A. Spence, C. Modahl, C. André, T. Palomeque, M. Smith, C. Drögemüller, Q.X. Yu, A. Dos Santos, G.P. Di Meo, D. Di Berardino, L. Fröhlich Archangelo, G. Odierna, A.D. Ditchfield, M. Heinrich, I. Garnería, M. Schmid, R. Kappler, M. Serrano, J.D. Liu, T. Haaf, U.-J. Kim, S. Holguin, Pilar Zaragoza, E. Schwinger, T. Hardt, Z. Yao, T.-I. Gan, C. Rodellar, T. Capriglione, R. Roy, I. Grandy, A. Woodroffe, E. Petitpierre, A. Splendiani, Y. Yonenaga-Yassuda, P. Nisi Cerioni, Manfred Schwerin, T. O’Sickey, G. Vonghia, E. Owens, J.A.M. Graves, K. Mennicke, P. Flodman, J. Martinez, S. Al-Hasani, F. Henrique-Silva, A. Beattie, M. Bina, E. Leuschner, Daniel Vaiman, L. Mays, Tom Goldammer, F. Zhou, O. Distl, L. Iannuzzi, Luca Ferretti, P. Hu, J.M. Pagnozzi, A. Geisinger, R. Nesbitt, D.Q. Wang, K. Diedrich, B.A. Roe, and P.D. Waters

Subjects
Index (economics), Statistics, Genetics, Subject (documents), Biology, Molecular Biology, Genetics (clinical)
Published
2002
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30. Discrimination of distinct subpopulations within a tumor with combined double immunophenotyping and interphase cytogenetics

Author

A Müller-Hermelink, W. Grote, Brigitte Schlegelberger, J. Deerberg, H Scherthan, and K. Weber-Matthiesen

Subjects
Pathology, medicine.medical_specialty, Histology, CD3 Complex, Follicular lymphoma, Fluorescent Antibody Technique, Biology, Immunofluorescence, Immunophenotyping, Cytogenetics, Antigen, Antigens, CD, Antigens, Neoplasm, Proto-Oncogene Proteins, medicine, Biomarkers, Tumor, Humans, Lymphoma, Follicular, In Situ Hybridization, medicine.diagnostic_test, Staining and Labeling, Cell cycle, medicine.disease, Antigens, CD20, Lymphocyte Subsets, Antigens, Differentiation, B-Lymphocyte, Proto-Oncogene Proteins c-bcl-2, Immunohistochemistry, Interphase, Female, Anatomy, Clone (B-cell biology)
Abstract

We describe a method that enables detection and immunophenotypical characterization of distinct subpopulations within a cytogenetically defined tumor clone. Coexisting normal cells do not hinder microscopic evaluation because they can be distinguished from cytogenetically aberrant tumor cells. This is also true when normal and neoplastic cells cannot be clearly distinguished by cytology or immunohistochemistry, i.e., if both constituents have similar immunophenotypes and morphology. The method is based on fluorescence double staining for two different antigens combined with interphase cytogenetic analysis. It is referred to as "Fluorescence immunophenotyping and Interphase Cytogenetics as a Tool for Investigation of Neoplasms (FICTION)." In a case of follicular lymphoma we demonstrate that FICTION can differentiate bcl-2-positive malignant and non-malignant cells and can verify the presence of bcl-2-positive but cytogenetically inconspicuous T-lymphocytes.

Published
1993

31. Localisation of the human nuclear factor I/X (NFI/X) gene to chromosome 19p13 and detection of five other related loci at 1p21-22, 1q42-43, 5q15, 11p13 and 20q13 by FISH

Author

E. L. Winnacker, H. Scherthan, and C. Seisenberger

Subjects
Genetics, Nuclear factor I, Restriction Mapping, Nuclear Proteins, Chromosome, Y box binding protein 1, Biology, Molecular biology, DNA-Binding Proteins, NFI Transcription Factors, Restriction map, Gene mapping, Sequence Homology, Nucleic Acid, CCAAT-Enhancer-Binding Proteins, Humans, Y-Box-Binding Protein 1, Nuclear protein, Chromosomes, Human, Pair 19, Gene, In Situ Hybridization, Fluorescence, Genetics (clinical), Transcription Factors
Abstract

Nuclear factor I (NFI) is a member of a family of dimeric DNA-binding proteins that are involved both in the initiation of adenovirus DNA replication and in the stimulation of transcriptional activation. We have used fluorescence in situ hybridisation (FISH) to map one of four known genes encoding an NFI protein, the human NFI/X gene, to chromosome 19p1.3. Secondary sites of hybridisation observed at 5p1.5, 1q4.2-4.4, 1p2.1-2.2, and 20p1.3 most likely are attributable to partial sequence homologies with related NFI genes.

Published
1993
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33. Subject Index Vol. 93, 2001

Author

N. Sampson, W. Lu, H. Neitzel, P.D. Waters, T. Brueckmann, W. Brenner, C. Mackie Ogilvie, A. Heller, H. Tönnies, B. Dutrillaux, M. Steinemann, C. Pendón, J. Bolívar, R.-D. Wegner, M. Lombard, C.J. Ye, A. Ishikawa, E. Zend-Ajusch, T. Nagase, Y.A. Wang, F. Richard, A. Kuroiwa, N. Rubtsov, E.R. Schmidt, C. Tuggle, C. Genêt, K. Gardiner, H. Enders, B. Zabel, A. Van Zeveren, M. Rocchi, H. Scherthan, A. Dalski, R.V. Rambau, J.P. Lambert, K. Stout, A. Dufke, B. Seipel, F.F.B. Elder, J.L. Wright, T. Namikawa, H. Hauser, E. Schwinger, M. Buceta, C. Pfeifer, S. Narayanswami, A.T. Kumamoto, H. Starke, V. Kalscheuer, J.G. Scammell, M. Stumm, K. Matsubara, V. Trifonov, C. Amid, K. Mrasek, G. Liu, A. Bahr, T. Haaf, A. Viñas, C. Iglesias, Z. Docherty, H. Mayrhofer, P. Kaiser, S.-E. Bikar, I. Chudoba, C.M. Tuck-Muller, J. Decker, L.J. Bechtel, H.H.Q. Heng, A. Winterpacht, M.M. Valdivia, C. Messaoudi, D. Reutzel, M. Van Poucke, C. Steinlein, S. Störkel, U. Claussen, T.J. Robinson, J.A.M. Graves, A. Niveleau, F. Grützner, A. Mujica, N. Nomura, W. Vogel, S. Naumann, M. Hughes, E.C. Akeson, S. Steinemann, I. Nanda, S. Bremer, S. Munsche, S.W. Bremer, P.D. Thomsen, F.J. García-Cozar, D. Prawitt, B.U. Zabel, B. Maurer, A. Astola, T. Liehr, F. Domínguez, M.T. Davisson, H. Hanson, T. Hankeln, L.J. Peelman, M.L. Houck, N. Reissmann, Y. Matsuda, J. Gómez-Márquez, M. Leipoldt, A. Cichutek, K.D. Zang, P. Moens, T. Paiss, D.S. Gallagher, M. Schmid, C.G. Mathew, S.A. Krawetz, F. Piumi, S. Schlaubitz, C. Zühlke, F. Boán, K. Benirschke, M. Yerle, I. Schubert, M. Mende, P.J. Kirby, L. Sánchez, and C. Maier

Subjects
Genetics, Index (economics), Subject (documents), Social science, Biology, Molecular Biology, Genetics (clinical)
Published
2001
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34. Subject Index Vol. 84, 1999

