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4. Search for dark matter, extra dimensions, and unparticles in monojet events in proton-proton collisions at root s=8TeV

Author

Khachatryan, V., Sirunyan, Bergauer, T., Dragicevic, M., Fruehwirth, R., Ghete, Hrubec, J., Jeitler, Krammer, M., Kraetschmer, D., Rahbaran, B., Rohringer, Taurok, A., Treberer, Treberspurg, Wulz, C. E., Mossolov, Alderweireldt, S., Bansal, De Wolf, E. A., Janssen, Ochesanu, S., Roland, Van Haevermaet, H., Van, Mechelen, Spilbeeck, A., Blekman, N., Heracleous, N., Kalogeropoulos, Lowette, S., Maes, Tavernier, S., Van, Doninck, G. P., Villella, I., Caillol, Lentdecker, G., Dobur, Grebenyuk, A., Leonard, T., Seva, T., Thomas, Wang, J., Adler, Costantini, S., Crucy, Garcia, G., Klein, Ryckbosch, D., Diblen, Thyssen, F., Tytgat, Basegmez, S., Beluffi, A., Ceard, L., Silveira, Da, Favart, D., Forthomme, Jez, P., Komm, Pagano, D., Perrini, A., Quertenmont, L., Selvaggi, Vizan, J. M., Beliy, N., Caebergs, H., Alda Junior, W. L., Alves, Dos Reis Martins, T., Pol, J., Custodio, A., Costa, Da, Oliveira Martins, C., Fonseca De Souza, Malek, M., Matos, Figueiredo, Prado Da Silva, W. L., Santaolalla, A., Tonelli Manganote, E. J., Vilela, Pereira, Dias, F. A., Fernandez Perez Tomei, Mercadante, P. G., Novaes, Aleksandrov, A., Genchev, Piperov, S., Rodozov, Dimitrov, A., Glushkov, Litov, L., Pavlov, Chen, H. S., Chen, Liang, S., Plestina, Liu, S., Mao, W., Avila, C., Chaparro, Sierra, Gomez Moreno, B., Sanabria, D., Polic, D., Puljak, Brigljevic, V., Kadija, Sudic, L., Attikis, Nicolaou, C., Ptochos, M., Finger, J. r., Radi, A., Calpas, Raidal, M., Tiko, Harkonen, J., Karimaki, J., Lampen, T., Lassila, Perini, Luukka, P., Maenpaa, Tuominiemi, J., Tuovinen, Besancon, M., Couderc, Fabbro, B., Faure, Givernaud, A., Gras, P., Locci, E., Malcles, Rosowsky, A., Titov, Busson, P., Charlot, Dobrzynski, L., Filipovic, Granier, Mastrolorenzo, L., Mine, I. N., Nguyen, M., Ochando, Sauvan, J. B., Sirois, Zabi, A., Agram, Brom, J. M., Chabert, Fontaine, J. C., Gele, Bihan, A. C., Van, Hove, Beaupere, N., Boudoul, Chasserat, J., Chierici, El Mamouni, H., Fan, Ille, B., Kurca, Perries, S., Alvarez, Sordini, V., Vander, Donckt, Xiao, H., Rurua, Bontenackels, M., Edelhoff, Klein, K., Ostapchuk, J., Schael, S., Sprenger, Zhukov, V., Ata, Duchardt, D., Erdmann, T., Heidemann, C., Hoepfner, Kreuzer, P., Merschmeyer, Padeken, K., Papacz, Sonnenschein, L., Teyssier, Cherepanov, V., Erdogan, Geisler, M., Ahmad, T., Kuessel, Y., Lingemann, Perchalla, L., Pooth, N., Behr, J., Behrenhoff, Bergholz, M., Bethani, A., Calligaris, L., Campbell, F., Pardos, C. Diez, Dooling, Eckstein, D., Eichhorn, Geiser, A., Gunnellini, Hempel, M., Horton, Kieseler, J., Kleinwort, Leonard, J., Lipka, Mankel, R., Marfin, B., Mnich, J., Mussgiller, Novgorodova, O., Nowak, D., Placakyte, R., Raspereza, Ron, E., Sahin, Schmidt, R., Schoerner, Sadenius, Trevino, A. D. R. Vargas, Walsh, Martin, M. Aldaya, Blobel, Garutti, E., Goebel, Haller, J., Hoeing, Kogler, R., Lange, Ott, J., Peiffer, C., Schettler, H., Schleper, Seidel, M., Sibille, Steinbrueck, G., Troendle, Barth, C., Baus, Chwalek, T., Boer, De, Feindt, M., Frensch, U., Katkov, I., Kornmayer, Lobelle, Mozer, M. U., Mueller, G., Rabbertz, K., Ratnikov, Stober, F. M., Ulrich, Weiler, T., Wolf, Geralis, T., Giakoumopoulou, Markou, A., Markou, Panagiotou, A., Saoulidou, X., Evangelou, I., Flouris, Manthos, N., Papadopoulos, Hajdu, C., Hidas, Vesztergombi, G., Zsigmond, Karancsi, J., Molnar, Raics, P., Trocsanyi, S. B., Bhatnagar, V., Dhingra, Kaur, M., Mittal, Ashok, Kumar, Arun, Ahuja, C., Kumar, A., Malhotra, Sharma, V., Banerjee, Dutta, S., Gomber, Modak, A., Mukherjee, Abdulsalam, A., Dutta, Mohanty, A. K., Pant, T., Banerjee, S., Chatterjee, S., Ganguly, S., Ghosh, G., Kumar, S., Maity, Mohanty, G. B., Parida, Mohammadi, Naseri, M., Mehdiabadi, Zeinali, M., Felcini, Barbone, L., Calabria, Creanza, D., Filippis, De, Iaselli