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2. Elective cancer surgery in COVID-19–Free surgical pathways during the SARS-cov-2 pandemic: An international, multicenter, comparative cohort study
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James C Glasbey, Dmitri Nepogodiev, Joana Ff Simoes, Omar Omar, Elizabeth Li, Mary L Venn, Mohammad Abou Chaar, Vita Capizzi, Daoud Chaudhry, Anant Desai, Jonathan G Edwards, Jonathan P Evans, Marco Fiore, Jose Flavio Videria, Samuel J Ford, Ian Ganyli, Ewen A Griffiths, Rohan R Gujjuri, Angelos G Kolias, Haytham Ma Kaafarani, Ana Minaya-Bravo, Siobhan C McKay, Helen M Mohan, Keith Roberts, Carlos San Miguel-Méndez, Peter Pockney, Richard Shaw, Neil J Smart, Grant D Stewart, Sudha Sundar, Raghavan Vidya, Aneel A Bhangu, James C Glasbey, Omar Omar, Aneel A Bhangu, Kwabena Siaw-Acheampong, Ruth A Benson, Edward Bywater, Daoud Chaudhry, Brett E Dawson, Jonathan P Evans, James C Glasbey, Rohan R Gujjuri, Emily Heritage, Conor S Jones, Sivesh K Kamarajah, Chetan Khatri, Rachel A Khaw, James M Keatley, Andrew Knight, Samuel Lawday, Elizabeth Li, Harvinder S Mann, Ella J Marson, Kenneth A McLean, Siobhan C McKay, Emily C Mills, Dmitri Nepogodiev, Gianluca Pellino, Maria Picciochi, Elliott H Taylor, Abhinav Tiwari, Joana Ff Simoes, Isobel M Trout, Mary L Venn, Richard Jw Wilkin, Aneel A Bhangu, James C Glasbey, Neil J Smart, Ana Minaya-Bravo, Jonathan P Evans, Gaetano Gallo, Susan Moug, Francesco Pata, Peter Pockney, Salomone Di Saverio, Abigail Vallance, Dale Vimalchandran, Ewen A Griffiths, Sivesh K Kamarajah, Richard Pt Evans, Philip Townend, Keith Roberts, Siobhan McKay, John Isaac, Sohei Satoi, John Edwards, Aman S Coonar, Adrian Marchbank, Edward J Caruana, Georgia R Layton, Akshay Patel, Alessandro Brunelli, Samuel Ford, Anant Desai, Alessandro Gronchi, Marco Fiore, Max Almond, Fabio Tirotta, Sinziana Dumitra, Angelos Kolias, Stephen J Price, Daniel M Fountain, Michael D Jenkinson, Peter Hutchinson, Hani J Marcus, Rory J Piper, Laura Lippa, Franco Servadei, Ignatius Esene, Christian Freyschlag, Iuri Neville, Gail Rosseau, Karl Schaller, Andreas K Demetriades, Faith Robertson, Alex Alamri, Richard Shaw, Andrew G Schache, Stuart C Winter, Michael Ho, Paul Nankivell, Juan Rey Biel, Martin Batstone, Ian Ganly, Raghavan Vidya, Alex Wilkins, Jagdeep K Singh, Dinesh Thekinkattil, Sudha Sundar, Christina Fotopoulou, Elaine Leung, Tabassum Khan, Luis Chiva, Jalid Sehouli, Anna Fagotti, Paul Cohen, Murat Gutelkin, Rahel Ghebre, Thomas Konney, Rene Pareja, Rob Bristow, Sean Dowdy, T S Shylasree, R Kottayasamy Seenivasagam, Joe Ng, Keiiji Fujiwara, Grant D Stewart, Benjamin Lamb, Krishna Narahari, Alan McNeill, Alexandra Colquhoun, John McGrath, Steve Bromage, Ravi Barod, Veeru Kasivisvanathan, Tobias Klatte, Joana Ff Simoes, Tom Ef Abbott, Sadi Abukhalaf, Michel Adamina, Adesoji O Ademuyiwa, Arnav Agarwal, Murat Akkulak, Ehab Alameer, Derek Alderson, Felix Alakaloko, Markus Albertsmeiers, Osaid Alser, Muhammad Alshaar, Sattar Alshryda, Alexis P Arnaud, Knut Magne Augestad, Faris Ayasra, José Azevedo, Brittany K Bankhead-Kendall, Emma Barlow, David Beard, Ruth A Benson, Ruth Blanco-Colino, Amanpreet Brar, Ana Minaya-Bravo, Kerry A Breen, Chris Bretherton, Igor Lima Buarque, Joshua Burke, Edward J Caruana, Mohammad Chaar, Sohini Chakrabortee, Peter Christensen, Daniel Cox, Moises Cukier, Miguel F Cunha, Giana H Davidson, Anant Desai, Salomone Di Saverio, Thomas M Drake, John G Edwards, Muhammed Elhadi, Sameh Emile, Shebani Farik, Marco Fiore, J Edward Fitzgerald, Samuel Ford, Tatiana Garmanova, Gaetano Gallo, Dhruv Ghosh, Gustavo Mendonça Ataíde Gomes, Gustavo Grecinos, Ewen A Griffiths, Madalegna GrÜndl, Constantine Halkias, Ewen M Harrison, Intisar Hisham, Peter J Hutchinson, Shelley Hwang, Arda Isik, Michael D Jenkinson, Pascal Jonker, Haytham Ma Kaafarani, Debby Keller, Angelos Kolias, Schelto Kruijff, Ismail Lawani, Hans Lederhuber, Sezai Leventoglu, Andrey Litvin, Andrew Loehrer, Markus W Löffler, Maria Aguilera Lorena, Maria Marta Modolo, Piotr Major, Janet Martin, Hassan N Mashbari, Dennis Mazingi, Symeon Metallidis, Ana Minaya-Bravo, Helen M Mohan, Rachel Moore, David Moszkowicz, Susan Moug, Joshua S Ng-Kamstra, Mayaba Maimbo, Ionut Negoi, Milagros Niquen, Faustin Ntirenganya, Maricarmen Olivos, Kacimi Oussama, Oumaima Outani, Marie Dione Parreno-Sacdalanm, Francesco Pata, Carlos Jose Perez Rivera, Thomas D Pinkney, Willemijn van der Plas, Peter Pockney, Ahmad Qureshi, Dejan Radenkovic, Antonio Ramos-De la Medina, Keith Roberts, April C Roslani, Martin Rutegård, Juan José Segura-Sampedro, Irène Santos, Sohei Satoi, Raza Sayyed, Andrew Schache, Andreas A Schnitzbauer, Justina O Seyi-Olajide, Neil Sharma, Richard Shaw, Sebastian Shu, Kjetil Soreide, Antonino Spinelli, Grant D Stewart, Malin Sund, Sudha Sundar, Stephen Tabiri, Philip Townend, Georgios Tsoulfas, Gabrielle H van Ramshorst, Raghavan Vidya, Dale Vimalachandran, Oliver J Warren, Duane Wedderburn, Naomi Wright, C Allemand, L Boccalatte, M Figari, M Lamm, J Larrañaga, C Marchitelli, F Noll, D Odetto, M Perrotta, J Saadi, L Zamora, C Alurralde, E L Caram, D Eskinazi, J P Mendoza, M Usandivaras, R Badra, A Esteban, J S García, P M García, J I Gerchunoff, S M Lucchini, M A NIgra, L Vargas, T Hovhannisyan, A Stepanyan, T Gould, R Gourlay, B Griffiths, S Gananadha, M McLaren, J Cecire, N Joshi, S Salindera, A Sutherland, J H Ahn, G Charlton, S Chen, N Gauri, R Hayhurst, S Jang, F Jia, C Mulligan, W Yang, G Ye, H Zhang, M Ballal, D Gibson, D Hayne, J Moss, T Richards, P Viswambaram, U G Vo, J Bennetts, T Bright, M Brooke-Smith, R Fong, B Gricks, Y H Lam, B S Ong, M Szpytma, D Watson, K Bagraith, S Caird, E Chan, C Dawson, D Ho, E Jeyarajan, S Jordan, A Lim, G J Nolan, A Oar, D Parker, H Puhalla, A Quennell, L Rutherford, P Townend, M Von Papen, M Wullschleger, A Blatt, D Cope, N Egoroff, M Fenton, J Gani, N Lott, P Pockney, N Shugg, M Elliott, D Phung, D Phan, D Townend, C Bong, J Gundara, A Frankel, S Bowman, G R Guerra, J Bolt, K Buddingh, N N Dudi-Venkata, S Jog, H M Kroon, T Sammour, R Smith, C Stranz, M Batstone, K Lah, W McGahan, D Mitchell, A Morton, A Pearce, M Roberts, G Sheahan, B Swinson, N Alam, S Banting, L Chong, P Choong, S Clatworthy, D Foley, A Fox, M W Hii, B Knowles, J Mack, M Read, A Rowcroft, S Ward, G Wright, M Lanner, I Königsrainer, M Bauer, C Freyschlag, M Kafka, F Messner, D Öfner, I Tsibulak, K Emmanuel, M Grechenig, R Gruber, M Harald, L Öhlberger, J Presl, A Wimmer, I Namazov, E Samadov, D Barker, R Boyce, S Corbin, A Doyle, A Eastmond, R Gill, A Haynes, S Millar, M O'Shea, G Padmore, N Paquette, E Phillips, S St John, K Walkes, N Flamey, P Pattyn, W Oosterlinck, J Van den Eynde, R Van den Eynde, A Gatti, C Nardi, R Oliva, R De Cicco, I Cecconello, P Gregorio, L Pontual Lima, U Ribeiro Junior, F Takeda, R M Terra, M Sokolov, B Kidane, S Srinathan, M Boutros, N Caminsky, G Ghitulescu, G Jamjoum, J Moon, J Pelletier, T Vanounou, S Wong, M Boutros, S Dumitra, A Kouyoumdjian, B Johnston, C Russell, M Boutros, S Demyttenaere, R Garfinkle, J Abou-Khalil, C Nessim, J Stevenson, F Heredia, A Almeciga, A Fletcher, A Merchan, L O Puentes, J Mendoza Quevedo, G Bacic, D Karlovic, D Krsul, M Zelic, I Luksic, M Mamic, B Bakmaz, I Coza, E Dijan, Z Katusic, J Mihanovic, I Rakvin, K Frantzeskou, N Gouvas, G Kokkinos, P Papatheodorou, I Pozotou, O Stavrinidou, A Yiallourou, L Martinek, M Skrovina, I Szubota, J Žatecký, V Javurkova, J Klat, T Avlund, P Christensen, J L Harbjerg, L H Iversen, D W Kjaer, Hø Kristensen, M Mekhael, A L Ebbehøj, P Krarup, N Schlesinger, H Smith, A Abdelsamed, A Y Azzam, H Salem, A Seleim, A Abdelmajeed, M Abdou, N E Abosamak, M Al Sayed, F Ashoush, R Atta, E Elazzazy, M Elhoseiny, M Elnemr, M S Elqasabi, M E Elsayed Hewalla, I Elsherbini, E Essam, M Eweda, I Ghallab, E Hassan, M Ibrahim, M Metwalli, M Mourad, M S Qatora, M Ragab, A Sabry, H Saifeldin, M Saleh Mesbah Mohamed Elkaffas, A Samih, A Samir Abdelaal, S Shehata, K Shenit, D Attia, N Kamal, N Osman, A M Abbas, Has Abd Elazeem, M M Abdelkarem, S Alaa, A K Ali, A Ayman, M G Azizeldine, H Elkhayat, S M Elghazaly, F A