Author

C.T. Lago, D.S. Gallagher, R. Bucala, Y. Zhang, M. Matsui, N. Montuori, M.A. Ferguson-Smith, G. Senger, U. Mahlknecht, M.G. Persico, J.F. Taylor, P. Miniou, C. Cassano, R. Banerjee, M. D’Urso, M.E. Durkin, A. Forabosco, T. Esposito, P. Maraschio, F. Nagai, A.J. Sainsbury, N. Inoue, M.A. Morris, Y. Nitta, T.E. Richardson, A. Geurts van Kessel, R. Stanyon, J. Lemke, J. Laborda, M. Bagga, F. Darroudi, Y. Koshizuka, L. Bartoloni, P.M. Kroisel, N. Taniguchi, T.C. van Stijn, G.P. Di Meo, A. Rott, E. Verdin, C.H. Kindler, T. Fujita, E. Viegas-Péquignot, F. Gianfrancesco, M. Rocchi, A. Plesch, A. Matsumoto, N.A. Affara, J.M. Lumsden, J.T.G. Schepens, E. Gubina, M. Svelto, B. Schlegelberger, G.F. Merkx, Y. Nakamura, T. Kinoshita, M. Jeanpierre, G.W. Montgomery, M.R. Speicher, O. Miyoshi, T. Fujii, J.E. Womack, G. De Saint-Basile, V. Baladrón, J.-M. Dupont, K. Patel, T. Usui, A. Haynes, H.-J. Heidebrecht, C.S. Yost, B. Scognamiglio, H. Tamura, L. Jennes, R. Kappler, R. Mazzarella, T. Cremer, M. D’Esposito, A. Kindler-Röhrborn, S. Thiel, Y. Endo, E.A. Lord, S.A. Cato, N.J. Lynch, Y. Yamaguchi, J. Fujii, M. Tucci, G. Baldassarre, A. Barra, M. Isomura, I. Chudoba, R. Dono, A. Gos, L. Viggiano, J. Takeda, H.-D. Mennel, M.F. Broom, B. Trueb, E. Petek, U. Claussen, J.-L.C. Blouin, V. Luu-The, G. Calamita, R. Albrechtsen, H. Satoh, Y. Yang, A. Bolzer, T.P.L. Smith, P. Soucy, P.C.M. O’Brien, J.M. Craig, R. Parwaresch, A. Ciccodicola, M.J. Ruiz-Hidalgo, T.S. Khurana, W.J. Schwaeble, A.T. Gray, G. Lembo, C.D. DeLozier-Blanchet, G. Viglietto, C.V. Beechey, S. Ikegawa, W.J.A.J. Hendriks, C.M. Stover, F.C. Nielsen, A.C. Jäger, I. Dufort, B. Wieringa, D. Molina Gomes, F. Yang, M. Egashira, D. Bourc’his, S.E. Antonarakis, E.R. Sampson, S.S. Kakar, M. Imhof, T. Lörch, A.M.J.M. van den Maagdenberg, K. Ohishi, L. Iannuzzi, P. Denny, U.M. Wewer, N. Niikawa, P. Cavagna, J. Schlegel, R. Hamaoka, L. Tiepolo, P. Rheault, N.L. Lòpez-Corrales, M.T.M. Schepens, K. Wagner, J. Wienberg, T.S. Sonstegard, W. Emberger, H. Scherthan, S.K. Davis, and E.P. Evans

Subjects
Genetics, Index (economics), Subject (documents), Social science, Biology, Molecular Biology, Genetics (clinical)
Published
1999
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35. Localization of the repetitive telomeric sequence (TTAGGG)n in two muntjac species and implications for their karyotypic evolution

Author

H, Scherthan

Subjects
Base Sequence, Deer, Sequence Homology, Nucleic Acid, Animals, Nucleic Acid Hybridization, Biological Evolution, Chromosomes, Repetitive Sequences, Nucleic Acid
Abstract

It has been suggested that the chromosome set of the Indian muntjac, Muntiacus muntjak vaginalis (female, 2n = 6; male, 2n = 7), evolved from small acrocentric chromosomes, such as those found in the complement of the Chinese muntjac, M. reevesi (2n = 46), by a series of tandem fusions and other rearrangements. The location of the highly conserved human telomeric sequence (TTAGGG)n in the metaphase chromosomes of M.m. vaginalis and its close relative, M. reevesi, was investigated by non-radioactive in situ hybridization. The (TTAGGG)n repeat was found adjacent to the centromeres in the short arm and at the telomeres in the long arm of M. reevesi acrocentric metaphase chromosomes. Tandem fusions present in the karyotype of M.m. vaginalis chromosomes were not reflected by interstitial signals of the telomere repeat, as these chromosomes displayed hybridization signals only at the ends of the chromatids. Mechanisms that might have played a role in the evolution of the reduced karyotype of the Indian muntjac are discussed.

Published
1990

36. Subject Index, Vol. 77, 1997

Author

A.S. Graphodatsky, G. Hardiman, J.A. Squire, L. Frönicke, P. Bosco, N. Ceratto, S. van Beersum, J.A.M. Graves, H.N. Seuánez, X. Estivill, N. Archidiacono, G. Novelli, G.G. Karpova, C.H.M. Mellink, E. Jenkins, M. Stacey, T. Fujiwara, M. Lovett, R. Knippers, R. Moyzis, M. Jeanpierre, P. Maccarone, J. Wienberg, M. Rocchi, C. Bendixen, S. Weremowicz, B.P. Chowdhary, Y. Yang, A. Pandita, M. Lachtermacher, N. Matas, K.-H. Lee, N. Miyasaka, T. Katagiri, F. Pelliccia, M.-J. Pébusque, R. Godbout, M. Gersh, R. Leube, F. Ugolini, M. Kai, S.-T. Lee, O. Miura, H.G. Brunner, O.V. Cheryaukene, K. Ohsugi, A. Tanzariello, M.A. Ferguson-Smith, A. Geurts van Kessel, P.C.M. O’Brien, W.G. Nash, A. Baldini, T.J. Robinson, M. Matsumoto, A. Pizzuti, Y. Nakamura, M. Mannens, V. Romano, A. Musio, J. Widmer, Déborah Bourc'his, A. Botta, K. Rojas, M.Z. Limongi, L.A. James, A.F. Davies, M. de Meulemeester, R.M. Brunner, C.H. van Os, J.H. Xia, T.K. Watanabe, E.M. Ladenburger, S.-H. Park, C. Rodellar, M. Pritchard, J.L. Kissil, A.S. Hewson, A. Arai, K.N. Sastry, P.M.T. Deen, P. Eydoux, J.A. McMahon, F.C. Canavez, L. Langbein, R. Toder, G. von Beust, M. Schmid, R. Houlgatte, T. Takahashi, P.A. Voûte, N.V. Vorobieva, J. Overhauser, R. Stanyon, E.I.B. Peerschke, K. Yamamoto, J.P. Park, T.K. Mohandas, S. Feo, C. Zijlstra, N.P. Mertvetsov, M. Steenman, U.W. Kenkare, S.A. Wilcox, J. Guimera, P. Zaragoza, N.A. de Haan, W.Y. Hung, J. Ragoussis, D. Birnbaum, M. Ogawa, H. Kobayashi, W. Engel, F. Shimizu, B. Hoebee, B. Ghebrehiwet, T. Ikeuchi, M. Chaffanet, W.R. Harrison, T. Goldammer, S. Ishikawa, E. Burt, K. Wiesmeijer, V. Jurecic, S.D. Pack, M.R. Koehler, B. Beatty, M. Nagata, E. Takahashi, J.F. Bazan, N. Lynch, M. Schwerin, Y. Yokoyama, G. Mirza, A. Fratello, D. Grady, D. Molina Gomes, F. Saito-Ohara, N. Hoggard, C. Dobkin, H. Scherthan, H. van Bokhoven, L.D. Matyakhina, R. Meneveri, A.P. McMahon, H. Murer, R. Marzella, K. Okui, J. Kissing, A. Risch, J.M. Varley, X.-L. Yao, M. Carter, X.-X. Zhang, H.S. Tenenhouse, S. Kurata, O.L. Serov, P.M. Borodin, M. Nadal, M.L. Filipenko, A. Rocchi, M. Kool, W. Schwaeble, H. Hayes, Y. Takei, H. Levéziel, S.J. O’Brien, P. Thygesen, C.H. Fan, H.X. Deng, M. Suzuki, H. Hameister, G.F.M. Merkx, R. Slater, P. Laurent, S. Sebastian, B. Redeker, R.A. Kastelein, E. Viegas-Péquignot, M.A. van Kuijck, L. Xu, M.A.M. Moreira, T. Kozaki, C.C. Morton, M.S. Aly, I.V. Koroleva, H. Kim, E. Sim, A. Ponce de León, A.B. Spurdle, A. Kimchi, A. Simons, G. Rainaldi, Y. Hey, P. Miniou, D. Wells, F.F.B. Elder, P. Riegman, D. Patterson, M. Schepens, S.N. Malchenko, L.A. Witters, L. Viggiano, S. Hirosawa, F. Yang, K.B.M. Reid, C. Elduque, C. Auffray, A.A. Bosma, N. Guo, J.-J. Cassiman, F.O. Fackelmayer, R.J.M. Bindels, A.T. Natarajan, B.-L. Lim, J.B. Searle, As. Ricco, N. Sakuragawa, L. Vatteroni, M.P. Hande, C.K. Ullrich, S. Okuno, T. Siddque, W. Bie, A. Westerveld, Y. Kuga, and B. Dallapiccola