, G., Maggi, Pompili, A., Pugliese, Silvestris, L., Singh, Zito, G., Abbiendi, Capiluppi, P., Castro, Cuffiani, M., Dallavalle, Fasanella, D., Giacomelli, Marcellini, S., Masetti, Siroli, G. P., Tosi, Cappello, G., Chiorboli, Potenza, R., Tricomi, Civinini, C., D'Alessandro, Gonzi, S., Gori, Sguazzoni, G., Tropiano, Fabbri, F., Piccolo, E., Tosi, S., Dinardo, Gerosa, R., Ghezzi, Malvezzi, S., Manzoni, Menasce, D., Moroni, S., Redaelli, N., Fatis, De, Cavallo, N., Guida, Di, Lista, L., Meola, Dall'Osso, M., Dorigo, Gasparini, F., Gasparini, Pazzini, J., Pegoraro, Simonetto, F., Torassa, A., Zumerle, G., Gabusi, Salvini, P., Vitulo, Ciangottini, D., Fano', Livio, Menichelli, M., Romeo, Spiezia, A., Androsov, Bernardini, J., Boccali, Ciocci, M. A., Dell'Orso, Giassi, A., Grippo, Martini, L., Messineo, Savoy Navarro, A., Serban, Squillacioti, P., Tenchini, Verdini, P. G., Vernieri, Re, D., Diemoz, Margaroli, F., Meridiani, Organtini, G., Paramatti, Arcidiacono, R., Argiro, C., Cartiglia, N., Casasso, Demaria, N., Finco, E., Monaco, V., Musich, Pacher, L., Pastrone, Potenza, A., Romero, A., Staiano, A., Tamponi, Casarsa, M., Cossutti, La Licata, C., Marone, T., Zanetti, A., Chang, K., Kim, D. H., Kim, S., Y. D., Oh, Park, J. Y., Song, S., Choi, Kim, H., Kim, Y., Choi, M., Kim, Ryu, M. S., Lee, J., Seo, Castilla Valdez, H., De La Cruz Burelo, Cruz, I., Lopez, Fernandez, Carrillo, S., Valencia, F. Vazquez, Pedraza, Ibarguen, H. A., Casimiro, Linares, Krofcheck, D., Butler, Ahmad, M., Hassan, A., Khurshid, T., Shah, Bluj, M., Boimska, M., Nawrocki, K., Romanowska, Rybinska, Zalewski, P., Brona, W., Doroba, K., Kalinowski, Misiura, M., Olszewski, Beirao Da Cruz E. Silva, C., Faccioli, Gallinaro, M., Nguyen, J., Varela, J., Vischia, Gorbunov, I., Kamenev, Lanev, A., Malakhov, Palichik, V., Perelygin, Shulha, S., Skatchkov, Golovtsov, V., Ivanov, V., Oreshkin, V., Smirnov, Vavilov, S., Vorobyev, Dermenev, A., Gninenko, Krasnikov, N., Pashenkov, Epshteyn, V., Gavrilov, Safronov, G., Semenov, Vlasov, E., Zhokin, Kirakosyan, M., Leonidov, Vinogradov, A., Belyaev, Dudko, L., Ershov, Kodolova, O., Lokhtin, Savrin, V., Snigirev, Bitioukov, S., Kachanov, Tourtchanovitch, L., Troshin, Volkov, A., Adzic, Milosevic, J., Maestre, Cerrada, M., Chamizo, Llatas, Delgado Peris, A., Dominguez, Vazquez, Fernandez Bedoya, C., Fernandez, Ramos, Fouz, M. C., Garcia, Abia, Hernandez, J. M., Josa, Martino, E., Perez Calero Yzquierdo, Quintario Olmeda, A., Redondo, Albajar, C., Troconiz, De, Cuevas, J., Fernandez, Menendez, Cabrillo, I. J., Calderon, Fernandez, M., Gomez, Marco, J., Marco, Munoz Sanchez, F. J., Piedra, Gomez, Rodriguez Marrero, A. Y., Ruiz, Jimeno, Vila, I., Vilar, Cortabitarte, Auzinger, G., Bachtis, D., Benaglia, A., Bendavid, Bernet, C., Bianchi, A., Bondu, O., Botta, Cerminara, G., Colafranceschi, D., Dabrowski, A., David, De Visscher, S., Dobson, Elliott Peisert, A., Eugster, Giffels, M., Gigi, Glege, F., Guida, Hammer, J., Hansen, V., Janot, P., Kousouris, Lourenco, C., Magini, Masetti, L., Meijers, F., Morovic, S., Mulders, Pape, L., Perez, Petrucciani, G., Pfeiffer, Piparo, D., Plagge, Sakulin, H., Schaefer, Sharma, A., Siegrist, Spiga, D., Steggemann, Treille, D., Tsirou, Woehri, H. K., Zeuner, Erdmann, W., Horisberger, Koenig, S., Kotlinski, Rohe, T., Bachmair, P., Buchmann, M. A., Casal, P., Grab, C., Hits, Marini, A. C., Del, Arbol, Naegeli, C., Nef, Pauss, F., Peruzzi, F. J., Rossini, M., Starodumov, Theofilatos, K., Wallny, Canelli, M. F., Chiochia, Hreus, T., Rikova, Ngadiuba, J., Robmann, Verzetti, M., Yang, Kuo, C. M., Lin, Chang, P., Chang, Chen, P. H., Dietz, K. Y., Lei, Y. J., Liu, Petrakou, E., Tzeng, Srimanobhas, N., Suwonjandee, Cerci, S., Dozen, S., Gokbulut, G., Gurpinar, Topaksu, A. Kayis, Onengut, Polatoz, A., Sogut, H., Vergili, M., Akin, Gamsizkan, H., Karapinar, Yalvac, M., Zeyrek, Kaya, O., Bahtiyar, Vardarli, F. I., Yucel, Brooke, J. J., Clement, Frazier, R., Goldstein, H. F., Jacob, J., Kreczko, Newbold, D. M., Paramesvaran, Smith, V. J., Williams, C., Brown, R. M., Cockerill, Harder, K., Harper, Shepherd