Monib, M A Nageh, M M Saad, M Salah, M Shahine, E A Yousof, A Youssef, A Eldaly, M ElFiky, A Nabil, G Amira, I Sallam, M Sherief, A Sherif, A Abdelrahman, H Aboulkassem, G Ghaly, R Hamdy, A Morsi, H Salem, G Sherif, H Abdeldayem, I Abdelkader Salama, M Balabel, Y Fayed, A E Sherif, D Bekele, J Kauppila, E Sarjanoja, O Helminen, H Huhta, J H Kauppila, C Beyrne, L Jouffret, L Lugans, L Marie-Macron, E Chouillard, B De Simone, J Bettoni, S Dakpé, B Devauchelle, N Lavagen, S Testelin, S Boucher, R Breheret, A Gueutier, A Kahn, J KÜn-Darbois, A Barrabe, Z Lakkis, A Louvrier, S Manfredelli, P Mathieu, A Chebaro, V Drubay, M El Amrani, C Eveno, K Lecolle, G Legault, L Martin, G Piessen, F R Pruvot, S Truant, P Zerbib, Q Ballouhey, B Barrat, J Laloze, H Salle, A Taibi, J Usseglio, D Bergeat, A Merdrignac, Roy B Le, L O Perotto, A Scalabre, A Aimé, A Ezanno, B Malgras, P Bouche, S Tzedakis, E Cotte, O Glehen, V Kepenekian, J Lifante, G Passot, A D'Urso, E Felli, D Mutter, P Pessaux, B Seeliger, J Bardet, R Berry, G Boddaert, S Bonnet, E Brian, C Denet, D Fuks, D Gossot, M Grigoroiu, A Laforest, Y Levy-Zauberman, C Louis-Sylvestre, A Moumen, G Pourcher, A Seguin-Givelet, E Tribillon, E Duchalais, F Espitalier, C Ferron, O Malard, U Bork, M Distler, J Fritzmann, J Kirchberg, C Praetorius, C Riediger, J Weitz, T Welsch, P Wimberger, K Beyer, C Kamphues, J Lauscher, F N Loch, C Schineis, M Albertsmeier, M Angele, A Kappenberger, H Niess, T Schiergens, J Werner, R Becker, J Jonescheit, I Pergolini, D Reim, C Boeker, I Hakami, J Mall, P Liokatis, W Smolka, K Nowak, T Reinhard, F Hölzle, A Modabber, P Winnand, M Knitschke, P Kauffmann, S Wolfer, J Kleeff, K Lorenz, C Michalski, U Ronellenfitsch, R Schneider, E Bertolani, A Königsrainer, M W Löffler, M Quante, C Steidle, L ÜberrÜck, C Yurttas, C S Betz, J Bewarder, A Böttcher, S Burg, C Busch, M Gosau, A Heuer, J Izbicki, T O Klatte, D Koenig, N Moeckelmann, C Nitschke, M Priemel, R Smeets, U Speth, S Thole, F G Uzunoglu, T Vollkommer, N Zeller, M J Battista, K Gillen, A Hasenburg, S Krajnak, V Linz, R Schwab, K Angelou, D Haidopoulos, A Rodolakis, P Antonakis, K Bramis, L Chardalias, I Contis, N Dafnios, D Dellaportas, G Fragulidis, A Gklavas, M Konstadoulakis, N Memos, I Papaconstantinou, A Polydorou, T Theodosopoulos, A Vezakis, M I Antonopoulou, D K Manatakis, N Tasis, N Arkadopoulos, N Danias, P Economopoulou, P Kokoropoulos, A Larentzakis, N Michalopoulos, J Selmani, T Sidiropoulos, V Tsaousis, P Vassiliu, K Bouchagier, S Klimopoulos, D Paspaliari, G Stylianidis, K Baxevanidou, K Bouliaris, P Chatzikomnitsa, M Efthimiou, A Giaglaras, C Kalfountzos, G Koukoulis, A M Ntziovara, K Petropoulos, K Soulikia, I Tsiamalou, K Zervas, S Zourntou, I Baloyiannis, A Diamantis, E Gkrinia, J Hajiioannou, C Korais, O Koukoura, K Perivoliotis, A Saratziotis, C Skoulakis, D Symeonidis, K Tepetes, G Tzovaras, D Zacharoulis, V Alexoudi, K Antoniades, I Astreidis, P Christidis, D Deligiannidis, T Grivas, O Ioannidis, I Kalaitsidou, L Loutzidou, A Mantevas, D Michailidou, K Paraskevopoulos, S Politis, A Stavroglou, D Tatsis, I Tilaveridis, K Vahtsevanos, G Venetis, I Karaitianos, T Tsirlis, A Charalabopoulos, T Liakakos, E Mpaili, D Schizas, E Spartalis, A Syllaios, C Zografos, C Anthoulakis, C Christou, V Papadopoulos, A Tooulias, D Tsolakidis, G Tsoulfas, D Zouzoulas, E Athanasakis, E Chrysos, J Tsiaoussis, S Xenaki, E Xynos, K Futaba, M F Ho, S F Hon, Twc Mak, Ssm Ng, C C Foo, B Banky, N Suszták, M Aremu, A Canas-Martinez, O Cullivan, C Murphy, P Owens, L Pickett, L Akmenkalne, J Byrne, M Corrigan, C Cullinane, A Daly, C Fleming, P Jordan, S Killeen, N Lynch, A McCarthy, H Mustafa, S O'Brien, P O'Leary, Was Syed, L Vernon, D Callanan, L Huang, A Ionescu, P Sheahan, I Balasubramanian, M Boland, K Conlon, D Evoy, N Fearon, T Gallagher, J Geraghty, H Heneghan, N Kennedy, D Maguire, D McCartan, E W McDermott, R S Prichard, D Winter, D Alazawi, C Barry, T Boyle, W Butt, E M Connolly, N Donlon, C Donohue, B A Fahey, R Farrell, C Fitzgerald, J Kinsella, J O Larkin, P Lennon, P J Maguire, P Mccormick, B J Mehigan, H Mohan, T Nugent, H O'Sullivan, N Ravi, J V Reynolds, A Rogers, P Shokuhi, J Smith, L A Smith, C Timon, Y Bashir, G Bass, T Connelly, B Creavin, H Earley, J A Elliott, A Gillis, D Kavanagh, P Neary, J O'riordan, I S Reynolds, D Rice, P Ridgway, M Umair, M Whelan, P Carroll, C Collins, K Corless, L Finnegan, A Fowler, A Hogan, M Kerin, A Lowery, P McAnena, K McKevitt, K Nizami, É Ryan, A Samy, J C Coffey, R Cunningham, M Devine, D Nally, C Peirce, S Tormey, N Hardy, P Neary, S O'Malley, M Ryan, S Macina, N M Mariani, E Opocher, A Pisani Ceretti, F Ferrari, F Odicino, E Sartori, C Cotsoglou, S Granieri, F Bianco, A Camillo, M Colledan, S Tornese, M F Zambelli, G Bissolotti, S Fusetti, F Lemma, M V Marino, A Mirabella, G Vaccarella, C Agostini, G Alemanno, I Bartolini, C Bergamini, A Bruscino, C Checcucci, R De Vincenti, A Di Bella, M Fambrini, L Fortuna, G Maltinti, P Muiesan, F Petraglia, P Prosperi, M N Ringressi, M Risaliti, F Sorbi, A Taddei, R Tucci, C Bassi, L Bortolasi, T Campagnaro, L Casetti, M De Pastena, A Esposito, M Fontana, A Guglielmi, L Landoni, G Malleo, G Marchegiani, S Nobile, S Paiella, C Pedrazzani, S Rattizzato, A Ruzzenente, R Salvia, G Turri, M Tuveri, P Bellora, G D'Aloisio, M Ferrari, E Francone, S Gentilli, H Nikaj, M Bianchini, M Chiarugi, F Coccolini, G Di Franco, N Furbetta, D Gianardi, S Guadagni, L Morelli, M Palmeri, D Tartaglia, G Anania, P Carcoforo, M Chiozza, A De Troia, M Koleva Radica, M Portinari, M G Sibilla, A Urbani, N Fabbri, C V Feo, S Gennari, S Parini, E Righini, L Ampollini, L Bellanti, M Bergonzani, G Bertoli, G Bocchialini, G D'Angelo, D Lanfranco, L Musini, T Poli, G P Santoro, A Varazzani, L Aguzzoli, G Borgonovo, C Castro Ruiz, S Coiro, G Falco, V D Mandato, V Mastrofilippo, M T Montella, V Annessi, M Zizzo, U Grossi, S Novello, M Romano, S Rossi, G Zanus, G Esposito, F Frongia, A Pisanu, M Podda, C Belluco, A Lauretta, G Montori, L Moras, M Olivieri, F Bussu, A G Carta, M L Cossu, P Cottu, A Fancellu, C F Feo, G C Ginesu, G Giuliani, M Madonia, T Perra, A Piras, A Porcu, D Rizzo, A M Scanu, A Tedde, M Tedde, P Delrio, D Rega, G Badalamenti, G Campisi, A Cordova, M Franza, G Maniaci, G Rinaldi, F Toia, M Calabrò, F Farnesi, E G Lunghi, A Muratore, N S Pipitone Federico, F Bàmbina, G D'Andrea, P Familiari, V Picotti, G De Palma, G Luglio, G Pagano, F P Tropeano, L Baldari, G A Beltramini, L Boni, E Cassinotti, A Gianni, L Pignataro, S Torretta, C Abatini, M Baia, D Biasoni, G Bogani, P Cadenelli, V Capizzi, Spb Cioffi, D Citterio, L V Comini, M Cosimelli, M Fiore, S Folli, M Gennaro, L Giannini, A Gronchi, M Guaglio, A Macchi, F Martinelli, V Mazzaferro, A Mosca, S Pasquali, C Piazza, F Raspagliesi, L Rolli, R Salvioni, G Sarpietro, C Sarre, L Sorrentino, A Agnes, S Alfieri, F Belia, A Biondi, V Cozza, A D'Amore, D D'Ugo, V De Simone, A Fagotti, G Gasparini, L Gordini, F Litta, C P Lombardi, L Lorenzon, A A Marra, F Marzi, A Moro, A Parello, E Perrone, R Persiani, C Ratto, F Rosa, G Saponaro, G Scambia, O Scrima, G Sganga, R Tudisco, A Belli, V Granata, F Izzo, R Palaia, R Patrone, F M Carrano, M M Carvello, A De Virgilio, F Di Candido, F Ferreli, F Gaino, G Mercante, V Rossi, A Spinelli, G Spriano, D M Donati, T Frisoni, E Palmerini, A Aprile, F Barra, P Batistotti, S Ferrero, P Fregatti, S Scabini, M Sparavigna, E Asti, D Bernardi, L Bonavina, A Lovece, L Adamoli, M Ansarin, S Cenciarelli, F Chu, R De Berardinis, U Fumagalli Romario, F Mastrilli, G Pietrobon, M Tagliabue, E Badellino, A Ferrero, R Massobrio, A De Manzoni Garberini, P Federico, P Maida, E Marra, G Marte, A Petrillo, T Tammaro, A Tufo, M Berselli, G Borroni, E Cocozza, L Conti, M Desio, L Livraghi, V Quintodei, A Rizzi, A Zullo, C Baldi, C Corbellini, G M Sampietro, P Cellerino, E Baldini, P Capelli, L Conti, S M Isolani, M Ribolla, A Bondurri, F Colombo, L Ferrario, C Guerci, A Maffioli, T Armao, M Ballabio, P Bisagni, A Gagliano, M Longhi, M Madonini, P PizziCni, A M Baietti, M Biasini, P Maremonti, F Neri, G M Prucher, S Ricci, F Ruggiero, A G Zarabini, R Barmasse, S