Subjects
Index (economics), Statistics, Genetics, Subject (documents), Biology, Molecular Biology, Genetics (clinical)
Published
1997
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37. Brief Gene Mapping Reports A / B / C / D / E

Author

E. Kemter, C. Fitzsimmons, J.E. Womack, U. Philipp, A. Rauch, A. Perucatti, G.P. Di Meo, M. Gille, S. Chadi-Taourit, H. Kuiper, U.A. Nuber, P. Savolainen, D. Varga, E. Bailey, W. Vogel, Peter Pearson, C. Maier, A.J. Gamel, G.-P. Shi, J.-C. Benichou, B. Gralak, J. Flynn, L. Arvestad, B. Patino-Garcia, D.B. Zimonjic, M.A. Brinton, L.V. Millon, X. Zhou, V. Boutreux, M.I. Nino-Soto, M.C.T. Penedo, T. Efferth, H.-H. Ropers, P.K. Basrur, R. Roy, R. Klose, G. Steding, N.C. Popescu, W. Engel, I. Chudoba, Y. Chen, U. Wick, C. Maisonhaute, C. Drögemüller, I. Michel, R.G.A. Faragher, G. Lindgren, E.P. Cribiu, O. Distl, Michael Schmid, C. Corso, G. Guérin, E.M. Parry, J. Liu, Marc Boelhauve, T. Goldammer, J.M. Parry, H. Scherthan, B. Brand-Saberi, J. Lundeberg, M. Rachidi, N. Hartmann, D. Incarnato, A.A. Zharkikh, P. Zaragoza, A.A. Perelygin, R. Hellio, M. Binns, S. Taourit, M. Perrocheau, T. Hasegawa, K.H. Røed, G. Evanno, A. Eggen, L. Iannuzzi, R.M. Brunner, C. Lopes, I.M. Adham, C. Rodellar, J.E. Swinburne, N. Ellis, B. Lausen, W.-H. Xu, T. Tozaki, D. Bernoco, C. Moran, T.L. Lear, Eckhard Wolf, W.A. King, T. Paiss, A. Guthrie, S.R. Kata, T. Leeb, L. Andersson, R. Dressel, A. Seager, R. Guyon, M. Kirsch, E. Piper, M.H.L. Green, E. Gebhart, L.A. Lyons, C. André, G. Cholewinski, and A. Reis

Subjects
Genetics, Gene mapping, Biology, Molecular Biology, Genetics (clinical)
Published
2005
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38. Absract