Themistocleous, C. H., Thea, Womersley, W. J., Worm, Buchmuller, O., Burton, Cutajar, M., Dauncey, Dunne, P., Ferguson, A., Hall, G., Iles, Kenzie, M., Lane, Malik, S., Marrouche, Nikitenko, A., Pela, Raymond, D. M., Rogerson, Tapper, A., Acosta, Hobson, P. R., Khan, Martin, W., Reid, Turner, M., Dittmann, Scarborough, T., Charaf, Rumerio, P., Avetisyan, Heister, A., Lawson, D., St John, J., Sulak, Christopher, G., Cutts, Garabedian, A., Heintz, Laird, E., Landsberg, Sinthuprasith, T., Speer, Breto, G., Sanchez, Chertok, M., Conway, R., Gardner, M., Mulhearn, M., Pellett, M., Shalhout, S., Smith, Tripathi, M., Wilbur, P., Farrell, C., Hauser, Takasugi, E., Valuev, Ellison, J., Gary, P., Kennedy, E., Lacroix, Luthra, A., Malberti, Sumowidagdo, S., Wimpenny, Cerati, G. B., Cittolin, Holzner, A., Kelley, Letts, J., Macneill, Pieri, M., Sani, Tu, Y., Vartak, Yoo, J., Barge, Geffert, P., George, J., Justus, C., Mccoll, W., West, C., Apresyan, Y., Di Marco, E., Duarte, Pena, C., Rogan, R., Xie, S., Zhu, Ferguson, T., Iiyama, Vorobiev, I., Cumalat, Gaz, A., Lopez, Stenson, K., Ulmer, Chatterjee, A., Chu, W., Kreis, B., Mirman, J. R., Ryd, A., Salvati, W. D., Thom, J., Thompson, Winstrom, L., Wittich, M., Anderson, J., Apollinari, Beretvas, A., Berryhill, Butler, J. N., Cheung, Elvira, V. D., Fisk, E., Gray, L., Green, Hanlon, J., Hare, Hooberman, B., Jindariani, Kaadze, K., Klima, Lipton, R., Marraffino, J. M., Outschoorn, Mason, D., Mcbride, Nahn, S., Newman, Holmes, Spiegel, L., Taylor, L., Vaandering, E. W., Vidal, Yang, F., Acosta, M., Cheng, T., Curry, Giovanni, G. P., Field, Hugon, J., Konigsberg, F., Matchev, K., Milenovic, Rinkevicius, A., Shchutska, M., Yelton, J., Zakaria, Linn, S., Markowitz, Adams, T., Askew, Hagopian, S., Hagopian, Kalakhety, H., Yumiceva, Bazterra, V. E., Berry, Cavanaugh, R., Evdokimov, Hofman, D. J., Khalatyan, O'Brien, C., Silkworth, Albayrak, E. A., Bilki, F., Haytmyradov, M., Merlo, Mestvirishvili, A., Moeller, Onel, Y., Ozok, P., Tiras, E., Wetzel, B. A., Blumenfeld, B., Bolognesi, A. V., Maksimovic, P., Martin, Bean, A., Benelli, R. P., Murray, M., Noonan, Stringer, R., Wang, Chakaberia, I., Ivanov, Maravin, Y., Saini, Gronberg, J., Calvert, B., Eno, Kellogg, R. G., Kolberg, Mignerey, A. C., Pedro, Tonwar, S. C., Apyan, Cali, I. A., Chan, Ceballos, G. Gomez, Goncharov, Lai, Y. S., Lee, Paus, C., Ralph, G. S. F., Stoeckli, F., Sumorok, J., Wyslouch, B., Dahmes, B., Benedetti, De, Klapoetke, K., Kubota, Singovsky, A., Tambe, Oliveros, S., Avdeeva, Dominguez, A., Suarez, D., Kravchenko, I., Lazo, Flores, Snow, G. R., Dolen, Kharchilava, A., Kumar, Barberis, E., Baumgartel, Massironi, A., Morse, D., Wood, D., Zhang, N., Odell, N., Pollack, Stoynev, S., Sung, Chan, K. M., Drozdetskiy, Karmgard, D. J., Kellams, Marinelli, N., Pearson, Valls, N., Wayne, Brinson, J., Bylsma, Hill, C., Hughes, H., Wulsin, H. W., Hebda, P., Hunt, Saka, H., Stickland, S. C., Zuranski, A., Brownson, Ramirez, Alagoz, E., Barnes, Bortoletto, D., Mattia, De, M. K., Jones, M., Jung, Pegna, D. Lopes, Maroussov, Silvers, D., Svyatkovskiy, Yoo, H. D., Zablocki, J., Adair, A., Akgun, Li, W., Michlin, Roberts, J., Zabel, R., de Barbaro, P., Demina, D., Bhatti, A., Ciesielski, Lungu, G., Mesropian, J. P., Contreras Campana, C., Contreras, Campana, Ferencek, D., Gershtein, Hidas, D., Lath, Rekovic, V., Salur, S., Stone, R., Rose, K., Spanier, Krutelyov, V., Montalvo, Perloff, A., Roe, Suarez, I., Tatarinov, J., Dragoiu, C., Dudero, K., Kunori, S., Appelt, E., Delannoy, W., Maguire, C., Mao, P., Snook, B., Tuo, Boutle, S., Cox, Ledovskoy, A., Gollapinni, S., Harr, Kankanamge, Lamichhane, P., Sturdy, Carlsmith, D., Cepeda, Hall Wilton, R., Herndon, Lanaro, A., Lazaridis, Mohapatra, A., Ojalvo, G., Ross, I., Sarangi, Woods, N., Cms, Collaboration, Santocchia, Attilio, and Fano, L