Mochet, L Morelli, A Usai, F Bianco, P Incollingo, S Mancini, L Marino Cosentino, A Sagnotta, R Fruscio, T Grassi, L C Nespoli, N Tamini, A Anastasi, B Bartalucci, A Bellacci, G Canonico, L Capezzuoli, C Di Martino, P Ipponi, C Linari, M Montelatici, T Nelli, G Spagni, L Tirloni, A Vitali, E Abate, M Casati, T Casiraghi, L Laface, M Schiavo, A Arminio, A Cotoia, V Lizzi, F Vovola, R Vergari, S D'Ugo, N Depalma, M G Spampinato, P Bartolucci, G Brachini, P Bruzzaniti, A Chiappini, V Chiarella, F Ciccarone, P M Cicerchia, B Cirillo, G De Toma, A Di Bartolomeo, E Fiori, G B Fonsi, G Franco, A Frati, M Giugliano, I Iannone, F La Torre, P Lapolla, C Leonardo, G Marruzzo, S Meneghini, A Mingoli, D Ribuffo, M Salvati, A Santoro, P Sapienza, A K Scafa, L Simonelli, M Zambon, G T Capolupo, F Carannante, M Caricato, G Mascianà, E Mazzotta, A Gattolin, M Migliore, R Rimonda, D Sasia, E Travaglio, M Cervellera, A Gori, L Sartarelli, V Tonini, M Giacometti, S Zonta, A Chessa, A Fiorini, C Norcini, G Colletti, M Confalonieri, A Costanzi, C Frattaruolo, G Mari, M Monteleone, A Bandiera, L Bocciolone, G Bonavina, M Candiani, G Candotti, P De Nardi, F Gagliardi, M Medone, P Mortini, G Negri, P Parise, M Piloni, P Sileri, A Vignali, A Belvedere, P Bernante, P Bertoglio, S Boussedra, E Brunocilla, R Cipriani, G Cisternino, E De Crescenzo, P De Iaco, G Dondi, F Frio, E Jovine, F Mineo Bianchi, J Neri, D Parlanti, A M Perrone, A P Pezzuto, M Pignatti, V Pinto, G Poggioli, M Ravaioli, M Rottoli, R Schiavina, M Serenari, M Serra, P Solli, M Taffurelli, M Tanzanu, M Tesei, T Violante, S Zanotti, F Borghi, D Cianflocca, S Di Maria Grimaldi, D Donati, E Gelarda, P Geretto, G Giraudo, M C Giuffrida, A Marano, S Palagi, L Pellegrino, C Peluso, V Testa, F Agresta, D Prando, M Zese, F Aquila, C Gambacciani, L Lippa, F Pieri, O S Santonocito, G Armatura, G Bertelli, A Frena, P Marinello, F Notte, S Patauner, G Scotton, S F Fulginiti, G Gallo, G Sammarco, G Vescio, P Balercia, L Catarzi, G Consorti, F Di Marzo, T Fontana, H Daiko, M Ishikawa, K Ishiyama, S Iwata, K Kanematsu, Y Kanemitsu, T Kato, A Kawai, E Kobayashi, M Kobayashi Kato, K Moritani, F Nakatani, J Oguma, Y Tanase, M Uno, M Al Abdallah, F Ayasra, Y Ayasra, A Qasem, F J Abu Za'nouneh, T Fahmawee, A Hmedat, A Ibrahim, K Obeidat, S Abdel Al, R Abdel Jalil, M K Abou Chaar, M Al-Masri, H Al-Najjar, F Alawneh, O Alsaraireh, M Elayyan, R Ghanem, I Lataifeh, G Z Alkadeeki, F S Al Maadany, N Aldokali, O Senossi, M T Subhi, D Burgan, E Kamoka, A I Kilani, A Salamah, M Salem, A Shuwayyah, E Abdulwahed, E Alshareea, N Aribi, S Aribi, M Biala, R Ghamgh, M Morgom, Z Aldayri, I Ellojli, A Kredan, S Bradulskis, E Dainius, E Kubiliute, J Kutkevicius, A Parseliunas, A Subocius, D Venskutonis, F Rasoaherinomenjanahary, J B Razafindrahita, L H Samison, E C Ong, K H Hamdan, M R Ibrahim, J A Tan, M R Thanapal, N Amin Sahid, F Hayati, J Jayasilan, R K Sriram, S Subramaniam, A Che Jusoh, A H Hussain, A S Mohamed Sidek, M F Mohd Yunus, J Y Soh, Mpk Wong, A D Zakaria, Z Zakaria, A Fadzli, N Q Fathi, P S Koh, Y T Liew, A C Roslani, C Y Tang, L Y Teoh, W J Wong, A S Yahaya, M R Alvarez, R Arrangoiz, F Cordera, M A De la Rosa Abaroa, A Gómez-Pedraza, R Hernandez, A Maffuz-Aziz, J A Posada, F C Becerra García, A Alfaro-Goldaracena, G A Buerba, R A Castillejos-Molina, C Chan, I Dominguez-Rosado, H Medina-Franco, Má Mercado, M Oropeza-Aguilar, E Peña Gómez Portugal, O E Posadas-Trujillo, F Rodriguez-Covarrubias, N Salgado-Nesme, C Sarre, M Vilatoba, Y Arkha, H Bechri, A El Ouahabi, M Y Oudrhiri, F Derkaoui Hassani, N El Abbadi, L Amrani, Z H Belkhadir, A Benkabbou, O Chakib, B El Ahmadi, Y El Bouazizi, H Essangri, A Ghannam, A M Majbar, R Mohsine, A Souadka, R Hompes, E M Meima-van Praag, Ajm Pronk, S Sharabiany, B Grotenhuis, L Hartveld, S Reijers, W Van Houdt, J Baaij, M Bolster-van Eenennaam, M De Graaff, D Sloothaak, P Van 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Gupta, J Steinke, S Thrumurthy, E Massie, K McGivern, D Rutherford, M Wilson, J Hardie, S Kazzaz, S Handa, M Kaushal, A Kler, P Patel, J Redfern, S Tezas, Y Aawsaj, S Amonkar, C Barry, L Blackwell, D Blake, J Carter, H Emerson, A Fisher, M Katory, P Korompelis, W McCormick, A Mustafa, L Pearce, N Ratnavelu, R Reehal, L Kretzmer, L Lalou, B Manku, I Parwaiz, J Stafford, M Abdelkarim, A Asqalan, T Gala, S Ibrahim, A Maw, R Mithany, R Morgan, G Sundaram Venkatesan, K Ang, E J Caruana, M F Chowdhry, A Mohammad, A Nakas, S Rathinam, M Boal, O Brown, S Dwerryhouse, S Higgs, A Vallance, E Boyd, V Irvine, A Kirk, G Bakolas, A Boulton, A Chandock, T Khan, M Kumar, P Agoston, A Bille, B Challacombe, S Fraser, K Harrison-Phipps, J King, G Mehra, L Mills, M Najdy, R Nath, L Okiror, J Pilling, V Rizzo, T Routledge, A Sayasneh, L Stroman, A Wali, M Fehervari, C Fotopoulou, N Habib, S Hamrang-Yousefi, Z Jawad, L Jiao, M Pai, J Ploski, P Rajagopal, S Saso, M Sodergren, D Spalding, S Laws, C Hardie, C McNaught, R Alam, A Budacan, J Cahill, M Kalkat, S Karandikar, L Kenyon, D Naumann, A Patel, J Ayorinde, T Chase, T Cuming, A Ghanbari, L Humphreys, S Tayeh, A Aboelkassem Ibrahim, R Bichoo, H Cao, Akw Chai, J Choudhury, C Evans, H Fitzjohn, H Ikram, M Langstroth, M Loubani, A McMillan, S Nazir, Ssa Qadri, A Robinson, E Ross, T Sehgal, A Wilkins, J Dixon, J Dunning, K Freystaetter, M Jha, S Lester, A Madhavan, S V Thulasiraman, Y Viswanath, T Curl-Roper, C Delimpalta, Ccl Liao, V Velchuru, E Westwood, E Belcher, G Bond-Smith, S Chidambaram, F Di Chiara, K Fasanmade, L Fraser, H Fu, M Ganau, S Gore, J Graystone, D Jeyaretna, H Khatkar, M Lami, M Maher, S Mastoridis, R Mihai, R Piper, S Prabhu, Obf Risk, U Selbong, K Shah, R Smillie, H Soleymani Majd, S Sravanam, D Stavroulias, G D Tebala, M Vatish, C Verberne, K Wallwork, S Winter, M I Bhatti, H Boyd-Carson, E Elsey, E Gemmill, P Herrod, M Jibreel, E Lenzi, T Saafan, D Sapre, T Sian, N Watson, A Athanasiou, G Bourke, L Bradshaw, A Brunelli, J Burke, P Coe, F Costigan, H Elkadi, M Ho, J Johnstone, A Kanatas, V Kantola, A Kaufmann, A Laios, S Lam, E MacInnes, S Munot, C Nahm, M Otify, C Pompili, I Smith, G Theophilou, G Toogood, R Wade, D Ward, C West, S Annamalai, C Ashmore, A Boddy, T Hossain, A Kourdouli, A Gvaramadze, A Jibril, L Prusty, D Thekkinkattil, A Harky, M Shackcloth, A Askari, C Chan, N Cirocchi, S Kudchadkar, K Patel, J Sagar, S Shaw, R Talwar, M Abdalla, R Edmondson, O Ismail, D Jones, K Newton, N Stylianides, A Aderombi, U Andaleeb, O Bajomo, K Beatson, W Garrett, M Mehmood, V Ng, R Al-Habsi, G S Divya, B Keeler, B Al-Sarireh, R Egan, R Harries, A Henry, M Kittur, Z Li, K Parkins, F Soliman, N Spencer, D Thompson, C Burgess, C Gemmell, C Grieco, M Hollyman, L Hunt, J Morrison, S Ojha, N Ryan, F Abbadessa, S Barnard, C Chan, N Dawe, J Hammond, Ali F Mahmoud, I McPherson, C Mellor, J Moir, S Pandanaboyana, J Powell, B Rai, A Rogers, C Roy, A Sachdeva, C Saleh, S Tingle, T Williams, J Manickavasagam, C McDonald, N McGrath, N McSorley, K Ragupathy, L Ramsay, A Solth, O Kakisi, K Seebah, I Shaikh, L Sreedharan, M Youssef, J Shah, P Ameerally, N McLarty, S Mills, A Shenfine, K Sahnan, J Abu, E Addae-Boateng, D Bratt, L Brock, N Burnside, S Cadwell-Sneath, K Gajjar, C Gan, C Grundy, K Hallam, K Hassell, M Hawari, A Joshi, H Khout, K Konstantinidi, Rxn Lee, D Nunns, R Schiemer, T Walton, H Weaver, L Whisker, K Williamson, J McVeigh, R Myatt, M A Williams, R Kaur, E Leung, S Sundar, M Michel, S Patil, S Ravindran, J Sarveswaran, L Scott, M Edmond, E King, M Almond, A Bhangu, O Breik, L D Cato, A Desai, S Ford, E Griffiths, M Idle, M Kamal, A Kisiel, R Kulkarni, Jkc Mak, T Martin, P Nankivell, A Parente, S Parmar, A M Pathanki, L Phelan, P Praveen, S Saeed, N Sharma, J Singh, F Tirotta, D Vijayan, A Geddes, J McCaul, J McMahon, A H Khan, F Khan, A Mansuri, S Mukherjee, M Patel, M Sarigul, S Singh, K L Tan, A Woodham, A Adiamah, H Brewer, A Chowdhury, J Evans, D Humes, J Jackman, A Koh, C Lewis-Lloyd, O Oyende, J Reilly, D Worku, P Cool, G Cribb, K Shepherd, C Bisset, S Moug, N Elson, G Faulkner, P Saleh, C Underwood, G Brixton, L Findlay, T Klatte, A Majkowska, J Manson, R Potter, A Bhalla, Z Chia, P