Author

Marietta Kaszkin, Volker Kinzel, Karl Maly, Irina Bichler, Florian Lang, Hans H. Grunicke, R. Pepperkok, R. Jakobi, P. Lorenz, W. Ansorge, W. Pyerin, P. Borowski, M. Harbers, A. Ludwig, T. Kischel, H. Hilz, K. Eckert, A. Granetzny, J. Fischer, R. Grosse, V. Manch, S. Wehner, B. Kornhuber, U. Ebener, K. Müller-Decker, G. Fürstenberger, I. Vogt, F. Marks, G. Graschew, A. Küsel, W. Hull, W. Lorenz, H. W. Thielmann, Gisela H. Degen, Alexius Freyberger, A. Müller, M. Linscheid, Ulrike Hindermeier, Ute Jorritsma, K. Golka, W. Föllmann, H. Peter, H. M. Bolt, S. Monnerjahn, D. N. Phillips, A. Never, A. Seidel, A. R. Glatt, K. Wiench, E. Frei, P. Schroth, M. Wiessler, T. Schäfer, M. Hergenhahn, E. Hecker, D. Proft, P. Bartholmes, R. S. Bagewadikar, B. Bertram, N. Frank, Hanno Leibersperger, Michael Gschwendt, Friedrich Marks, S. Fasco, Peter Plein, Karin Schiess, Lothar Seidler, T. Jacobi, E. Besemfelder, M. Stephan, W. D. Lehmann, M. Grell, B. Thoma, P. Scheurich, Markus Meyer, Hans Grunicke, G. Jaques, B. Wegmann, K. Ravemann, Odilia Popanda, Heinz Walter Thielmann, H. Voss, U. Wirkner, Dieter Werner, D. Strand, A. Kalmes, H. -P. Walther, B. Mechler, S. Volker Schirrmacher, V. Kinzel, R. Hess, H. -G. Hanagarth, C. Hässler, G. Brandner, Christian Ertel, B. Gückel, V. Schirrmacher, B. A. Kyewski, U. Bogdahn, P. Jachimczak, J. Schneider, W. Brysch, W. Schlingensiepen, D. Drenkard, C. Behl, J. Winkler, R. Apfel, J. Meixensberger, K. Stulle, P. Marquardt, H. P. Vollmers, J. Müller, H. -K. Müller-Hermelink, M. Schuermann, G. Seemann, Angelika Ptok, M. Ptok, T. E. Carey, M. Steffen, U. C. Nitz, B. Everding, F. Hölzel, G. Kantwerk-Funke, G. Boll, K. S. Zänker, P. Hölzel, J. Heymanns, C. Hennig, M. Rotsch, K. Havemann, Jürgen R. Fischer, Sabine Stehr, Harald Lahm, Peter Drings, Peter H. Krammer, M. Kirsch, A. Strubel, A. Kist, R. Hinn, H. Fischer, A. Buttler, G. Schackert, S. Friedenauer, D. Lindner, B. Marczynski, H. Karcls, H. W. Goergens, B. Epe, E. Müller, D. Schütze, S. Boiteux, E. Eder, C. Deininger, C. Hoffman, E. Scherer, E. Vermeulen, H. J. van Kranen, J. Bax, R. A. Woutersen, C. F. van Kreijl, B. Schurich, H. Hagedorn, E. Kamp, G. Eisenbrand, B. Spiegelhalder, U. Bolm-Audorff, H. G. Bienfait, R. Preussmann, C. -D. Wacker, H. Kehl, Z. Akkan, J. Ries, M. Meger, S. E. Shephard, D. Gunz, W. K. Lutz, A. R. Tricker, R. Kurnar, M. Siddiqi, P. Mende, B. Pfundstein, A. Scholl, C. Janzowski, D. Jacob, P. Goelzer, I. Henn, H. Zankl, K. -H. Zimlich, Barbara Gansewendt, Ricarda Thier, K. R. Schroeder, E. Hallier, G. Moeckel, W. Heiden, M. Waldherr-Teschner, J. Brickmann, H. Roeser, G. Krauter, G. Scherer, A. Krätschmer, H. Hauenstein, F. Adlkofer, R. C. Fernando, H. H. Schmeiser, W. Nicklas, Wolfgang Pfau, David H. Phillips, S. Scheckenbach, S. Cantoreggi, Monika Leutbecher, H. Ottenwälder, U. Föst, P. M. Baumgart, H. -C. Kliem, S. Data, C. Pfeiffer, A. Fuchs, P. Schmezer, F. Kuchenmeister, B. L. Pool-Zober, U. M. Liegibel, B. L. Pool-Zobel, L. Steeb, H. Friesel, Th. Schneider, H. R. Scherf, A. Buchmann, R. Bauer-Hofmann, J. Mahr, M. Schwarz, R. Schmidt, F. Rippmann, B. Steinbauer, P. Zlfu, B. Bunk, W. Hefter, K. Klinga, M. R. Berger, L. W. Robertson, G. Luebeck, S. Moolgavkar, U. Torsten, M. Kowalczyk-Wagner, H. Weitzel, Ch. Zechel, H. Peters, F. Anders, S. Ambs, T. Kirchner, H. -G. Neumann, C. Einig, E. Eigenbrodt, D. Oesterle, E. Deml, G. Weisse, U. Gerbracht, H. Stumpf, E. Filsingcr, P. Bannasch, W. Muster, P. Cikryt, P. Münzel, E. Röhrdanz, K. W. Bock, H. -P. Lipp, T. Wiesmüller, H. Hagenmaier, D. Schrenk, A. Karger, G. Bauer, P. Höfler, M. Götschl, E. Viesel, J. Jürgensmeier, D. Schaefer, G. Picht, J. Kiefer, P. Krieg, R. Schnapke, S. Feil, E. Wagner, U. Schleenbecker, A. Anders, M. M. Gross, S. Unger, E. J. Stanbridge, Petra Boukamp, Ulrich Pascheberg, Norbert E. Fusenig, H. Abken, U. H. Weidle, F. Grummt, K. Willecke, R. Schäfer, A. Hajnal, I. Balmer, R. Klemenz, P. E. Goretzki, H. Reishaus, M. Demeure, H. Haubruck, J. Lyons, H. D. Röher, Sylvia Trouliaris, Angelika Hadwiger-Fangmeier, Elke Simon, Heiner Niemann, Teruko Tamura, G. Westphal, Elke Turner, H. Karels, M. Blaszkewicz, Helga Stopper, Dietmar Schiffmann, Umberto De Boni, M. Schuler, R. Schnitzler, M. Metzler, E. Pfeiffer, R. Aulenbacher, T. Langhof, K. R. Schröder, K. Saal, H. K. Müller-Hermelink, W. Henn, G. Seitz, P. Lagoda, A. Christmann, N. Blin, C. Welter, D. Adam, D. Fömzler, C. Winkler, W. Mäueler, M. Schartl, B. Theisinger, G. Schüder, U. Rüther, C. Nunnensiek, H. A. G. Müller, W. Rupp, M. Lüthgens, P. Jipp, I. Kinzler, M. Gulich, H. J. Seidel, O. H. Clark, F. McCormick, H. R. Bourne, F. Gieseler, F. Boege, H. Biersack, B. Spohn, M. Clark, K. Wilms, Fritz Boege, Frank Gieseler, Harald Biersack, Michael Clark, Klaus Wllms, Axel Polack, Lothar Strobl, Regina Feederle, Matthias Schweizer, Dirk Eick, Georg W. Bornkamm, M. Kopun, H. Scherthan, C. Granzow, P. Janiaud, D. Rueß, B. M. Mechler, P. G. Strauss, V. Erfle, M. Fritsche, C. Haessler, H. Christiansen, J. Schestag, N. M. Christiansen, F. Lampert, Wolfgang A. Schulz, Andreas Hasse, Helmut Sies, G. Orend, I. Kuhlmann, W. Doerfler, A. Behn-Krappa, I. Hölker, U. Sandaradura de Silva, Ute Smola, Dagmar Hennig, Angelika Hadviger-Fangmeier, Burkhard Schütz, R. Kerler, H. M. Rabes, G. Dölken, A. A. Fauser, R. Kerkert, U. Ragoczy, R. Fritzen, W. Lange, J. Finke, B. Nowicki, E. Schalipp, W. Siegert, R. Mertelsmann, U. Schilling, H. J. Sinn, W. Maier-Borst, E. A. Friedrich, E. Löhde, M. Lück, H. Raude, H. Schlicker, G. Barzen, E. Kraas, J. Milleck, R. Keymer, S. Störkel, T. Reichert, F. Steinbach, R. Lippold, W. Thoenes, W. Wagner, K. -A. Reiffen, A. Bardosi, D. Brkovic, H. -J. Gabius, B. Brandt, C. Jackisch, D. Seitzer, M. Hillebrand, F. A. Habermann, null Zeindl-Eberhart, null Evelyn, C. Robl, V. Röttgen, C. Nowak, H. -B. Richter-Reichhelm, V. Waldmann, B. Suchy, Ch. Zietz, M. Sarafoff, Richard Ostermayr, Hartmut M. Rabes, J. Lorenz, T. Friedberg, W. Paulus, R. Ferlinz, F. Oesch, E. Jähde, K. -H. Glüsenkamp, L. F. Tietze, M. F. Rajewsky, G. Chen, K. -J. Hutter, J. Bullerdiek, W. J. Zeller, M. Schirner, M. R. Schneider, P. Zbu, M. Gebelein, B. Naser-Hijazi, Nancy E. Hynes, M. Reinhardt, P. Heyl, D. Schmähl, P. Presek, U. Liebenhoff, D. Findik, G. H. Hartmann, C. Kliesch, F. Albert, S. Kunze, M. Wannnenmacher, J. Boese-Landgraf, E. Lorenz, D. Albrecht, M. Dulce, K. R. Aigner, N. Thiem, H. Müller, M. Leonardi, A. Justh, M. Lutz, E. Lang, C. W. v. d. Lieth, H. Sinn, B. R. Betsch, Jan Georg Hengstler, Jürgen Fuchs, Franz Oesch, F. J. Busch, A. B. C. Cato, G. Schied, W. Tang, B. Richter, C. Schaefer, D. K. Kelleher, P. Vaupel, D. Mundt, H. H. Bartsch, H. Meden, M. Meyer, K. Vehmeyer, R. Mull, W. Kuhn, S. Hoffmann, D. Berger, H. Fiebig, Ch. Moog, B. Luu, S. Frühauf, B. K. Keppler, A. Galeano, P. Valenzuela-Paz, T. Klenner, H. Stadler, G. Golomb, E. Breuer, R. Voegeli, P. Hilgard, H. R. Nowrousian, P. Aulenbacher, B. Winterhalter, C. Granson, M. Stöhr, H. Ponstingl, P. Drings, H. Osswald, S. B. Sobottka, E. Amtmann, G. Sauer, B. Hornung, S. Volland, S. Kahl, R. Gerspach, B. Matz, J. Schmidt, M. Lipp, G. Brehm, A. Luz, S. Wendel, P. G. Strauß, V. Erflte, S. Greehmann, A. Zobel, F. Kalkbrenner, G. Vorbrüggen, K. Moelling, T. Iftner, A. H. Müller, P. G. Fuchs, H. Pfister, Klaus Cichutek, Iris Treinies, Matthias Lang, C. Braun, J. Denner, S. Norley, R. Kurth, L. Music, O. D. Wiestler, A. Aguzzi, A. von Deimling, M. Schneemann, R. Elbl, P. Kleihues, H. Land, H. -P. Hohn, M. Höök, H. -W. Denker, W. Kemmner, K. Zaar, Peter A. Jones, R. Kath, M. Herlyn, P. Maier, H. P. Schawalder, J. Elsner, W. Parzefall, E. Erber, R. Sedivy, R. Schulte-Hermann, J. Hemmer, P. Tomakidi, P. Boukamp, D. Breitkreutz, N. E. Fusenig, F. Kallinowski, W. Strauss, A. L. Brownell, I. D. Bassukas, G. Vester, B. Maurer-Schultze, L. Langbein, H. Kosmehl, D. Katenkamp, Eberhard Spiess, Günther Trefz, Werner Ebert, Peter Jordan, Dieter Kübler, Rosemarie B. Lichtner, Marion Wiedemuth, Annette Kittmann, Axel Ullrich, Khashayarsha Khazaie, Aiga Kowitz, Guni Kadmon, Peter Altevogt, U. H. Frixen, J. Behrens, J. Schipper, M. Sachs, H. Birchmeier, R. Hackenberg, Th. Hawighorst, J. Hofmann, H. Beato, K. -D. Schulz, C. Erbil, M. Maasberg, L. A. Kunz, A. Simm, G. Adam, W. Mueller-Klieser, Andreas M. Kaufmann, Michael Stoeck, A. Hülsen, S. Game, M. Donnelly, H. -J. Stark, K. -H. Schlingensiepen, U. Kurzik-Dumke, B. Phannavong, D. Gundacker, E. Gateff, S. Gabius, S. S. Joshi, H. Franz, N. J. John, R. Grümmer, H. W. Denker, M. W. Gross, and U. Karbach