Published
2015

5. Vascular endothelial growth factor receptor-1 contributes to resistance to anti-epidermal growth factor receptor drugs in human cancer cells

Author

BIANCO R, ROSA R, DAMIANO V, DANIELE G, GELARDI T, GAROFALO S, TARALLO V, FALCO S, MELISI D, BENELLI R, ALBINI A, RYAN A, TORTORA G., CIARDIELLO, Fortunato, Bianco, R, Rosa, R, Damiano, V, Daniele, G, Gelardi, T, Garofalo, S, Tarallo, V, De, Falco, S, Melisi, D, Benelli, R, Albini, A, Ryan, A, Ciardiello, Fortunato, and Tortora, G.

Published
2008

6. VEGF Receptor 1 contributes to resistance to anti-EGFR drugs in human cancer cells

Author

BIANCO, ROBERTO, TORTORA, GIAMPAOLO, Rosa R, Damiano V, Daniele G, Gelardi T, Garofalo S, Tarallo V, De Falco S, Melisi D, Benelli R, Albini A, Ryan A, Ciardiello F, Bianco, Roberto, Rosa, R, Damiano, V, Daniele, G, Gelardi, T, Garofalo, S, Tarallo, V, De Falco, S, Melisi, D, Benelli, R, Albini, A, Ryan, A, Ciardiello, F, and Tortora, Giampaolo

Subjects
resistance, EGFR, VEGFR-1
Published
2008

12. Simple method for in vitro bladder urothelium regeneration on a heterologous acellular matrix

Author

Campodonico, F., Michelazzi, A., Benelli, R., and Toncini, C.

Subjects
Bladder -- Research, Bladder -- Properties, Regeneration (Biology) -- Research, Regeneration (Biology) -- Methods, Health
Abstract

Byline: F. Campodonico (1), A. Michelazzi (2), R. Benelli (3), C. Toncini (4) Author Affiliation: (1) Department of Urology, University of Genoa, Largo R. Benzi 10, 16132, Genoa, Italy (2) Department of Pediatric Surgery, Largo G. Gaslini 5, 16148 , Genoa, Italy (3) National Institute for Cancer Research, Largo R. Benzi 10, 16132, Genoa, Italy (4) Department of Pathology S Martino Hospital, Largo R. Benzi 10, Italy, 16132, Genoa, Italy Article History: Accepted Date: 10/12/2002 Online Date: 18/07/2003

Published
2003

14. HIV-1 TAT PROTEIN MIMICRY OF CHEMOKINES

Author

Albini, A, Ferrini, S, Benelli, R, Sforzini, S, Giunciuglio, D, Aluigi, Mg, Proudfoot, Aei, Alquani, S, Wells, Tnc, Mariani, Giuliano, Rabin, R, and Farber, J.

Published
1998

18. HIV-1 tat acts as a growth factor and induces angiogenic activity in BK virus/tat transgenic mice

Author

Barbanti-Brodano, G., Sampaolesi, R., Diana Campioni, Lazzarin, L., Altavilla, G., Possati, L., Masiello, L., Benelli, R., Albini, A., and Corallini, A.

Subjects
Mice, Base Sequence, Neovascularization, Pathologic, BK Virus, Gene Products, tat, Molecular Sequence Data, Papillomavirus Infections, HIV-1, Animals, Humans, Mice, Transgenic, tat Gene Products, Human Immunodeficiency Virus, Growth Substances
Published
1994

22. Anti-angiogenesis and angioprevention: mechanisms, problems and perspectives

Author

Bisacchi, D., Benelli, R., Vanzetto, C., Ferrari, N., Tosetti, F., and Albini, A.

Subjects
*CANCER treatment, *NEOVASCULARIZATION, *CARCINOGENESIS, *TUMORS, *DRUGS
Abstract

The recognition that angiogenesis is a key early event in tumor progression and metastasis has led to the development of new strategies for cancer therapy. The generation of a new blood vessel network under physiological conditions is regulated by the concerted action of activators and inhibitors. Perturbation of this balance, as it occurs in solid tumor growth and metastasis, appears to be a critical point in tumorigenesis. This has led to the “angiogenic switch” hypothesis: the point at which a tumor acquires the potential to induce angiogenesis is a critical step towards malignancy. Based on experimental evidence, prevention of blood vessel development appears to be the mechanism of action of many successful chemopreventive drugs of natural or synthetic origin: a novel concept that we termed “angioprevention”. The hypothesis that anti-angiogenesis is at the basis of tumor prevention also suggests that many anti-angiogenic drugs could be used for chemoprevention in higher risk populations or in early intervention. There is a growing body of experimental evidence that anti-angiogenic strategies will contribute to the future therapy of cancer, several compounds with anti-angiogenic properties are now under clinical investigation including anti-inflammatory coumpounds, as inflammation may play a key role in angiogenesis. We must persevere in the development of novel, powerful and safer angiogenesis inhibitors and in the use of anti-angiogenic drugs in combination with other natural or synthetic anti-cancer agents in a biological therapy strategy. [Copyright &y& Elsevier]

Published
2003
Full Text
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30. Vascular endothelial growth factor regulates angiogenesis and vascular permeability in Kaposi's sarcoma

Author

Cornali, E., Zietz, C., Benelli, R., Weninger, W., Masiello, L., Breier, G., Tschachler, E., Albini, A., and Sturzl, M.