Daliya, A Goyal, E Grimley, A Hamad, A Kumar, F L Malcolm, E Theophilidou, J Bowden, N Campain, I Daniels, C Evans, G Fowler, J John, L Massey, F McDermott, J McGrath, A McLennan, M Ng, J Pascoe, N Rajaretnam, S Bulathsinhala, B Davidson, G Fusai, C Hidalgo Salinas, N Machairas, T Pissanou, J M Pollok, D A Raptis, F Soggiu, H Tzerbinis, S E Xyda, A Beamish, E Davies, R Foulkes, D Magowan, H Nassa, R Ooi, C Price, L Smith, F Solari, A Tang, G Williams, Y Al-Tamimi, A Bacon, N Beasley, D Chew, M Crank, N Ilenkovan, M Macdonald, B Narice, O Rominiyi, A Thompson, I Varley, T Drake, E Harrison, G Linder, J Mayes, R McGregor, R Skipworth, V Zamvar, E Davies, P Hawkin, T Raymond, O Ryska, R Baron, D Dunne, S Gahunia, C Halloran, N Howes, R McKinney, F McNicol, J Russ, P Szatmary, J R Tan, A Thomas, P Whelan, A Anzak, A Banerjee, O Fuwa, F Hughes, J D Jayasinghe, C Knowles, H Kocher, I Leal Silva, F S Ledesma, A Minicozzi, L Navaratne, R Rahman, R Ramamoorthy, C Sohrabi, M Thaha, B Thakur, M Venn, V Yip, R Baumber, J Parry, S Evans, L Jeys, G Morris, M Parry, J Stevenson, N Ahmadi, G Aresu, Z M Barrett-Brown, A S Coonar, H Durio Yates, D Gearon, J Hogan, M King, A Peryt, I S Pradeep, C Smith, M Adishesh, R Atherton, K Baxter, M Brocklehurst, M Chaudhury, N Krishnamohan, J McAleer, G Owens, E Parkin, P Patkar, I Phang, A Aladeojebi, M Ali, B Barmayehvar, A Gaunt, M Gowda, E Halliday, M Kitchen, F Mansour, M Thomas, D Zakai, N Abbassi-Ghadi, H Assalaarachchi, A Currie, M Flavin, A Frampton, M Hague, C Hammer, J Hopper, J Horsnell, S Humphries, A Kamocka, T K Madhuri, S Preston, P Singh, J Stebbing, A Tailor, D Walker, F Aljanadi, M Jones, P Mhandu, C O'Donnell, R Turkington, Z Al-Ishaq, S Bhasin, A S Bodla, A Burahee, A Crichton, R Fossett, N Pigadas, S Pickford, E Rahman, D Snee, R Vidya, N Yassin, F Colombo, D Fountain, M T Hasan, K Karabatsou, R Laurente, O Pathmanaban, A Al-Mukhtar, S Brown, J Edwards, A Giblin, C Kelty, M Lee, G Lye, T Newman, A Sharkey, C Steele, N Sureshkumar Shah, E Whitehall, R Athwal, A Baker, L Jones, C Konstantinou, S Ramcharan, S Singh, J Vatish, R Wilkin, M Ethunandan, G K Sekhon, H Shields, R Singh, F Wensley, S Lawday, A Lyons, T Abbott, S Anwar, K Ghufoor, C Sohrabi, E Chung, R Hagger, A Hainsworth, A Karim, H Owen, A Ramwell, K Williams, C Baker, A Davies, J Gossage, M Kelly, W Knight, J Hall, G Harris, G James, C Kang, D J Lin, A D Rajgor, T Royle, R Scurrah, B Steel, L J Watson, D Choi, R Hutchison, A Jain, V Luoma, H Marcus, R May, A Menon, B Pramodana, L Webber, I A Aneke, P Asaad, B Brown, J Collis, S Duff, A Khan, F Moura, B Wadham, H Warburton, T Elmoslemany, M Jenkinson, C Millward, R Zakaria, S Mccluney, C Parmar, S Shah, J Allison, M S Babar, B Collard, S Goodrum, K Lau, A Patel, R Scott, E Thomas, H Whitmore, D Balasubramaniam, B Jayasankar, S Kapoor, A Ramachandran, A Elhamshary, Smb Imam, K Kapriniotis, V Kasivisvanathan, J Lindsay, S Rakhshani-Moghadam, N Beech, M Chand, L Green, N Kalavrezos, H Kiconco, R McEwen, C Schilling, D Sinha, J Pereca, J Singh, S Chopra, D Egbeare, R Thomas, T Combellack, Sef Jones, M Kornaszewska, M Mohammed, A Sharma, G Tahhan, V Valtzoglou, J Williams, P Eskander, K Gash, L Gourbault, M Hanna, T Maccabe, C Newton, J Olivier, S Rozwadowski, E Teh, D West, H Al-Omishy, M Baig, H Bates, G Di Taranto, K Dickson, N Dunne, C Gill, D Howe, D Jeevan, A Khajuria, K Martin-Ucar AMcEvoy, P Naredla, V Ng, S Robertson, M Sait, D R Sarma, S Shanbhag, T Shortland, S Simmonds, J Skillman, N Tewari, G Walton, M A Akhtar, A Brunt, J McIntyre, K Milne, M M Rashid, A Sgro, K E Stewart, A Turnbull, M Aguilar Gonzalez, S Talukder, C Boyle, D Fernando, K Gallagher, A Laird, D Tham, M Bath, P Patki, C Sohrabi, C Tanabalan, T Arif, C Magee, T Nambirajan, S Powell, R Vinayagam, I Flindall, A Hanson, V Mahendran, S Green, M Lim, L MacDonald, V Miu, L Onos, K Sheridan, R Young, F Alam, O Griffiths, C Houlden, R Jones, V S Kolli, A K Lala, S Leeson, R Peevor, Z Seymour, L Chen, E Henderson, A Loehrer, K Brown, D Fleming, A Haynes, C Heron, C Hill, H Kay, E Leede, K McElhinney, K Olson, E C Osterberg, C Riley, P Srikanth, M Thornhill, D Blazer, G DiLalla, E S Hwang, W Lee, M Lidsky, J Plichta, L Rosenberger, R Scheri, K Shah, K Turnage, J Visgauss, S Zani, J Farma, J Clark, D Kwon, E Etchill, H E Gabre-Kidan AJenny, A Kent, M Ladd, C Long, H Malapati, A Margalit, S Rapaport, J Rose, K Stevens, L Tsai, D Vervoort, P Yesantharao, A Dehal, D Klaristenfeld, K Huynh, L Brown, I Ganly, J Mullinax, N Gusani, J Hazelton, J Maines, J S Oh, A Ssentongo, P Ssentongo, M Azam, A Choudhry, W Marx, J Fleming, A Fuson, J Gigliotti, A Ovaitt, Y Ying, M K Abel, V Andaya, K Bigay, M A Boeck, L Chen, H Chern, C Corvera, I El-Sayed, A Glencer, P Ha, Bcs Hamilton, C Heaton, K Hirose, D M Jablons, K Kirkwood, L Z Kornblith, J R Kratz, R Lee, P N Miller, E Nakakura, B Nunez-Garcia, R O'Donnell, D Ozgediz, P Park, B Robinson, A Sarin, B Sheu, M Varma, K Wai, R Wustrack, M J Xu, D Beswick, J Goddard, J Manor, J Song, T Fullmer, C Gaskill, N Gross, K Kiong, C L Roland, S N Zafar, M Abdallah, A Abouassi, M Almasri, G Kulkarni, H Marwan, M Mehdi, S Aoun, V S Ban, H H Batjer, J Caruso, D Abbott, A Acher, T Aiken, J Barrett, E Foley, P Schwartz, S N Zafar, A Hawkins, A Maiga, J Laufer, S Scasso
- Subjects
Aged, 80 and over ,Male ,Critical Care ,SARS-CoV-2 ,International Cooperation ,COVID-19 ,Middle Aged ,Cohort Studies ,Logistic Models ,Postoperative Complications ,Elective Surgical Procedures ,Neoplasms ,Outcome Assessment, Health Care ,Humans ,Female ,Epidemics ,Aged - Abstract
PURPOSE As cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19–free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway. PATIENTS AND METHODS This international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19–free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation). RESULTS Of 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19–free surgical pathways. Patients who underwent surgery within COVID-19–free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19–free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score–matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19–free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76). CONCLUSION Within available resources, dedicated COVID-19–free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks.
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- 2021
3. Comparison of the effects of alendronate and risedronate on bone mineral density and bone turnover markers in postmenopausal osteoporosis
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Sarioglu, Mengu, Tuzun, Cigdem, Unlu, Zeliha, Tikiz, Canan, Taneli, Fatma, and Uyanik, B. Sami.
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- 2006
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4. Incidence and Prognosis of CMV Disease in HIV–Infected Patients before and after Introduction of Combination Antiretroviral Therapy
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Salzberger, B., Hartmann, P., Hanses, F., Uyanik, B., Cornely, O. A., Wöhrmann, A., and Fätkenheuer, G.
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- 2005
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5. The involvement of DNA damage response pathway in nuclear reorganization during netotic initiation
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Uyanik, B., primary, Grigorash, B. B., additional, Uyanik, B., additional, and Demidov, O. N., additional
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- 2019
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6. Effect of long-term alcohol abuse on male sexual function and serum gonadal hormone levels
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Gümüs, B., Yiĝitoĝlu, M. R., Lekili, M., Uyanik, B. S., Müezzinoĝlu, T., and Büyüksu, C.
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- 1998
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7. Serum lipid fractions, nitric oxide and plasma endothelin-1 levels in actinic keratosis
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Sacar, T., Gunduz, K., Var, A., and Uyanik, B. S.