Subjects
Cancer Research, Oncology, General Medicine
Published
1991
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39. Mammalian meiotic telomeres: protein composition and redistribution in relation to nuclear pores.

Author

H, Scherthan, M, Jerratsch, B, Li, S, Smith, M, Hultn, T, Lock, and T, de Lange

Abstract

Mammalian telomeres consist of TTAGGG repeats, telomeric repeat binding factor (TRF), and other proteins, resulting in a protective structure at chromosome ends. Although structure and function of the somatic telomeric complex has been elucidated in some detail, the protein composition of mammalian meiotic telomeres is undetermined. Here we show, by indirect immunofluorescence (IF), that the meiotic telomere complex is similar to its somatic counterpart and contains significant amounts of TRF1, TRF2, and hRap1, while tankyrase, a poly-(ADP-ribose)polymerase at somatic telomeres and nuclear pores, forms small signals at ends of human meiotic chromosome cores. Analysis of rodent spermatocytes reveals Trf1 at mouse, TRF2 at rat, and mammalian Rap1 at meiotic telomeres of both rodents. Moreover, we demonstrate that telomere repositioning during meiotic prophase occurs in sectors of the nuclear envelope that are distinct from nuclear pore-dense areas. The latter form during preleptotene/leptotene and are present during entire prophase I.

Published
2000

40. DNA Damage and Repair in PBMCs after Internal Ex Vivo Irradiation with [ 223 Ra]RaCl 2 and [ 177 Lu]LuCl 3 Mixtures.

Author

Strobel I, Schumann S, Müller J, Buck AK, Port M, Lassmann M, Eberlein U, and Scherthan H

Subjects
Humans, Male, Adult, DNA Breaks, Double-Stranded radiation effects, Radioisotopes, Lutetium, Female, Histones metabolism, Leukocytes, Mononuclear radiation effects, Leukocytes, Mononuclear metabolism, DNA Repair radiation effects, DNA Damage radiation effects
Abstract

The combination of high and low LET radionuclides has been tested in several patient studies to improve treatment response. Radionuclide mixtures can also be released in nuclear power plant accidents or nuclear bomb deployment. This study investigated the DNA damage response and DNA double-strand break (DSB) repair in peripheral blood mononuclear cells (PBMCs) after internal exposure of blood samples of 10 healthy volunteers to either no radiation (baseline) or different radionuclide mixtures of the α- and β-emitters [ 223 Ra]RaCl 2 and [ 177 Lu]LuCl 3 , i.e., 25 mGy/75 mGy, 50 mGy/50 mGy and 75 mGy/25 mGy, respectively. DSB foci and γ-H2AX α-track enumeration directly after 1 h of exposure or after 4 h or 24 h of repair revealed that radiation-induced foci (RIF) and α-track induction in 100 cells was similar for mixed α/β and pure internal α- or β-irradiation, as were the repair rates for all radiation qualities. In contrast, the fraction of unrepaired RIF (Q β ) in PBMCs after mixed α/β-irradiation (50% 223 Ra & 50% 177 Lu: Q β = 0.23 ± 0.10) was significantly elevated relative to pure β-irradiation (50 mGy: Q β, pure = 0.06 ± 0.02), with a similar trend being noted for all mixtures. This α-dose-dependent increase in persistent foci likely relates to the formation of complex DNA damage that remains difficult to repair.

Published
2024
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41. Modelling the In Vivo and Ex Vivo DNA Damage Response after Internal Irradiation of Blood from Patients with Thyroid Cancer.

Author

Schumann S, Scherthan H, Hartrampf PE, Göring L, Buck AK, Port M, Lassmann M, and Eberlein U

Subjects
Humans, Middle Aged, Male, Female, Adult, Aged, DNA Damage, Iodine Radioisotopes therapeutic use, Tumor Suppressor p53-Binding Protein 1 metabolism, Histones metabolism, Leukocytes, Mononuclear metabolism, Leukocytes, Mononuclear radiation effects, Models, Biological, Thyroid Neoplasms radiotherapy, Thyroid Neoplasms blood, Thyroid Neoplasms pathology, Thyroid Neoplasms genetics, DNA Repair, DNA Breaks, Double-Stranded radiation effects
Abstract

This work reports on a model that describes patient-specific absorbed dose-dependent DNA damage response in peripheral blood mononuclear cells of thyroid cancer patients during radioiodine therapy and compares the results with the ex vivo DNA damage response in these patients. Blood samples of 18 patients (nine time points up to 168 h post-administration) were analyzed for radiation-induced γ-H2AX + 53BP1 DNA double-strand break foci (RIF). A linear one-compartment model described the absorbed dose-dependent time course of RIF (Parameters: c characterizes DSB damage induction; k 1 and k 2 are rate constants describing fast and slow repair). The rate constants were compared to ex vivo repair rates. A total of 14 patient datasets could be analyzed; c from 0 to 0.04 h -1 , k (range: 0.19-3.03 h 2 from 0 to 0.04 h -1 . On average, 96% of the damage is repaired quickly with k 1 > 1.1 h -1 ). Two patient subgroups were distinguished by k 1 < 0.6 h n = 6, k 1 > 1.1 h -1 ; n = 8, k 1 < 0.6 h -1 ). A weak correlation with patient age was observed. While induction of RIF was similar among ex vivo and in vivo, the respective repair rates failed to correlate. The lack of correlation between in vivo and ex vivo repair rates and the applicability of the model to other therapies will be addressed in further studies.

Published
2024
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42. The Influence of Computed Tomography Contrast Agent on Radiation-Induced Gene Expression and Double-Strand Breaks.

Author

Schüle S, Bunert F, Hackenbroch C, Beer M, Ostheim P, Stewart S, Port M, Scherthan H, and Abend M

Subjects
Humans, Male, Female, Adult, Gene Expression Regulation radiation effects, Gene Expression Regulation drug effects, DNA Breaks, Double-Stranded radiation effects, DNA Breaks, Double-Stranded drug effects, Contrast Media, Tomography, X-Ray Computed
Abstract

After nuclear scenarios, combined injuries of acute radiation syndrome (ARS) with, e.g., abdominal trauma, will occur and may require contrast-enhanced computed tomography (CT) scans for diagnostic purposes. Here, we investigated the effect of iodinated contrast agents on radiation-induced gene expression (GE) changes used for biodosimetry (AEN, BAX, CDKN1A, EDA2R, APOBEC3H) and for hematologic ARS severity prediction (FDXR, DDB2, WNT3, POU2AF1), and on the induction of double-strand breaks (DSBs) used for biodosimetry. Whole blood samples from 10 healthy donors (5 males, 5 females, mean age: 28 ± 2 years) were irradiated with X rays (0, 1 and 4 Gy) with and without the addition of iodinated contrast agent (0.016 ml contrast agent/ml blood) to the blood prior to the exposure. The amount of contrast agent was set to be equivalent to the blood concentration of an average patient (80 kg) during a contrast-enhanced CT scan. After irradiation, blood samples were incubated at 37°C for 20 min (DSB) and 8 h (GE, DSB). GE was measured employing quantitative real-time polymerase chain reaction. DSB foci were revealed by γH2AX + 53BP1 immunostaining and quantified automatically in >927 cells/sample. Radiation-induced differential gene expression (DGE) and DSB foci were calculated using the respective unexposed sample without supplementation of contrast agent as the reference. Neither the GE nor the number of DSB foci was significantly (P = 0.07-0.94) altered by the contrast agent application. However, for some GE and DSB comparisons with/without contrast agent, there were weakly significant differences (P = 0.03-0.04) without an inherent logic and thus are likely due to inter-individual variation. In nuclear events, the diagnostics of combined injuries can require the use of an iodinated contrast agent, which, according to our results, does not alter or influence radiation-induced GE changes and the quantity of DSB foci. Therefore, the gene expression and γH2AX focus assay can still be applied for biodosimetry and/or hematologic ARS severity prediction in such scenarios., (©2024 by Radiation Research Society. All rights of reproduction in any form reserved.)