Subjects
Physiological aspects, Development and progression, Vascular endothelium -- Physiological aspects, Kaposi's sarcoma -- Development and progression, Neovascularization -- Physiological aspects, Platelet-derived growth factor -- Physiological aspects
Abstract

Cornali, E.; Zietz, C.; Benelli, R.; Weninger, W.; Masiello, L.; Breier, G.; Tschachler, E.; Albini, A.; Sturzl, M. 'Vascular Endothelial Growth Factor Regulates Angiogenesis and Vascular Permeability in Kaposi's sarcoma.' [...]

Published
1997

31. The beta-core fragment of human chorionic gonadotrophin inhibits growth of Kaposi's sarcoma-derived cells and a new immortalized Kaposi's sarcoma cell line

Author

Albini, A., Paglieri, I., Orengo, G., Carlone, S., Aluigi, M.G., Demarchi, R., Matteucci, C., Mantovani, A., Carozzi, F., Donini, S., and Benelli, R.

Subjects
Physiological aspects, Growth, Company growth, Kaposi's sarcoma -- Physiological aspects, Chorionic gonadotropins -- Physiological aspects -- Growth, Cancer cells -- Growth -- Physiological aspects, Chorionic gonadotropin -- Physiological aspects -- Growth
Abstract

Albini, A.; Paglieri, I.; Orengo, G.; Carlone, S.; Aluigi, M.G.; Demarchi, R.; Matteucci, C.; Mantovani, A.; Carozzi, F.; Donini, S.; Benelli, R. 'The Beta-Core Fragment of Human Chorionic Gonadotrophin Inhibits [...]

Published
1997

32. The HIV-tat protein is a heparin-binding angiogenic growth factor

Author

Albini, A., Benelli, R., Presta, N., Rusnati, M., Ziche, M., Rubartelli, A., Bussolino, F., and Noonan, D.

Subjects
Physiological aspects, Development and progression, HIV infections -- Development and progression, Neovascularization -- Physiological aspects, HIV infection -- Development and progression
Abstract

According to an abstract submitted by the authors to the 87th Annual Meeting of the American Association for Cancer Research, held April 20-24, 1996, in Washington, D.C., 'HIV-1-tat has been [...]

Published
1996

34. Two new Kaposi's sarcoma cell lines characterized.

Author

Benelli, R.

Abstract

Reports on the establishment and characterization of two Kaposi's sarcoma (KS) cells from cultures obtained from patients with AIDS and in a non-AIDS patient. KS as an opportunistic lesion in HIV-positive patients; KS description; Relationship between KS and immune deficiency virus infection; Characteristics of KS lesions; Testing of angiogenic response from KS-cell supernatants.

Published
1994

40. Glycogen synthase kinase 3 regulates cell death and survival signaling in tumor cells under redox stress

Author

Simona Minghelli, Roberto Benelli, Barbara Cardinali, Alessandro Poggi, Francesca Tosetti, Adriana Albini, Roberta Venè, Giuseppe Arena, Nicoletta Ferrari, Douglas M. Noonan, Venè, R, Cardinali, B, Arena, G, Ferrari, N, Benelli, R, Minghelli, S, Poggi, A, Noonan, D, Albini, A, and Tosetti, F

Subjects
Cancer Research, Cell Survival, Tretinoin, Biology, medicine.disease_cause, lcsh:RC254-282, Cell Line, Antineoplastic Agent, chemistry.chemical_compound, Glycogen Synthase Kinase 3, GSK-3, Cell Line, Tumor, medicine, Gene Silencing, Phosphorylation, GSK3B, Mitogen-Activated Protein Kinase 1, Glycogen Synthase Kinase 3 beta, Mitogen-Activated Protein Kinase 3, Cell Death, Kinase, Apoptosi, Oxidative Stre, Glutathione, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Cell biology, Glucose, chemistry, Drug Resistance, Neoplasm, Neoplasm, Signal transduction, Bardoxolone, Reactive Oxygen Specie, Oxidation-Reduction, Oxidative stress, Heme Oxygenase-1, Human, Signal Transduction
Abstract

Targeting tumor-specific metabolic adaptations is a promising anticancer strategy when tumor defense mechanisms are restrained. Here, we show that redox-modulating drugs including the retinoid N-(4-hydroxyphenyl)retinamide (4HPR), the synthetic triterpenoid bardoxolone (2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid methyl ester), arsenic trioxide (As2O3), and phenylethyl isothiocyanate (PEITC), while affecting tumor cell viability, induce sustained Ser9 phosphorylation of the multifunctional kinase glycogen synthase kinase 3β (GSK3β). The antioxidant N-acetylcysteine decreased GSK3β phosphorylation and poly(ADP-ribose) polymerase cleavage induced by 4HPR, As2O3, and PEITC, implicating oxidative stress in these effects. GSK3β phosphorylation was associated with up-regulation of antioxidant enzymes, in particular heme oxygenase-1 (HO-1), and transient elevation of intracellular glutathione (GSH) in cells surviving acute stress, before occurrence of irreversible damage and death. Genetic inactivation of GSK3β or transfection with the non-phosphorylatable GSK3β-S9A mutant inhibited HO-1 induction under redox stress, while tumor cells resistant to 4HPR exhibited increased GSK3β phosphorylation, HO-1 expression, and GSH levels. The above-listed findings are consistent with a role for sustained GSK3β phosphorylation in a signaling network activating antioxidant effector mechanisms during oxidoreductive stress. These data underlie the importance of combination regimens of antitumor redox drugs with inhibitors of survival signaling to improve control of tumor development and progression and overcome chemoresistance.