- Published
- 2005
8. Nuclear protein phosphatase Wip1 regulate sensitivity of human colorectal cancer cells to DNA damaging anti-cancer agents
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Grigorash, B. B., primary, Uyanik, B., additional, Kochetkova, E. Yu., additional, and Demidov, O. N., additional
- Published
- 2019
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9. DNA damage-induced phosphatase Wip1 in regulation of hematopoiesis, immune system and inflammation
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Uyanik , B, Grigorash , B B, Goloudina , A R, Demidov , O N, Lipides - Nutrition - Cancer [Dijon - U1231] ( LNC ), Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale ( INSERM ), and Institute of Cytology of the Russian Academy of Science (St. Petersburg)
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Hematopoietic cells ,Wip1 phosphatase ,Pro-inflammatory environment ,[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology - Abstract
International audience; PP2C serine-threonine phosphatase, Wip1, is an important regulator of stress response. Wip1 controls a number of critical cellular functions: proliferation, cell cycle arrest, senescence and programmed cell death, apoptosis or autophagy. Ppm1d, the gene encoding Wip1 phosphatase, is expressed in hematopoietic progenitors, stem cells, neutrophils, macrophages B and T lymphocytes in bone marrow and peripheral blood. The Wip1-/- mice display immunodeficiency, abnormal lymphoid histopathology in thymus and spleen, defects in B- and T-cell differentiation, as well as susceptibility to viral infection. At the same time, Wip1 knockout mice exhibit pro-inflammatory phenotype in skin and intestine in the model of inflammatory bowel disease (IBD) with elevated levels of inflammation-promoting cytokines TNF-α, IL-6, IL-12, IL-17. Several Wip1 downstream targets can mediate Wip1 effects on hematopoietic system including, p53, ATM, p38MAPK kinase, NFkB, mTOR. Here, we summarized the current knowledge on the role of Wip1 in the differentiation of various hematopoietic lineages and how Wip1 deficiency affects the functions of immune cells.
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- 2017
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10. The effect of smoking on neutrophil/lymphocyte and platelet/lymphocyte ratio and platelet indices: a retrospective study
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Tulgar, Y. K., Cakar, S., Tulgar, S., Dalkilic, O., Cakiroglu, B., Uyanik, B. S., and Maltepe Üniversitesi
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Platelet/lymphocyte ratio ,Neutrophil/lymphocyte ratio ,Smoking ,Neutrophil ,Platelet ,Lymphocyte - Abstract
WOS: 000382460900024, PubMed ID: 27460742, OBJECTIVE: Smoking commonly leads to death. Although the neutrophil/lymphocyte Ratio, platelet/lymphocyte ratio and platelet indices have been shown to be important for the diagnosis, prognosis and severity of some diseases, the smoking status of patients in these studies has not been well defined. In this study, we compared ratios derived from complete blood count and platelet indices to smoking status and length in smokers and non-smokers. PATIENTS AND METHODS: The data of healthy males and females aged between 18-60 years who presented to our institute for a routine checkup were collected, and subjects were divided in two groups-smokers and non-smokers. The presence of medical history or laboratory results which could affect inflammatory response, formed our exclusion criteria. All complete blood count results were noted and persons' smoking habits were calculated as pack/years. RESULTS: White blood cell, neutrophil, basophil and eosinophil counts; mean corpuscular volume, red cell distribution width and neutrophil/lymphocyte ratio were significantly higher in smokers when compared to non-smokers (p
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- 2016
11. The effect of smoking on neutrophil/ lymphocyte and platelet/lymphocyte ratio and platelet indices: A retrospective study
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Tulgar, Y. K., Cakar, S., Tulgar, S., Dalkilic, O., Basri Cakiroglu, Uyanik, B. S., and Maltepe Üniversitesi
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ComputingMilieux_MANAGEMENTOFCOMPUTINGANDINFORMATIONSYSTEMS ,ComputingMethodologies_PATTERNRECOGNITION ,Neutrophil/lymphocyte ratio ,ComputerSystemsOrganization_COMPUTER-COMMUNICATIONNETWORKS ,Neutrophil ,Platelet ,Smoking ,Lymphocyte ,Platelet/lymphocyte ratio ,InformationSystems_MISCELLANEOUS - Abstract
PubMed ID: 27460742, OBJECTIVE: Smoking commonly leads to death. Although the neutrophil/lymphocyte Ratio, platelet/lymphocyte ratio and platelet indices have been shown to be important for the diagnosis, prognosis and severity of some diseases, the smoking status of patients in these studies has not been well defined. In this study, we compared ratios derived from complete blood count and platelet indices to smoking status and length in smokers and non-smokers. PATIENTS AND METHODS: The data of healthy males and females aged between 18-60 years who presented to our institute for a routine check-up were collected, and subjects were divided in two groups - smokers and non-smokers. The presence of medical history or laboratory results which could affect inflammatory response, formed our exclusion criteria. All complete blood count results were noted and persons' smoking habits were calculated as pack/years. RESULTS: White blood cell, neutrophil, basophil and eosinophil counts; mean corpuscular volume, red cell distribution width and neutrophil/lymphocyte ratio were significantly higher in smokers when compared to non-smokers (p
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- 2016
12. DNA damage-induced phosphatase Wip1 in regulation of hematopoiesis, immune system and inflammation
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Uyanik, B, primary, Grigorash, B B, additional, Goloudina, A R, additional, and Demidov, O N, additional
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- 2017
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13. Assessing the reliability of coronary artery calcium score in symptomatic patients: challenging the 'power of zero'
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Basaran, O, Beyoglu, B, Bastug, H, Demirci, E, Akdeniz, H, Dereli, H, and Uyanik, B S
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- 2024
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14. Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy
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Clausse, V, primary, Goloudina, A R, additional, Uyanik, B, additional, Kochetkova, E Y, additional, Richaud, S, additional, Fedorova, O A, additional, Hammann, A, additional, Bardou, M, additional, Barlev, N A, additional, Garrido, C, additional, and Demidov, O N, additional
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- 2016
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15. The relations between serum sex hormones and in and out of bone ALP isoenzymes in healthy adults
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Uyanik, B, AYTEKİN, Metin, Yar, B, Yigitoglu, MR, Ari, Z, Tavli, T, Telli, T, and Akyidiz, M
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- 1999
16. The relation of sex hormones with the serum lipid and lipoprotein levels in men diagnosed coronary artery disease by angyography
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Tavli, T, Telli, T, Akyildiz, M, Uyanik, B, AYTEKİN, Metin, Yigitoglu, MR, and Ozilgili, H
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- 1999
17. A neonatal case of citrullinemia with urolithiasis
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Ozkozaci T, Akin M, Atay Z, Uyanik B, Nuhoglu C, and Ceran O
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Male ,Citrullinemia ,diagnosis ,etiology ,lcsh:R ,Infant ,lcsh:Medicine ,Newborn ,urine ,drug therapy ,Consanguinity ,Ammonia ,blood ,Citrulline ,Humans - Published
- 2004
18. Transient thermoelectricity in a vibrating quantum dot in Kondo regime
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Goker, A., primary and Uyanik, B., additional
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- 2012
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19. Interactions of Thyroid Hormones; Insulin-like Growth Factor-1 (IGF-1), IGF Binding Proteins, and Nutritional Anthropometric Parameters in School Children with Goiter Detected by Palpation
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Ersoy, B., primary, Gunes, H. S., additional, Uyanik, B. S., additional, Taneli, F., additional, and Gunay, T., additional
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- 2009
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20. Low levels of high density lipoprotein cholesterol in Turkish children: An important risk factor
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IŞsLCAN, AKIN, primary, YIǦITOǦL̈, M RAMAZAN, additional, VURGUN, NUREDDIN, additional, UYANIK, B SAMI, additional, and AKYILDIZ, MUHITTIN, additional
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- 2007
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21. Comparison of the effects of alendronate and risedronate on bone mineral density and bone turnover markers in postmenopausal osteoporosis
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Sarioglu, Mengu, primary, Tuzun, Cigdem, additional, Unlu, Zeliha, additional, Tikiz, Canan, additional, Taneli, Fatma, additional, and Uyanik, B. Sami., additional
- Published
- 2004
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- View/download PDF
22. The protective mechanisms of defibrotide on liver ischaemia-reperfusion injury
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Aydemir, E. O., primary, Var, A., additional, Uyanik, B. S., additional, Ilkgül, Ö., additional, Aydede, H., additional, and Sakarya, A., additional
- Published
- 2003
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23. Endothelial Dysfunction in Preeclampsia
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Var, Ahmet, primary, Yildirim, Yasemin, additional, Onur, Ece, additional, Kuscu, N. Kemal, additional, Uyanik, B. Sami, additional, Goktalay, Kayhan, additional, and Guvenc, Yesim, additional
- Published
- 2003
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24. Clomiphene citrate does not adversely affect endometrial leukemia inhibitory factor levels
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Kuscu, N. K., primary, Koyuncu, F. M., additional, Var, A., additional, Laçin, S., additional, Uyanik, B. S., additional, and Ceylan, E., additional
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- 2002
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25. Increased Lipoprotein (a) and Its Relationships with Other Parameters of Lipoprotein Metabolism in Chronic Renal Failure Treated by Hemodialysis.
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YIGITOGLU, M. Ramazan, primary, POLAT, M. Fevzi, additional, AKÇAY, Fatih, additional, ARI, Zeki, additional, UYANIK, B. Sami, additional, and ÖZILGILI, Hilal M., additional
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- 1997
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26. Effects of Passive Exposure to Tobacco, Socioeconomic Status and a Family History of Essential Hypertension on Lipid Profiles in Children.
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ISCAN, Akin, primary, UYANIK, B. Sami, additional, VURGUN, Nureddin, additional, ECE, Aydin, additional, and YIGITOGLU, M. Ramazan, additional
- Published
- 1996
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27. Clomiphene citrate does not adversely affect endometrial leukemia inhibitory factor levels.
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Kuşşcu, N. K., Koyuncu, F. M., Var, A., Laçin, S., Uyanik, B. S., and Ceylan, E.
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- 2002
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28. VARİKOSELLİ HASTALARIN SEMEN PLAZMASINDA ANTİOKSİDAN SEVİYESİ.
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GÜMÜŞ, B., UYANIK, B. S., LEKİLİ, M., YİĞİTOĞLU, M. R., TEMELTAŞ, G., and BÜYÜKSU, C.
- Published
- 2001
29. Low levels of high density lipoprotein cholesterol in Turkish children: An important risk factor.
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IŞsLCAN, AKIN, YIǦITOǦL̈, M RAMAZAN, VURGUN, NUREDDIN, UYANIK, B SAMI, and AKYILDIZ, MUHITTIN
- Published
- 1998
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30. G-3. Nuclear protein phosphatase Wip1 regulate sensitivity of human colorectal cancer cells to DNA damaging anti-cancer agents.
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Grigorash, Bogdan B., Uyanik, B., Kochetkova, Elena Yu., and Demidov, Oleg N.
- Subjects
- *
NUCLEAR proteins , *PHOSPHOPROTEIN phosphatases , *DNA damage , *CANCER cells , *COLORECTAL cancer , *DNA mismatch repair - Published
- 2019
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31. Atherogenic profile in preeclampsia.