Published
2024
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43. Short-term Effects of Non-invasive Physical Plasma Treatment on Genomic Stability.

Author

Gelbrich N, Muhtadi R, Scherthan H, and Stope MB

Subjects
Humans, Caspase 3 genetics, DNA chemistry, Genomic Instability, DNA Repair, DNA Damage
Abstract

Background/aim: The application of non-invasive physical plasma (NIPP) generates reactive oxygen species. These can lead to chemical oxidation of cellular molecules including DNA. On the other hand, NIPP can induce therapeutically intended apoptosis, which also leads to DNA fragmentation in the late phase. Therefore, to assess unwanted genotoxic effects, the formation of DNA damage was investigated in this study in discrimination from apoptotic processes., Materials and Methods: Mutation events after NIPP application were analyzed in CCL-93 fibroblast cells using the hypoxanthine phosphoribosyl transferase assay. Additionally, DNA single-strand breaks (SSB) and double-strand breaks (DSB) were quantified by performing the alkaline comet assay, and terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. DSBs were quantified by phospho-histone 2AX-p53-binding protein 1 co-localization DSB focus assay. The data were compared with cell death quantification by the caspase-3/7 apoptosis assay., Results: Treatment with NIPP led to exceedingly rapid damage to genomic DNA and the appearance of DNA SSBs and DSBs in the initial 4 h. However, damage decreased again within the first 4-8 h, then the late phase began, characterized by DNA DSB and increasing caspase-3/7 activation., Conclusion: Although NIPP treatment leads to extremely rapid damage to genomic DNA, this damage is reversed very quickly by efficient DNA-repair processes. As a consequence, only those cells whose genome damage can be repaired actually survive and proliferate. Persistent genotoxic effects were not observed in the cell system used., (Copyright © 2024, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Published
2024
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44. Nano-Architecture of Persistent Focal DNA Damage Regions in the Minipig Epidermis Weeks after Acute γ-Irradiation.

Author

Scherthan H, Geiger B, Ridinger D, Müller J, Riccobono D, Bestvater F, Port M, and Hausmann M

Subjects
Animals, Swine, Swine, Miniature genetics, Swine, Miniature metabolism, Dose-Response Relationship, Radiation, DNA Damage, Chromatin, Epidermis metabolism, Discoidin Domain Receptors genetics, Discoidin Domain Receptors metabolism, Histones metabolism, DNA Repair
Abstract

Exposure to high acute doses of ionizing radiation (IR) can induce cutaneous radiation syndrome. Weeks after such radiation insults, keratinocyte nuclei of the epidermis exhibit persisting genomic lesions that present as focal accumulations of DNA double-strand break (DSB) damage marker proteins. Knowledge about the nanostructure of these genomic lesions is scarce. Here, we compared the chromatin nano-architecture with respect to DNA damage response (DDR) factors in persistent genomic DNA damage regions and healthy chromatin in epidermis sections of two minipigs 28 days after lumbar irradiation with ~50 Gy γ-rays, using single-molecule localization microscopy (SMLM) combined with geometric and topological mathematical analyses. SMLM analysis of fluorochrome-stained paraffin sections revealed, within keratinocyte nuclei with perisitent DNA damage, the nano-arrangements of pATM, 53BP1 and Mre11 DDR proteins in γ-H2AX-positive focal chromatin areas (termed macro-foci). It was found that persistent macro-foci contained on average ~70% of 53BP1, ~23% of MRE11 and ~25% of pATM single molecule signals of a nucleus. MRE11 and pATM fluorescent tags were organized in focal nanoclusters peaking at about 40 nm diameter, while 53BP1 tags formed nanoclusters that made up super-foci of about 300 nm in size. Relative to undamaged nuclear chromatin, the enrichment of DDR protein signal tags in γ-H2AX macro-foci was on average 8.7-fold (±3) for 53BP1, 3.4-fold (±1.3) for MRE11 and 3.6-fold (±1.8) for pATM. The persistent macro-foci of minipig epidermis displayed a ~2-fold enrichment of DDR proteins, relative to DSB foci of lymphoblastoid control cells 30 min after 0.5 Gy X-ray exposure. A lasting accumulation of damage signaling and sensing molecules such as pATM and 53BP1, as well as the DSB end-processing protein MRE11 in the persistent macro-foci suggests the presence of diverse DNA damages which pose an insurmountable problem for DSB repair.

Published
2023
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45. Postirradiation temperature influences DSB repair and dicentric chromosome formation-potential impact for dicentric chromosome analysis in interlaboratory comparisons.

Author

Beinke C, Port M, and Scherthan H

Subjects
Temperature, Cytogenetics, Chromosomes genetics, DNA Breaks, Double-Stranded, DNA Repair
Abstract

The objective was to investigate the influence of different pre-storage temperatures in the dicentric chromosome analysis (DCA) protocol (22°C vs. 37°C) by using γ-H2AX + 53BP1 foci as a marker for deoxyribonucleic acid (DNA) double-strand break (DSB) damage induction and repair and the formation of dicentric chromosomes as a result of mis-repair. Repair of γ-H2AX + 53BP1 DSB foci was absent in samples that were incubated for 2 h at 22°C after exposure of 0.5 and 1.2 Gy. When 0.5- and 1.2-Gy-exposed samples were incubated at 37°C for 2 h, there was an average decline of 31 and 52% of DSB foci, respectively. This indicated that DNA repair occurred. There was a 27% decrease in dicentric chromosome yield at 1.2 Gy and a 15% decrease at 3.5 Gy after post-irradiation incubation for 2 h at 37°C relative to the observed dicentric frequencies at 22°C. Recommended to re-phase: our data suggested that there were more open DSBs after a 2-h incubation at 22°C, which contributed to more mis-repair and dicentric formation from the start of culture. Our findings are corroborated by publications showing that lesion interaction based on enzymatic activity is suppressed below 21°C. As such temperature variations can be a source of variation in DCA during interlaboratory comparison studies, we propose to establish a common guide for the standardisation of pre-culture conditions in cytogenetic dosimetry proficiency testing., (© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Published
2023
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46. Radiation-induced double-strand breaks by internal ex vivo irradiation of lymphocytes: Validation of a Monte Carlo simulation model using GATE and Geant4-DNA.