Published
2014

41. Neutrophils as a key cellular target for angiostatin: implications for regulation of angiogenesis and inflammation

Author

Monica Morini, Fabio Carrozzino, Marco A. Cassatella, Douglas M. Noonan, Leonardo Santi, Roberto Benelli, Adriana Albini, Simona Minghelli, Nicoletta Ferrari, Benelli, R, Morini, M, Carrozzino, F, Ferrari, N, Minghelli, S, Santi, L, Cassatella, M, Noonan, D, and Albini, A

Subjects
Chemokine, Angiogenesis, Neutrophils, Receptors, Cell Surface, Biochemistry, Receptors, Interleukin-8B, Neovascularization, Chemokine receptor, Mice, Cell Movement, Genetics, medicine, Animals, CXC chemokine receptors, Molecular Biology, Angiostatins, Neutrophils cellular target angiostatin: angiogenesis and inflammation, Inflammation, Angiostatin, biology, Dose-Response Relationship, Drug, Neovascularization, Pathologic, Chemistry, Interleukin-8, Chemotaxis, Plasminogen, Angiomotin, Peptide Fragments, Cancer research, biology.protein, medicine.symptom, Biotechnology
Abstract

Angiostatin effectively blocks tumor angiogenesis through still poorly understood mechanisms. Given the close association between immune and vascular regulation, we investigated the effects of angiostatin on angiogenesis-associated leukocytes. Angiostatin inhibited the migration of monocytes and, even more markedly, neutrophils. Angiostatin blocked chemotaxis of neutrophils to CXCR2 chemokine receptor agonists (IL-8, MIP-2, and GRO alpha), formyl-Met-Leu-Phe (fMLP), and 12-O-tetradecanoylphorbol 13-acetate, and repressed fMLP-induced mitochondrial activity. Two different angiostatin forms (kringles 1-4 and 1-3) were effective, whereas whole plasminogen had no effect. IL-8, MIP-2, and GRO alpha induced intense angiogenic reactions in vivo, but no angiogenic response to these factors was observed in neutropenic mice, demonstrating an essential role for neutrophils. Angiostatin potently inhibited chemokine-induced angiogenesis in vivo, and consistent with in vitro observations, both angiostatin forms were active and whole plasminogen had little effect. Angiostatin inhibition of angiogenesis in vivo was accompanied by a striking reduction in the number of recruited leukocytes. In vivo, the inflammatory agent lipopolysaccharide also induced extensive leukocyte infiltration and angiogenesis that were blocked by angiostatin. Neutrophils expressed mRNAs for ATP synthase and angiomotin, two known angiostatin receptors. These data show that angiostatin directly inhibits neutrophil migration and neutrophil-mediated angiogenesis and indicate that angiostatin might inhibit inflammation.

Published
2002

42. Prevalence of hybrid TLR4 + M2 monocytes/macrophages in peripheral blood and lung of systemic sclerosis patients with interstitial lung disease.

Author

Gotelli E, Soldano S, Feghali-Bostwick C, Montagna P, Campitiello R, Contini P, Mora M, Benelli R, Hysa E, Paolino S, Pizzorni C, Sulli A, Smith V, and Cutolo M

Subjects
Humans, Middle Aged, Female, Male, Adult, Aged, Lung immunology, Lung pathology, Lung metabolism, Biomarkers, Macrophages, Alveolar immunology, Macrophages, Alveolar metabolism, Scleroderma, Systemic immunology, Scleroderma, Systemic complications, Scleroderma, Systemic blood, Toll-Like Receptor 4 metabolism, Lung Diseases, Interstitial immunology, Lung Diseases, Interstitial etiology, Monocytes immunology, Monocytes metabolism, Macrophages immunology, Macrophages metabolism
Abstract