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Var, Ahmet, Kuşcu, Kemal N., Koyuncu, Faik, Uyanik, B. Sami, Onur, Ece, Yildirim, Yasemin, and Oruç, Semra
- Subjects
PREECLAMPSIA ,PREGNANCY complications ,OBSTETRICAL emergencies ,PREGNANT women ,PREGNANCY - Abstract
Atherosis is accepted to underlie the pathogenesis of preeclampsia, therefore we aimed to determine malonyldialdehyde (MDA) levels as a marker of lipid peroxidation, and lipoprotein(a) (Lp(a)), apolipoprotein A-1 (Apo A-1) and apolipoprotein B (Apo B) levels as a marker of atherogenic profile in preeclamptic and normal pregnant women. Twenty preeclamptic and 20 gestational-age matched normal pregnant patients were enrolled in the study, mean gestational ages for the preeclamptic and the control group were 33.9±1.4 and 35.5±0.7 weeks, respectively. Blood was withdrawn from the patients soon after diagnosis, and from the controls at their routine prenatal visits. MDA levels was significantly higher in preeclamptic patients (P=0.0003), but no difference was observed in Apo A-1 and Apo B and Lp(a) levels between the 2 groups. We consider that higher MDA was due to oxidative stress seen in preeclampsia, and similar Apo A-1 and Apo B and Lp(a) levels were due to lack of systemic atherosis. [ABSTRACT FROM AUTHOR]
- Published
- 2003
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32. Can red cell distribution width and mean platelet volume serve as a marker for chronic prostatitis?
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Dogan, A. N., Cakiroglu, B., Hazar, A. I., RAMAZAN GOZUKUCUK, and Uyanik, B. S.
33. Narghile (hookah) smoking and carboxyhemoglobin levels.
- Author
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Uyanik B, Arslan ED, Akay H, Erçelik E, and Tez M
- Published
- 2011
34. U-1. The involvement of DNA damage response pathway in nuclear reorganization during netotic initiation.
- Author
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Uyanik, Burhan, Grigorash, Bogdan B., Uyanik, B., and Demidov, Oleg N.
- Subjects
- *
DNA damage - Published
- 2019
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35. A template-based code generator for web applications
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Burak Uyanik, Veysel Harun Şahin, Uyanik, B, Sahin, VH, Sakarya Üniversitesi/Bilgisayar Ve Bilişim Bilimleri Fakültesi/Yazılım Mühendisliği Bölümü, Şahin, Veysel Harun, and Sakarya Üniversitesi
- Subjects
web architecture ,Software engineering ,General Computer Science ,Computer science ,business.industry ,Process (computing) ,Code size ,web application ,computer.software_genre ,Engineering ,Software engineering,template-based code generation,web architecture,web ,Operating system ,Code (cryptography) ,Web application ,Code generation ,Template based ,Electrical and Electronic Engineering ,template-based code generation ,business ,computer - Abstract
The importance and usage of web applications grow every day. Today from small businesses to large-scale corporations, many institutions prefer web applications for both their internal and external services. Code size and complexity of these kinds of applications grow rapidly. This brings up the question of how to improve the development process of web applications. A solution can be to use code generators. This paper introduces a template-based code generator to improve the development process of web applications. The code generator was developed and integrated into a real-life web application. Today, the web application together with the code generator is actively used in industry. This proves that an effective integration of a template-based code generator into a real-life large-scale web application can be achieved. In addition, the effectiveness of automatic code generation to manual implementation was shown with experimentation. Throughout the experiments, bug-free code generation was observed. Also, 98.95% improvement in average development time, 93.97% improvement in average test run count, and 49.37% improvement in average code size was achieved. Fast particles like bullets are trying to pierce the structures in front of it. Studies to prevent this effect have been an ongoing effort of humanity since the early ages.Armor design studies against bullets and piercing pieces continue to be the focus of attention. For this purpose, tens of materials have been tried in hundreds of studies. Various structures are designed in many geometric variations and forms, and ballistic behavior is measured in test environments. Plate designs are predominantly formed with aluminum, ceramic and armor steel plates. These materials are used as the front and back support layers . This hard metal material structure has been tried to meet the need for easy movement and portability by including it in the fabric.In some studies, selected metal sheet materials have been tested with various thicknesses and sequences, ballistic performances have been determined, and impact resistance properties have been determined.In this review article, summaries of some of the studies conducted in recent years are presented, and it is aimed to create a target and perspective for future studies._x000D_ _x000D_ Amaç: Hematolojik parametrelerin prostat biyopsisi sonuçları üzerindeki öngörücü rolünü değerlendirmek Yöntem: Ocak 2014-Nisan 2016 tarihleri arasında ultrason eşliğinde prostat biyopsisi yapılan hastaları değerlendirdik. Hastalar histopatolojik sonuçlarına göre iki gruba ayrıldı: prostat kanseri saptanan ve saptanmamış hastalar. Biyopsi öncesi eritrosit sayısı, nötrofil sayısı, lenfosit sayısı, trombosit sayısı, hemoglobin düzeyi, hematokrit, kırmızı hücre dağılım genişliği, ortalama trombosit hacmi, trombosit dağılım genişliği ve trombosit incelemesi yapıldı. Ek olarak, nötrofil lenfosit oranları ve trombosit lenfosit oranları hesaplandı. Bu parametreler iki grup arasında karşılaştırıldı ve istatistiksel olarak analiz edildi. Bulgular: Prostat kanseri 38 hastada (%30,25) ve benign prostat hastalıkları (prostat hiperplazisi veya kronik prostatit) 88 hastada (%69,85) tespit edildi. Prostat kanserli hastalar ile eritrosit sayısı, nötrofil sayısı, lenfosit sayısı, trombosit sayısı, hemoglobin düzeyi, hematokrit,eritrosit dağılım genişliği, ortalama trombosit hacmi ve trombosit dağılımı genişliği açısından benign durumları olan hastalar arasında istatistiksel olarak anlamlı bir fark yoktu. Ek olarak, gruplar arasında nötrofil/lenfosit oranı ve trombosit/lenfosit oranı açısından istatistiksel olarak anlamlı bir fark yoktu. Sonuç: Hematolojik parametreler prostat biyopsi sonuçlarını öngörmede önemli bir rol oynamaz. Bu konunun daha fazla değerlendirilmesi için daha ileri çalışmalara ihtiyaç vardır."
- Published
- 2020
36. Hazardous genomic bioeffects of home Wi-Fi systems
- Author
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Sevgi Durna Daştan, Sinan Soylu, Mustafa Duman, Taner Daştan, Halime Hanım Pençe, Bülent Uyanık, Mustafa Turan, Atilla Kurt, Aydin Zilan, Dastan, S.D., Cumhuriyet University, Faculty of Veterinary Medicine, Department of Zootechnics and Animal Nutrition, Division of Biometry and Genetics, Sivas, Turkey -- Soylu, S., Cumhuriyet University, Faculty of Medicine, Department of General Surgery, Sivas, Turkey -- Pence, H.H., Department of Biochemistry, Saglik Bilimleri University School of Medicine, Istanbul, Turkey -- Uyanik, B., Bağcılar Education and Research Hospital, Department of Medical Genetics, Istanbul, Turkey -- Duman, M., Saglik Bilimleri University School of Medicine, Kartal Kosuyolu Yuksek Ihtisas Hospital, Department of Gastrointestinal Surgery, Istanbul, Turkey -- Kurt, A., Cumhuriyet University, Faculty of Medicine, Department of General Surgery, Sivas, Turkey -- Dastan, T., Bingol University, Faculty of Arts and Science, Department of Chemistry, Bingol, Turkey -- Zilan, A., Saglik Bilimleri University Bagcilar Education and Research Hospital, Department of General Surgery, Istanbul, Turkey -- Turan, M., Saglik Bilimleri University Bagcilar Education and Research Hospital, Department of General Surgery, Istanbul, Turkey, and UYANIK, BÜLENT
- Subjects
0301 basic medicine ,Microarray ,Microarray analysis techniques ,Cognitive Neuroscience ,Total rna ,Dastan S. D. , SOYLU S., Pence H. H. , Uyanik B., Duman M., KURT A., Dastan T., Zilan A., Turan M., -Hazardous genomic bioeffects of home Wi-Fi systems-, NeuroQuantology, cilt.16, ss.12-19, 2018 ,Rat brain ,Atomic and Molecular Physics, and Optics ,Emf exposure ,Andrology ,03 medical and health sciences ,030104 developmental biology ,Developmental Neuroscience ,Wireless radiofrequency ,Gene expression ,Electromagnetic field ,MRNA ,Gene - Abstract
Objective of this study is to investigate the changes of whole genom gene expression levels in rat brain induced by 2,4 GHz Wireless Fidelity Radiofrequency Electromagnetic Field (WiFi RF-EMF). Total RNA was extracted immediately and purified from the rat brain, after 12 hours/day exposed or sham-exposed to a frequency of 2,4 GHz WiFi RF-EMF for 14 days. Roche-Nimblegene-Agilent Microarray System was applied to investigate the changes of gene expression in rat brain. Roche-Nimblegene-Agilent Genespring Software for Microarray Analysis was used in bioenformatic analysis. After 14 days of WiFi RF-EMF exposure, 69 genes in experimental group showed statistical significant down regulation compared with the control group. Ten genes in experimental group showed statistical significant up regulation compared with the control group. In this study, it was detected that WiFi RF-EMF exposure to brain cells resulted with the down and up regulation of transcription level of some important genes. © 2018, Anka Publishers. All rights reserved., T-678, This work was supported by Cumhuriyet University BAP Fund with the Project Number T-678.
- Published
- 2018
37. Serum NMR metabolomics in distinct subtypes of hematologic malignancies.
- Author
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Gul AZ, Selek S, Bekiroglu S, Demirel M, Cakir FB, and Uyanik B
- Abstract
Hematologic malignancies encompass a diverse array of subtypes, contributing to substantial heterogeneity that poses challenges in predicting clinical outcomes. Leveraging the capabilities of nuclear magnetic resonance holds substantial promise in the detection of serum biomarkers and individual metabolic alterations in patients. This study involved the analysis of the sera from patients with acute myeloid leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphoma to investigate the affected metabolites and their associated pathways. The quantitative one-dimensional (1D) 1H nuclear magnetic resonance method was employed to identify alterations. Metabolite annotations were validated using two-dimensional (2D) analyses. Discriminating chemometric models and receiver operating characteristic curves were created using the MetaboAnalyst platform. The findings revealed significant alterations in the serum levels of amino acid catabolism products, citrate cycle intermediates, and phospholipids. The acute myeloid leukemia group showed differences in glucogenic amino acids related to the glycolysis pathway, whereas the chronic lymphocytic leukemia and non-Hodgkin lymphoma groups displayed variances in fumarate and acetate levels linked to the citrate cycle pathway. In the leukemia groups, higher levels of products from the protein degradation pathway were observed. The biomarker panels for each malignancy group exhibited outstanding discrimination from controls. Healthy individuals differed distinctly from patients, indicating commonly observed metabolic adaptation patterns among frequent hematologic malignancies. The small cohort study using nuclear magnetic resonance metabolomics in various hematologic malignancy subtypes revealed significant changes in serum amino acid and protein degradation end-product levels, suggesting prolonged leukocyte lifespan and increased energy demand., Competing Interests: Conflict of Interest Disclosure The authors do not have any conflicts of interest to declare in relation to this work., (Copyright © 2025 International Society for Experimental Hematology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2025
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38. Non-syndromic Congenital Sodium Diarrhea: A Novel Mutation in the SLC9A3 Gene.
- Author
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Hosnut FO, Sahin G, Uyanik B, Ceylaner S, and Akcaboy M
- Abstract
Competing Interests: Disclosure The authors report no conflicts of interest in this work.
- Published
- 2025
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39. Clonal haematopoiesis - a novel entity that modifies pathological processes in elderly.