Author

Salas-Ramirez M, Maigne L, Fois G, Scherthan H, Lassmann M, and Eberlein U

Abstract

This study describes a method to validate a radiation transport model that quantifies the number of DNA double-strand breaks (DSB) produced in the lymphocyte nucleus by internal ex vivo irradiation of whole blood with the radionuclides 90 Y, 99m Tc, 123 I, 131 I, 177 Lu, 223 Ra, and 225 Ac in a test vial using the GATE/Geant4 code at the macroscopic level and the Geant4-DNA code at the microscopic level., Methods: The simulation at the macroscopic level reproduces an 8 mL cylindrical water-equivalent medium contained in a vial that mimics the geometry for internal ex vivo blood irradiation. The lymphocytes were simulated as spheres of 3.75 µm radius randomly distributed, with a concentration of 125 spheres/mL. A phase-space actor was attached to each sphere to register all the entering particles. The simulation at the microscopic level for each radionuclide was performed using the Geant4-DNA tool kit, which includes the clustering example centered on a density-based spatial clustering of applications with noise (DBSCAN) algorithm. The irradiation source was constructed by generating a single phase space from the sum of all phase spaces. The lymphocyte nucleus was defined as a water sphere of a 3.1 µm radius. The absorbed dose coefficients for lymphocyte nuclei (d Lymph ) were calculated and compared with macroscopic whole blood absorbed dose coefficients (d Blood ). The DBSCAN algorithm was used to calculate the number of DSBs. Lastly, the number of DSB∙cell -1 ∙mGy -1 (simulation) was compared with the number of radiation-induced foci per cell and absorbed dose (RIF∙cell -1 ∙mGy -1 ) provided by experimental data for gamma and beta emitting radionuclides. For alpha emitters, d Lymph and the number of α-tracks∙100 cell -1 ∙mGy -1 and DBSs∙µm -1 were calculated using experiment-based thresholds for the α-track lengths and DBSs/track values. The results were compared with the results of an ex vivo study with 223 Ra., Results: The d Lymph values differed from the d Blood values by -1.0% ( 90 Y), -5.2% ( 99m Tc), -22.3% ( 123 I), 0.35% ( 131 I), 2.4% ( 177 Lu), -5.6% ( 223 Ra) and -6.1% ( 225 Ac). The number of DSB∙cell -1 ∙mGy -1 for each radionuclide was 0.015 DSB∙cell -1 ∙mGy -1 ( 90 Y), 0.012 DSB∙cell -1 ∙mGy -1 ( 99m Tc), 0.014DSB∙cell -1 ∙mGy -1 ( 123 I), 0.012 DSB∙cell -1 ∙mGy -1 ( 131 I), and 0.016 DSB∙cell -1 ∙mGy -1 ( 177 Lu). These values agree very well with experimental data. The number of α-tracks∙100 cells -1 ∙mGy -1 for 223 Ra and 225 Ac where 0.144 α-tracks∙100 cells -1 ∙mGy -1 and 0.151 α-tracks∙100 cells -1 ∙mGy -1 , respectively. These values agree very well with experimental data. Moreover, the linear density of DSBs per micrometer α-track length were 11.13 ± 0.04 DSB/µm and 10.86 ± 0.06 DSB/µm for 223 Ra and 225 Ac, respectively., Conclusion: This study describes a model to simulate the DNA DSB damage in lymphocyte nuclei validated by experimental data obtained from internal ex vivo blood irradiation with radionuclides frequently used in diagnostic and therapeutic procedures in nuclear medicine., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: M. Lassmann has received institutional grants by IPSEN Pharma, Nordic Nanovector, and Novartis. No other potential conflicts of interest relevant to this article exist., (Copyright © 2023. Published by Elsevier GmbH.)

Published
2023
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47. The order of sequential exposure of U2OS cells to gamma and alpha radiation influences the formation and decay dynamics of NBS1 foci.

Author

Tartas A, Lundholm L, Scherthan H, Wojcik A, and Brzozowska B

Subjects
Gamma Rays, DNA Breaks, Double-Stranded, DNA Damage, Green Fluorescent Proteins, Alpha Particles, Records
Abstract

DNA double strand breaks (DSBs) are a deleterious form of DNA damage. Densely ionising alpha radiation predominantly induces complex DSBs and sparsely ionising gamma radiation-simple DSBs. We have shown that alphas and gammas, when applied simultaneously, interact in producing a higher DNA damage response (DDR) than predicted by additivity. The mechanisms of the interaction remain obscure. The present study aimed at testing whether the sequence of exposure to alphas and gammas has an impact on the DDR, visualised by live NBS1-GFP (green fluorescent protein) focus dynamics in U2OS cells. Focus formation, decay, intensity and mobility were analysed up to 5 h post exposure. Focus frequencies directly after sequential alpha → gamma and gamma → alpha exposure were similar to gamma alone, but gamma → alpha foci quickly declined below the expected values. Focus intensities and areas following alpha alone and alpha → gamma were larger than after gamma alone and gamma → alpha. Focus movement was most strongly attenuated by alpha → gamma. Overall, sequential alpha → gamma exposure induced the strongest change in characteristics and dynamics of NBS1-GFP foci. Possible explanation is that activation of the DDR is stronger when alpha-induced DNA damage precedes gamma-induced DNA damage., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. This does not alter our adherence to PLOS ONE policies on sharing data and materials., (Copyright: © 2023 Tartas et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Published
2023
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48. RENEB Inter-Laboratory Comparison 2021: The Gamma-H2AX Foci Assay.

Author

Moquet J, Ainsbury E, Balázs K, Barnard S, Hristova R, Lumniczky K, Port M, Roessler U, Scherthan H, Staynova A, Szatmári T, Wojewodzka M, and Abend M

Subjects
Humans, Retrospective Studies, Laboratories, Dose-Response Relationship, Radiation, Radiometry methods, Biological Assay methods
Abstract

The Running the European Network of biological and retrospective dosimetry (RENEB) network of laboratories has a range of biological and physical dosimetry assays that can be deployed in the event of a radiation incident to provide exposure assessment. To maintain operational capability and provide training, RENEB runs regular inter-laboratory comparison (ILC) exercises. The RENEB ILC2021 was carried out with all the biological and physical dosimetry assays employed in the network. The focus of this paper is to evaluate the results from 6 laboratories that took part using the gamma-H2AX radiation-induced foci assay. For two laboratories this was their first RENEB ILC. Blood samples were homogenously exposed to 240 kVp X rays (1 Gy/min) to provide calibration data, (0-4 Gy), and a few weeks later three blind coded test samples, (0, 1.2 and 3.5 Gy) were prepared. All samples were allowed a 2 h repair time at 37°C before being transported, on ice packs, to the participating laboratories. On arrival, the samples were processed, scored either manually or automatically for gamma-H2AX foci and dose estimates for the 3 blind coded samples sent to the organizing laboratory. The temperature of samples during transit and the time taken to report the dose estimates were recorded. Subsequent examination of the data from each laboratory used the doses estimates to assign triage categories to the samples. After receipt of the samples, the quickest report of dose estimates was 4.6 h. Analysis of variance revealed that the laboratory carrying out the assay had a significant effect on the foci yield (P < 0.001) for the calibration data, but not on the dose estimates of the blind coded samples (P = 0.101). All laboratories correctly identified the unirradiated and irradiated samples, although the dose estimates for the latter tended to under-estimate the dose. Two participants seriously under-estimated the dose for the highly exposed sample, which resulted in the sample being placed in the lowest triage category not the highest. However, this under-estimation resulted from the samples not remaining cold during shipment, due to a delay in transit and was not related to the experience of the participating laboratory. Overall, the RENEB network laboratories have demonstrated it is possible to quickly identify a recent whole-body acute exposure using the gamma-H2AX assay within the conditions of the ILC. In addition, an ILC provides a useful training and harmonization exercise for laboratories., (©2023 by Radiation Research Society. All rights of reproduction in any form reserved.)

Published
2023
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49. RENEB Inter-Laboratory Comparison 2021: Inter-Assay Comparison of Eight Dosimetry Assays.