Introduction: Systemic sclerosis (SSc) is a complex autoimmune connective tissue disease characterized by microvascular damage, immune system reactivity and progressive fibrosis of skin and internal organs. Interstitial lung disease is the leading cause of death for SSc patients (SSc-ILD), and the process of lung fibrosis involves also circulating monocytes and alveolar macrophages., Methods: Current study aimed to identify monocyte/macrophage phenotypes in lung and peripheral blood of SSc-ILD patients by immunostaining and flow cytometry, respectively. Single immunostaining was performed using primary antibodies against CD68 (pan-macrophage marker), CD80, CD86, TLR4 (M1 markers), CD163, CD204, and CD206 (M2 markers). Flow cytometry analysis included the evaluation of CD45, CD14, CD16 (monocyte lineage), CD1c (dendritic lineage), together with M1 and M2 activation markers on circulating monocytes. Protein synthesis of TLR4 and M2 markers was also investigated in cultured monocytes-derived macrophages (MDMs) from SSc-ILD patients by Western Blotting., Results: Lung samples were obtained from 9 SSc-ILD patients (50 ± 9 years old) and 5 control non-SSc patients without lung fibrosis (58 ± 23 years old). Alveolar macrophages (CD68 + cells) showed a significantly higher positivity of M1 and M2 markers in SSc-ILD lung samples than in controls (p<0.05 for CD80, p<0.01 for CD86, p<0.001 for CD68, p<0.0001 for TLR4, CD163, CD204 and CD206). In CD68 positive areas of SSc-ILD samples, a significantly higher percentage of TLR4, CD163, CD204, and CD206 positive cells was observed compared to CD80 and CD86 positive cells (p<0.001 in both cases), suggesting the possible presence of hybrid TLR4 + M2 macrophages (CD68 + CD80 - CD86 - TLR4 + CD163 + CD204 + CD206 + cells) in SSc-ILD samples. A second cohort of 26 SSc-ILD patients (63 ± 14 years old) and 14 SSc patients without ILD (63 ± 19 years old) was recruited for flow cytometry analysis of circulating monocytes. Again, a significantly higher percentage of hybrid TLR4 + M2 monocytes (CD1c - CD80 - TLR4 + CD163 + CD204 + CD206 + cells) was found in SSc-ILD positive than SSc-ILD negative patients (p<0.05). Moreover, the protein synthesis of TLR4 and M2 markers was also found higher in cultured MDMs obtained from SSc-ILD patients than in MDMs from SSc patients without ILD and this increase was significantly higher for CD163 (p<0.05) and CD206 (p<0.01)., Conclusions: The presence of hybrid TLR4 + M2 markers on both circulating monocytes and resident lung macrophages in SSc-ILD patients, is reported for the first time. Therefore, the detection of circulating hybrid TLR4 + M2 monocytes in SSc-ILD might represent a further potential biomarker of progressive organ fibrosis, to be searched in blood samples of SSc patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationship that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Gotelli, Soldano, Feghali-Bostwick, Montagna, Campitiello, Contini, Mora, Benelli, Hysa, Paolino, Pizzorni, Sulli, Smith and Cutolo.)

Published
2024
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43. Epidermal Growth Factor Receptor Targeting in Colorectal Carcinoma: Antibodies and Patient-Derived Organoids as a Smart Model to Study Therapy Resistance.

Author

Tardito S, Matis S, Zocchi MR, Benelli R, and Poggi A

Subjects
Humans, Animals, Cetuximab pharmacology, Cetuximab therapeutic use, Antibodies, Monoclonal pharmacology, Antibodies, Monoclonal therapeutic use, Protein Kinase Inhibitors pharmacology, Protein Kinase Inhibitors therapeutic use, Molecular Targeted Therapy methods, Panitumumab pharmacology, Panitumumab therapeutic use, Antineoplastic Agents, Immunological pharmacology, Antineoplastic Agents, Immunological therapeutic use, Signal Transduction drug effects, Colorectal Neoplasms drug therapy, Colorectal Neoplasms pathology, Colorectal Neoplasms metabolism, ErbB Receptors antagonists & inhibitors, ErbB Receptors metabolism, Organoids metabolism, Organoids drug effects, Drug Resistance, Neoplasm drug effects
Abstract

Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide. Therefore, the need for new therapeutic strategies is still a challenge. Surgery and chemotherapy represent the first-line interventions; nevertheless, the prognosis for metastatic CRC (mCRC) patients remains unacceptable. An important step towards targeted therapy came from the inhibition of the epidermal growth factor receptor (EGFR) pathway, by the anti-EGFR antibody, Cetuximab, or by specific tyrosine kinase inhibitors (TKI). Cetuximab, a mouse-human chimeric monoclonal antibody (mAb), binds to the extracellular domain of EGFR thus impairing EGFR-mediated signaling and reducing cell proliferation. TKI can affect the EGFR biochemical pathway at different steps along the signaling cascade. Apart from Cetuximab, other anti-EGFR mAbs have been developed, such as Panitumumab. Both antibodies have been approved for the treatment of KRAS-NRAS wild type mCRC, alone or in combination with chemotherapy. These antibodies display strong differences in activating the host immune system against CRC, due to their different immunoglobulin isotypes. Although anti-EGFR antibodies are efficient, drug resistance occurs with high frequency. Resistant tumor cell populations can either already be present before therapy or develop later by biochemical adaptations or new genomic mutations in the EGFR pathway. Numerous efforts have been made to improve the efficacy of the anti-EGFR mAbs or to find new agents that are able to block downstream EGFR signaling cascade molecules. Indeed, we examined the importance of analyzing the anti-EGFR antibody-drug conjugates (ADC) developed to overcome resistance and/or stimulate the tumor host's immunity against CRC growth. Also, patient-derived CRC organoid cultures represent a useful and feasible in vitro model to study tumor behavior and therapy response. Organoids can reflect tumor genetic heterogeneity found in the tissue of origin, representing a unique tool for personalized medicine. Thus, CRC-derived organoid cultures are a smart model for studying the tumor microenvironment and for the preclinical assay of anti-EGFR drugs., Competing Interests: The authors declare no conflicts of interest.

Published
2024
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44. Antibody-Drug Conjugate Made of Zoledronic Acid and the Anti-CD30 Brentuximab-Vedotin Exert Anti-Lymphoma and Immunostimulating Effects.