- Author
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Belotserkovskaya E, Golotin V, Uyanik B, and Demidov ON
- Abstract
Progress in the development of new sequencing techniques with wider accessibility and higher sensitivity of the protocol of deciphering genome particularities led to the discovery of a new phenomenon - clonal haematopoiesis. It is characterized by the presence in the bloodstream of elderly people a minor clonal population of cells with mutations in certain genes, but without any sign of disease related to the hematopoietic system. Here we will review this recent advancement in the field of clonal haematopoiesis and how it may affect the disease's development in old age., (© 2023. Cell Death Differentiation Association (ADMC).)
- Published
- 2023
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40. HSPB5 Inhibition by NCI-41356 Reduces Experimental Lung Fibrosis by Blocking TGF-β1 Signaling.
- Author
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Tanguy J, Boutanquoi PM, Burgy O, Dondaine L, Beltramo G, Uyanik B, Garrido C, Bonniaud P, Bellaye PS, and Goirand F
- Abstract
Idiopathic pulmonary fibrosis is a chronic, progressive and lethal disease of unknown etiology that ranks among the most frequent interstitial lung diseases. Idiopathic pulmonary fibrosis is characterized by dysregulated healing mechanisms that lead to the accumulation of large amounts of collagen in the lung tissue that disrupts the alveolar architecture. The two currently available treatments, nintedanib and pirfenidone, are only able to slow down the disease without being curative. We demonstrated in the past that HSPB5, a low molecular weight heat shock protein, was involved in the development of fibrosis and therefore was a potential therapeutic target. Here, we have explored whether NCI-41356, a chemical inhibitor of HSPB5, can limit the development of pulmonary fibrosis. In vivo, we used a mouse model in which fibrosis was induced by intratracheal injection of bleomycin. Mice were treated with NaCl or NCI-41356 (six times intravenously or three times intratracheally). Fibrosis was evaluated by collagen quantification, immunofluorescence and TGF-β gene expression. In vitro, we studied the specific role of NCI-41356 on the chaperone function of HSPB5 and the inhibitory properties of NCI-41356 on HSPB5 interaction with its partner SMAD4 during fibrosis. TGF-β1 signaling was evaluated by immunofluorescence and Western Blot in epithelial cells treated with TGF-β1 with or without NCI-41356. In vivo, NCI-41356 reduced the accumulation of collagen, the expression of TGF-β1 and pro-fibrotic markers (PAI-1, α-SMA). In vitro, NCI-41356 decreased the interaction between HSPB5 and SMAD4 and thus modulated the SMAD4 canonical nuclear translocation involved in TGF-β1 signaling, which may explain NCI-41356 anti-fibrotic properties. In this study, we determined that inhibition of HSPB5 by NCI-41356 could limit pulmonary fibrosis in mice by limiting the synthesis of collagen and pro-fibrotic markers. At the molecular level, this outcome may be explained by the effect of NCI-41356 inhibiting HSPB5/SMAD4 interaction, thus modulating SMAD4 and TGF-β1 signaling. Further investigations are needed to determine whether these results can be transposed to humans.
- Published
- 2023
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41. Analysis of ACE2 and TMPRSS2 coding variants as a risk factor for SARS-CoV-2 from 946 whole-exome sequencing data in the Turkish population.
- Author
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Duman N, Tuncel G, Bisgin A, Bozdogan ST, Sag SO, Gul S, Kiraz A, Balta B, Erdogan M, Uyanik B, Canbek S, Ata P, Geckinli BB, Arslan Ates E, Alavanda C, Yesim Ozdemir S, Sezer O, Ozgon GO, Gurkan H, Guler K, Boga I, Kaya N, Alemdar A, Sayan M, Dundar M, Ergoren MC, and Temel SG
- Subjects
- Angiotensin-Converting Enzyme 2 genetics, Humans, Peptidyl-Dipeptidase A genetics, Retrospective Studies, Risk Factors, Serine Endopeptidases genetics, Exome Sequencing, Angiotensin-Converting Enzyme 2 metabolism, COVID-19 epidemiology, COVID-19 genetics, SARS-CoV-2 genetics
- Abstract
Heterogeneity in symptoms associated with COVID-19 in infected patients remains unclear. ACE2 and TMPRSS2 gene variants are considered possible risk factors for COVID-19. In this study, a retrospective comparative genome analysis of the ACE2 and TMPRSS2 variants from 946 whole-exome sequencing data was conducted. Allele frequencies of all variants were calculated and filtered to remove variants with allele frequencies lower than 0.003 and to prioritize functional coding variants. The majority of detected variants were intronic, only two ACE2 and three TMPRSS2 nonsynonymous variants were detected in the analyzed cohort. The main ACE2 variants that putatively have a protective or susceptibility effect on SARS-CoV-2 have not yet been determined in the Turkish population. The Turkish genetic makeup likely lacks any ACE2 variant that increases susceptibility to SARS-CoV-2 infection. TMPRSS2 rs75603675 and rs12329760 variants that were previously defined as common variants that have different allele frequencies among populations and may have a role in SARS-CoV-2 attachment to host cells were determined in the population. Overall, these data will contribute to the formation of a national variation database and may also contribute to further studies of ACE2 and TMPRSS2 in the Turkish population and differences in SARS-CoV-2 infection among other populations., (© 2022 Wiley Periodicals LLC.)
- Published
- 2022
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42. SETDB1 fuels the lung cancer phenotype by modulating epigenome, 3D genome organization and chromatin mechanical properties.
- Author
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Zakharova VV, Magnitov MD, Del Maestro L, Ulianov SV, Glentis A, Uyanik B, Williart A, Karpukhina A, Demidov O, Joliot V, Vassetzky YS, Mège RM, Piel M, Razin SV, and Ait-Si-Ali S
- Subjects
- Humans, Epigenome, Histone-Lysine N-Methyltransferase genetics, Histone-Lysine N-Methyltransferase metabolism, Heterochromatin, Phenotype, Chromatin genetics, Lung Neoplasms genetics
- Abstract
Imbalance in the finely orchestrated system of chromatin-modifying enzymes is a hallmark of many pathologies such as cancers, since causing the affection of the epigenome and transcriptional reprogramming. Here, we demonstrate that a loss-of-function mutation (LOF) of the major histone lysine methyltransferase SETDB1 possessing oncogenic activity in lung cancer cells leads to broad changes in the overall architecture and mechanical properties of the nucleus through genome-wide redistribution of heterochromatin, which perturbs chromatin spatial compartmentalization. Together with the enforced activation of the epithelial expression program, cytoskeleton remodeling, reduced proliferation rate and restricted cellular migration, this leads to the reversed oncogenic potential of lung adenocarcinoma cells. These results emphasize an essential role of chromatin architecture in the determination of oncogenic programs and illustrate a relationship between gene expression, epigenome, 3D genome and nuclear mechanics., (© The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research.)
- Published
- 2022
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- View/download PDF
43. Evaluation of Glycogen Storage Patients: Report of Twelve Novel Variants and New Clinical Findings in a Turkish Population.
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Ersoy M, Uyanik B, and Gedikbasi A
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- Child, Child, Preschool, Female, Genetic Association Studies, Genomics, Glycogen metabolism, Humans, Infant, Infant, Newborn, Male, Mutation, Retrospective Studies, Turkey epidemiology, United States, Glycogen Storage Disease epidemiology, Glycogen Storage Disease genetics
- Abstract
Glycogen storage diseases (GSDs) are clinically and genetically heterogeneous disorders that disturb glycogen synthesis or utilization. Although it is one of the oldest inherited metabolic disorders, new genetic methods and long-time patient follow-ups provide us with unique insight into the genotype-phenotype correlations. The aim of this study was to share the phenotypic features and molecular diagnostic results that include new pathogenic variants in our GSD cases. Twenty-six GSD patients were evaluated retrospectively. Demographic data, initial laboratory and imaging features, and current findings of the patients were recorded. Molecular analysis results were classified as novel or previously defined variants. Novel variants were analyzed with pathogenicity prediction tools according to American College of Medical Genetics and Genomics (ACGM) criteria. Twelve novel and rare variants in six different genes were associated with the disease. Hearing impairment in two patients with GSD I, early peripheral neuropathy after liver transplantation in one patient with GSD IV, epilepsy and neuromotor retardation in three patients with GSD IXA were determined. We characterized a heterogeneous group of all diagnosed GSDs over a 5-year period in our institution, and identified novel variants and new clinical findings. It is still difficult to establish a genotype-phenotype correlation in GSDs.
- Published
- 2021
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44. Inhibition of the DNA damage response phosphatase PPM1D reprograms neutrophils to enhance anti-tumor immune responses.
- Author
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Uyanik B, Goloudina AR, Akbarali A, Grigorash BB, Petukhov AV, Singhal S, Eruslanov E, Chaloyard J, Lagorgette L, Hadi T, Baidyuk EV, Sakai H, Tessarollo L, Ryffel B, Mazur SJ, Lirussi F, Garrido C, Appella E, and Demidov ON
- Subjects
- Animals, Antineoplastic Agents, Cell Line, Tumor, Cell Proliferation, Female, Humans, Lung, Mice, Mice, Inbred C57BL, Mice, Knockout, Phenotype, T-Lymphocytes, Tumor Microenvironment, Tumor Suppressor Protein p53 genetics, Tumor Suppressor Protein p53 metabolism, DNA Damage, Immunity, Neutrophils metabolism, Protein Phosphatase 2C genetics, Protein Phosphatase 2C metabolism
- Abstract
PPM1D/Wip1 is a negative regulator of the tumor suppressor p53 and is overexpressed in several human solid tumors. Recent reports associate gain-of-function mutations of PPM1D in immune cells with worse outcomes for several human cancers. Here we show that mice with genetic knockout of Ppm1d or with conditional knockout of Ppm1d in the hematopoietic system, in myeloid cells, or in neutrophils all display significantly reduced growth of syngeneic melanoma or lung carcinoma tumors. Ppm1d knockout neutrophils infiltrate tumors extensively. Chemical inhibition of Wip1 in human or mouse neutrophils increases anti-tumor phenotypes, p53-dependent expression of co-stimulatory ligands, and proliferation of co-cultured cytotoxic T cells. These results suggest that inhibition of Wip1 in neutrophils enhances immune anti-tumor responses.