Author

Port M, Barquinero JF, Endesfelder D, Moquet J, Oestreicher U, Terzoudi G, Trompier F, Vral A, Abe Y, Ainsbury L, Alkebsi L, Amundson SA, Badie C, Baeyens A, Balajee AS, Balázs K, Barnard S, Bassinet C, Beaton-Green LA, Beinke C, Bobyk L, Brochard P, Brzoska K, Bucher M, Ciesielski B, Cuceu C, Discher M, D Oca MC, Domínguez I, Doucha-Senf S, Dumitrescu A, Duy PN, Finot F, Garty G, Ghandhi SA, Gregoire E, Goh VST, Güçlü I, Hadjiiska L, Hargitai R, Hristova R, Ishii K, Kis E, Juniewicz M, Kriehuber R, Lacombe J, Lee Y, Lopez Riego M, Lumniczky K, Mai TT, Maltar-Strmečki N, Marrale M, Martinez JS, Marciniak A, Maznyk N, McKeever SWS, Meher PK, Milanova M, Miura T, Monteiro Gil O, Montoro A, Moreno Domene M, Mrozik A, Nakayama R, O'Brien G, Oskamp D, Ostheim P, Pajic J, Pastor N, Patrono C, Pujol-Canadell M, Prieto Rodriguez MJ, Repin M, Romanyukha A, Rößler U, Sabatier L, Sakai A, Scherthan H, Schüle S, Seong KM, Sevriukova O, Sholom S, Sommer S, Suto Y, Sypko T, Szatmári T, Takahashi-Sugai M, Takebayashi K, Testa A, Testard I, Tichy A, Triantopoulou S, Tsuyama N, Unverricht-Yeboah M, Valente M, Van Hoey O, Wilkins RC, Wojcik A, Wojewodzka M, Younghyun L, Zafiropoulos D, and Abend M

Subjects
Retrospective Studies, Cytokinesis, Electron Spin Resonance Spectroscopy, Biological Assay, Blood Specimen Collection
Abstract

Tools for radiation exposure reconstruction are required to support the medical management of radiation victims in radiological or nuclear incidents. Different biological and physical dosimetry assays can be used for various exposure scenarios to estimate the dose of ionizing radiation a person has absorbed. Regular validation of the techniques through inter-laboratory comparisons (ILC) is essential to guarantee high quality results. In the current RENEB inter-laboratory comparison, the performance quality of established cytogenetic assays [dicentric chromosome assay (DCA), cytokinesis-block micronucleus assay (CBMN), stable chromosomal translocation assay (FISH) and premature chromosome condensation assay (PCC)] was tested in comparison to molecular biological assays [gamma-H2AX foci (gH2AX), gene expression (GE)] and physical dosimetry-based assays [electron paramagnetic resonance (EPR), optically or thermally stimulated luminescence (LUM)]. Three blinded coded samples (e.g., blood, enamel or mobiles) were exposed to 0, 1.2 or 3.5 Gy X-ray reference doses (240 kVp, 1 Gy/min). These doses roughly correspond to clinically relevant groups of unexposed to low exposed (0-1 Gy), moderately exposed (1-2 Gy, no severe acute health effects expected) and highly exposed individuals (>2 Gy, requiring early intensive medical care). In the frame of the current RENEB inter-laboratory comparison, samples were sent to 86 specialized teams in 46 organizations from 27 nations for dose estimation and identification of three clinically relevant groups. The time for sending early crude reports and more precise reports was documented for each laboratory and assay where possible. The quality of dose estimates was analyzed with three different levels of granularity, 1. by calculating the frequency of correctly reported clinically relevant dose categories, 2. by determining the number of dose estimates within the uncertainty intervals recommended for triage dosimetry (±0.5 Gy or ±1.0 Gy for doses <2.5 Gy or >2.5 Gy), and 3. by calculating the absolute difference (AD) of estimated doses relative to the reference doses. In total, 554 dose estimates were submitted within the 6-week period given before the exercise was closed. For samples processed with the highest priority, earliest dose estimates/categories were reported within 5-10 h of receipt for GE, gH2AX, LUM, EPR, 2-3 days for DCA, CBMN and within 6-7 days for the FISH assay. For the unirradiated control sample, the categorization in the correct clinically relevant group (0-1 Gy) as well as the allocation to the triage uncertainty interval was, with the exception of a few outliers, successfully performed for all assays. For the 3.5 Gy sample the percentage of correct classifications to the clinically relevant group (≥2 Gy) was between 89-100% for all assays, with the exception of gH2AX. For the 1.2 Gy sample, an exact allocation to the clinically relevant group was more difficult and 0-50% or 0-48% of the estimates were wrongly classified into the lowest or highest dose categories, respectively. For the irradiated samples, the correct allocation to the triage uncertainty intervals varied considerably between assays for the 1.2 Gy (29-76%) and 3.5 Gy (17-100%) samples. While a systematic shift towards higher doses was observed for the cytogenetic-based assays, extreme outliers exceeding the reference doses 2-6 fold were observed for EPR, FISH and GE assays. These outliers were related to a particular material examined (tooth enamel for EPR assay, reported as kerma in enamel, but when converted into the proper quantity, i.e. to kerma in air, expected dose estimates could be recalculated in most cases), the level of experience of the teams (FISH) and methodological uncertainties (GE). This was the first RENEB ILC where everything, from blood sampling to irradiation and shipment of the samples, was organized and realized at the same institution, for several biological and physical retrospective dosimetry assays. Almost all assays appeared comparably applicable for the identification of unexposed and highly exposed individuals and the allocation of medical relevant groups, with the latter requiring medical support for the acute radiation scenario simulated in this exercise. However, extreme outliers or a systematic shift of dose estimates have been observed for some assays. Possible reasons will be discussed in the assay specific papers of this special issue. In summary, this ILC clearly demonstrates the need to conduct regular exercises to identify research needs, but also to identify technical problems and to optimize the design of future ILCs.

Published
2023
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50. Initial experience on abdominal photon-counting computed tomography in clinical routine: general image quality and dose exposure.

Author

Becker BV, Kaatsch HL, Nestler K, Overhoff D, Schneider J, Dillinger D, Piechotka J, Brockmann MA, Ullmann R, Port M, Scherthan H, and Waldeck S

Subjects
Humans, Retrospective Studies, Radiation Dosage, Signal-To-Noise Ratio, Phantoms, Imaging, Tomography, X-Ray Computed methods, DNA
Abstract

Objectives: Photon-counting computed tomography has lately found its way into clinical routine. The new technique could offer substantial improvements regarding general image quality, image noise, and radiation dose reduction. This study evaluated the first abdominal examinations in clinical routine and compared the results to conventional computed tomography., Methods: In this single-center retrospective study, 66 patients underwent photon-counting and conventional abdominal CT. Four radiologists assessed general image quality, image noise, and image artifacts. Signal-to-noise ratio and dose properties of both techniques within the clinical application were compared. An ex vivo phantom study revealed the radiobiological impact by means of DNA double-strand break foci in peripheral blood cells by enumerating γ-H2AX+53BP1 foci., Results: General image quality in accordance with the Likert scale was found superior for photon-counting CT (4.74 ± 0.46 vs. 4.25 ± 0.54; p < 0.001). Signal-to-noise ratio (p < 0.001) and also dose exposure were higher for photon-counting CT (DLP: 419.2 ± 162.2 vs. 372.3 ± 236.6 mGy*cm; p = 0.0435). CT exposure resulted in significantly increased DNA damage in comparison to sham control (p < 0.001). Investigation of the average foci per cell and radiation-induced foci numbers revealed significantly elevated numbers (p = 0.004 and p < 0.0001, respectively) after photon-counting CT., Conclusion: Photon-counting CT in abdominal examinations showed superior results regarding general image quality and signal-to-noise ratio in clinical routine. However, this seems to be traded for a significantly higher dose exposure and corresponding double-strand break frequency. Optimization of standard protocols in further clinical applications is required to find a compromise regarding picture quality and dose exposure., Key Points: • Photon-counting computed tomography promises to enhance the diagnostic potential of medical imaging in clinical routine. • Retrospective single-center study showed superior general image quality accompanied by higher dose exposure in initial abdominal PCCT protocols compared to state-of-the-art conventional CT. • A simultaneous ex vivo phantom study revealed correspondingly increased frequencies of DNA double-strand breaks after PCCT., (© 2022. The Author(s).)

Published
2023
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