- Published
- 2021
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- View/download PDF
45. Nanofitins targeting heat shock protein 110: An innovative immunotherapeutic modality in cancer.
- Author
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Marcion G, Hermetet F, Neiers F, Uyanik B, Dondaine L, Dias AMM, Da Costa L, Moreau M, Bellaye PS, Collin B, Gobbo J, Briand L, Seigneuric R, Kitten O, Cinier M, and Garrido C
- Subjects
- Animals, Cell Line, Tumor, Colorectal Neoplasms diagnostic imaging, Colorectal Neoplasms metabolism, Female, Humans, Lymphocytes, Tumor-Infiltrating drug effects, Macrophages drug effects, Mice, Peptide Fragments chemistry, Peptide Fragments pharmacology, Peptide Library, Positron-Emission Tomography, Tumor Microenvironment drug effects, Xenograft Model Antitumor Assays, Colorectal Neoplasms drug therapy, HSP110 Heat-Shock Proteins antagonists & inhibitors, Macrophages metabolism, Peptide Fragments administration & dosage
- Abstract
The presence of an inactivating heat shock protein 110 (HSP110) mutation in colorectal cancers has been correlated with an excellent prognosis and with the ability of HSP110 to favor the formation of tolerogenic (M2-like) macrophages. These clinical and experimental results suggest a potentially powerful new strategy against colorectal cancer: the inhibition of HSP110. In this work, as an alternative to neutralizing antibodies, Nanofitins (scaffold ~7 kDa proteins) targeting HSP110 were isolated from the screening of a synthetic Nanofitin library, and their capacity to bind (immunoprecipitation, biolayer interferometry) and to inhibit HSP110 was analyzed in vitro and in vivo. Three Nanofitins were found to inhibit HSP110 chaperone activity. Interestingly, they share a high degree of homology in their variable domain and target the peptide-binding domain of HSP110. In vitro, they inhibited the ability of HSP110 to favor M2-like macrophages. The Nanofitin with the highest affinity, A-C2, was studied in the CT26 colorectal cancer mice model. Our PET/scan experiments demonstrate that A-C2 may be localized within the tumor area, in accordance with the reported HSP110 abundance in the tumor microenvironment. A-C2 treatment reduced tumor growth and was associated with an increase in immune cells infiltrating the tumor and particularly cytotoxic macrophages. These results were confirmed in a chicken chorioallantoic membrane tumor model. Finally, we showed the complementarity between A-C2 and an anti-PD-L1 strategy in the in vivo and in ovo tumor models. Overall, Nanofitins appear to be promising new immunotherapeutic lead compounds., (© 2021 UICC.)
- Published
- 2021
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46. Lactobacillus stress protein GroEL prevents colonic inflammation.
- Author
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Dias AMM, Douhard R, Hermetet F, Regimbeau M, Lopez TE, Gonzalez D, Masson S, Marcion G, Chaumonnot K, Uyanik B, Causse SZ, Rieu A, Hadi T, Basset C, Chluba J, Grober J, Guzzo J, Neiers F, Ortega-Deballon P, Demidov ON, Lirussi F, and Garrido C
- Subjects
- Animals, Chaperonin 60 therapeutic use, Colon physiopathology, Disease Models, Animal, Inflammation drug therapy, Limosilactobacillus reuteri drug effects, Limosilactobacillus reuteri metabolism, Mice, Inbred BALB C, Statistics, Nonparametric, Mice, Chaperonin 60 pharmacology, Colon drug effects, Inflammation prevention & control, Lactobacillus metabolism
- Abstract
Background: We previously showed that supernatants of Lactobacillus biofilms induced an anti-inflammatory response by affecting the secretion of macrophage-derived cytokines, which was abrogated upon immunodepletion of the stress protein GroEL., Methods: We purified GroEL from L. reuteri and analysed its anti-inflammatory properties in vitro in human macrophages isolated from buffy coats, ex vivo in explants from human biopsies and in vivo in a mouse model of DSS induced intestinal inflammation. As a control, we used GroEL purified (LPS-free) from E. coli., Results: We found that L. reuteri GroEL (but not E. coli GroEL) inhibited pro-inflammatory M1-like macrophages markers, and favored M2-like markers. Consequently, L. reuteri GroEL inhibited pro-inflammatory cytokines (TNFα, IL-1β, IFNγ) while favouring an anti-inflammatory secretome. In colon tissues from human biopsies, L. reuteri GroEL was also able to decrease markers of inflammation and apoptosis (caspase 3) induced by LPS. In mice, we found that rectal administration of L. reuteri GroEL (but not E. coli GroEL) inhibited all signs of haemorrhagic colitis induced by DSS including intestinal mucosa degradation, rectal bleeding and weight loss. It also decreased intestinal production of inflammatory cytokines (such as IFNγ) while increasing anti-inflammatory IL-10 and IL-13. These effects were suppressed when animals were immunodepleted in macrophages. From a mechanistic point of view, the effect of L. reuteri GroEL seemed to involve TLR4, since it was lost in TRL4
-/- mice, and the activation of a non-canonical TLR4 pathway., Conclusions: L. reuteri GroEL, by affecting macrophage inflammatory features, deserves to be explored as an alternative to probiotics.- Published
- 2021
- Full Text
- View/download PDF
47. Disrupted oxidative stress resistance: A homozygous mutation in the catalytic (TLDc) domain of TBC1D24 gene associated with epileptic encephalopathy.
- Author
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Uzunhan TA and Uyanik B
- Subjects
- Child, Preschool, Consanguinity, Female, Humans, Infant, Infant, Newborn, Male, Mutation, Missense, Pedigree, Catalytic Domain genetics, GTPase-Activating Proteins genetics, Oxidative Stress genetics, Spasms, Infantile genetics
- Published
- 2020
- Full Text
- View/download PDF
48. Selecting the first chemical molecule inhibitor of HSP110 for colorectal cancer therapy.
- Author
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Gozzi GJ, Gonzalez D, Boudesco C, Dias AMM, Gotthard G, Uyanik B, Dondaine L, Marcion G, Hermetet F, Denis C, Hardy L, Suzanne P, Douhard R, Jego G, Dubrez L, Demidov ON, Neiers F, Briand L, Sopková-de Oliveira Santos J, Voisin-Chiret AS, and Garrido C
- Subjects
- Animals, Antineoplastic Agents toxicity, Cell Proliferation, Colorectal Neoplasms metabolism, Colorectal Neoplasms pathology, Crystallography, X-Ray, HSP110 Heat-Shock Proteins chemistry, HSP110 Heat-Shock Proteins metabolism, Humans, Mice, Models, Molecular, STAT3 Transcription Factor metabolism, Antineoplastic Agents chemistry, Antineoplastic Agents therapeutic use, Colorectal Neoplasms drug therapy, HSP110 Heat-Shock Proteins antagonists & inhibitors
- Abstract
Pro-survival stress-inducible chaperone HSP110 is the only HSP for which a mutation has been found in a cancer. Multicenter clinical studies demonstrated a direct association between HSP110 inactivating mutation presence and excellent prognosis in colorectal cancer patients. Here, we have combined crystallographic studies on human HSP110 and in silico modeling to identify HSP110 inhibitors that could be used in colorectal cancer therapy. Two molecules (foldamers 33 and 52), binding to the same cleft of HSP110 nucleotide-binding domain, were selected from a chemical library (by co-immunoprecipitation, AlphaScreening, Interference-Biolayer, Duo-link). These molecules block HSP110 chaperone anti-aggregation activity and HSP110 association to its client protein STAT3, thereby inhibiting STAT3 phosphorylation and colorectal cancer cell growth. These effects were strongly decreased in HSP110 knockdown cells. Foldamer's 33 ability to inhibit tumor growth was confirmed in two colorectal cancer animal models. Although tumor cell death (apoptosis) was noted after treatment of the animals with foldamer 33, no apparent toxicity was observed, notably in epithelial cells from intestinal crypts. Taken together, we identified the first HSP110 inhibitor, a possible drug-candidate for colorectal cancer patients whose unfavorable outcome is associated to HSP110.
- Published
- 2020
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49. HSP110 translocates to the nucleus upon genotoxic chemotherapy and promotes DNA repair in colorectal cancer cells.
- Author
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Causse SZ, Marcion G, Chanteloup G, Uyanik B, Boudesco C, Grigorash BB, Douhard R, Dias AMM, Dumetier B, Dondaine L, Gozzi GJ, Moussay E, Paggetti J, Mirjolet C, de Thonel A, Dubrez L, Demidov ON, Gobbo J, and Garrido C
- Subjects
- Animals, Cell Line, Tumor, Cell Nucleus drug effects, DNA Breaks, Double-Stranded drug effects, DNA Damage drug effects, DNA Damage genetics, DNA End-Joining Repair drug effects, DNA-Binding Proteins genetics, HCT116 Cells, Humans, Ku Autoantigen genetics, Mice, Mice, Inbred NOD, Mice, SCID, Oxaliplatin pharmacology, Translocation, Genetic drug effects, Cell Nucleus genetics, Colorectal Neoplasms drug therapy, Colorectal Neoplasms genetics, DNA End-Joining Repair genetics, HSP110 Heat-Shock Proteins genetics, Mutagens pharmacology, Translocation, Genetic genetics
- Abstract
A multicenter clinical study demonstrated the presence of a loss-of-function HSP110 mutation in about 15% of colorectal cancers, which resulted from an alternative splicing and was produced at the detriment of wild-type HSP110. Patients expressing low levels of wild-type HSP110 had excellent outcomes (i.e. response to an oxaliplatin-based chemotherapy). Here, we show in vitro, in vivo, and in patients' biopsies that HSP110 co-localizes with DNA damage (γ-H2AX). In colorectal cancer cells, HSP110 translocates into the nucleus upon treatment with genotoxic chemotherapy such as oxaliplatin. Furthermore, we show that HSP110 interacts with the Ku70/Ku80 heterodimer, an essential element of the non-homologous end joining (NHEJ) repair machinery. We also demonstrate by evaluating the resolved 53BP1 foci that depletion in HSP110 impairs repair steps of the NHEJ pathway, which is associated with an increase in DNA double-strand breaks and in the cells' sensitivity to oxaliplatin. HSP110-depleted cells sensitization to oxaliplatin-induced DNA damage is abolished upon re-expression of HSP110. Confirming a role for HSP110 in DNA non-homologous repair, SCR7 and NU7026, two inhibitors of the NHEJ pathway, circumvents HSP110-induced resistance to chemotherapy. In conclusion, HSP110 through its interaction with the Ku70/80 heterodimer may participate in DNA repair, thereby inducing a protection against genotoxic therapy.
- Published
- 2019
- Full Text
- View/download PDF
50. Novel isatin-derived molecules activate p53 via interference with Mdm2 to promote apoptosis.
- Author
-
Fedorova O, Daks A, Petrova V, Petukhov A, Lezina L, Shuvalov O, Davidovich P, Kriger D, Lomert E, Tentler D, Kartsev V, Uyanik B, Tribulovich V, Demidov O, Melino G, and Barlev NA
- Subjects
- Animals, Apoptosis Regulatory Proteins genetics, Cell Line, Tumor, Histones metabolism, Humans, Imidazoles pharmacology, Isatin analogs & derivatives, Mice, Piperazines pharmacology, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins c-mdm2 antagonists & inhibitors, Antineoplastic Agents pharmacology, Apoptosis drug effects, Isatin pharmacology, Proto-Oncogene Proteins c-mdm2 metabolism, Tumor Suppressor Protein p53 metabolism
- Abstract
The p53 protein is a key tumor suppressor in mammals. In response to various forms of genotoxic stress p53 stimulates expression of genes whose products induce cell cycle arrest and/or apoptosis. An E3-ubiquitin ligase, Mdm2 (mouse-double-minute 2) and its human ortholog Hdm2, physically interact with the amino-terminus of p53 to mediate its ubiquitin-mediated degradation via the proteasome. Thus, pharmacological inhibition of the p53-Mdm2 interaction leads to overall stabilization of p53 and stimulation of its anti-tumorigenic activity. In this study we characterize the biological effects of a novel class of non-genotoxic isatin Schiff and Mannich base derivatives (ISMBDs) that stabilize p53 on the protein level. The likely mechanism behind their positive effect on p53 is mediated via the competitive interaction with Mdm2. Importantly, unlike Nutlin, these compounds selectively promoted p53-mediated cell death. These novel pharmacological activators of p53 can serve as valuable molecular tools for probing p53-positive tumors and set up the stage for development of new anti-cancer drugs.
- Published
- 2018
- Full Text
- View/download PDF
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