Author

Morelli F, Matis S, Benelli R, Salvini L, Zocchi MR, and Poggi A

Subjects
Humans, Cell Line, Tumor, Hodgkin Disease drug therapy, Hodgkin Disease pathology, Hodgkin Disease immunology, Apoptosis drug effects, Cell Proliferation drug effects, Zoledronic Acid pharmacology, Zoledronic Acid therapeutic use, Immunoconjugates pharmacology, Immunoconjugates therapeutic use, Immunoconjugates chemistry, Brentuximab Vedotin pharmacology, Brentuximab Vedotin therapeutic use, Ki-1 Antigen metabolism, Ki-1 Antigen immunology
Abstract

Relevant advances have been made in the management of relapsed/refractory (r/r) Hodgkin Lymphomas (HL) with the use of the anti-CD30 antibody-drug conjugate (ADC) brentuximab-vedotin (Bre-Ved). Unfortunately, most patients eventually progress despite the excellent response rates and tolerability. In this report, we describe an ADC composed of the aminobisphosphonate zoledronic acid (ZA) conjugated to Bre-Ved by binding the free amino groups of this antibody with the phosphoric group of ZA. Liquid chromatography-mass spectrometry, inductively coupled plasma-mass spectrometry, and matrix-assisted laser desorption ionization-mass spectrometry analyses confirmed the covalent linkage between the antibody and ZA. The novel ADC has been tested for its reactivity with the HL/CD30 + lymphoblastoid cell lines (KMH2, L428, L540, HS445, and RPMI6666), showing a better titration than native Bre-Ved. Once the HL-cells are entered, the ADC co-localizes with the lysosomal LAMP1 in the intracellular vesicles. Also, this ADC exerted a stronger anti-proliferative and pro-apoptotic (about one log fold) effect on HL-cell proliferation compared to the native antibody Bre-Ved. Eventually, Bre-Ved-ZA ADC, in contrast with the native antibody, can trigger the proliferation and activation of cytolytic activity of effector-memory Vδ2 T-lymphocytes against HL-cell lines. These findings may support the potential use of this ADC in the management of r/r HL.

Published
2024
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45. EGFR-Targeted Antibody-Drug Conjugate to Different Aminobisphosphonates: Direct and Indirect Antitumor Effects on Colorectal Carcinoma Cells.

Author

Pisheh L, Matis S, Taglieri M, Di Gregorio L, Benelli R, and Poggi A

Abstract

Antibody--drug conjugates (ADCs) are a promising delivery system that involves linking a monoclonal antibody (mAb) to a specific drug, such as a cytotoxic agent, to target tumor cells. This new class of antitumor therapy acts as a "biological missile" that can destroy tumor cells while increasing the therapeutic index and decreasing toxicity. One of the most critical factors in ADC design is selecting a target antigen that is highly expressed on the surface of cancer cells. In this study, we conjugated Cetuximab (Cet), a monoclonal antibody that targets the epidermal growth factor receptor (EGFR), to aminobisphosphonates (N-BPs) such as ibandronate (IBA) or risedronate (RIS) or zoledronate (ZA). Cetuximab is administered to patients with metastatic colorectal carcinoma (mCRC) with a wild-type (WT) EGFR transduction pathway. Also, it is well established that N-BPs can trigger the antitumor activity of Vδ2 T cells in both in vitro and in vivo experimental models. The resulting ADCs were added in co-culture to assess the effect on CRC cell line proliferation and sensitivity to Vδ2 T antitumor lymphocytes in comparison with the native antibody. These assays have been performed both in conventional and 3D spheroid cultures. We found that all three ADCs can increase the inhibitory effect on cell proliferation of the WT-EGFR cell line Caco-2 while only Cet-RIS and Cet-ZA can increase the cytotoxicity mediated by Vδ2 T cells against both WT and EGFR-mutated CRC cell lines (Caco-2, DLD-1, and HCT-116). Also, the ADCs can trigger the cell proliferation of Vδ2 T cells present in peripheral blood and tumor specimens. Our findings indicate that anti-EGFR antibodies bound to N-BPs can improve the antitumor effects of the native antibody possibly increasing the therapeutic effect., Competing Interests: The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Published
2024
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47. Cyclic fasting bolsters cholesterol biosynthesis inhibitors' anticancer activity.

Author

Khalifa A, Guijarro A, Ravera S, Bertola N, Adorni MP, Papotti B, Raffaghello L, Benelli R, Becherini P, Namatalla A, Verzola D, Reverberi D, Monacelli F, Cea M, Pisciotta L, Bernini F, Caffa I, and Nencioni A

Subjects
Diet, Insulin, Cholesterol, Simvastatin pharmacology, Simvastatin therapeutic use, Fasting
Abstract

Identifying oncological applications for drugs that are already approved for other medical indications is considered a possible solution for the increasing costs of cancer treatment. Under the hypothesis that nutritional stress through fasting might enhance the antitumour properties of at least some non-oncological agents, by screening drug libraries, we find that cholesterol biosynthesis inhibitors (CBIs), including simvastatin, have increased activity against cancers of different histology under fasting conditions. We show fasting's ability to increase CBIs' antitumour effects to depend on the reduction in circulating insulin, insulin-like growth factor-1 and leptin, which blunts the expression of enzymes from the cholesterol biosynthesis pathway and enhances cholesterol efflux from cancer cells. Ultimately, low cholesterol levels through combined fasting and CBIs reduce AKT and STAT3 activity, oxidative phosphorylation and energy stores in the tumour. Our results support further studies of CBIs in combination with fasting-based dietary regimens in cancer treatment and highlight the value of fasting for drug repurposing in oncology., (© 2023. The Author(s).)

Published
2023
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48. SB202190 Predicts BRAF-Activating Mutations in Primary Colorectal Cancer Organoids via Erk1-2 Modulation.

Author

Costa D, Venè R, Coco S, Longo L, Tosetti F, Scabini S, Mastracci L, Grillo F, Poggi A, and Benelli R

Subjects
Humans, Protein Kinase Inhibitors pharmacology, Mutation, ErbB Receptors genetics, Organoids metabolism, Proto-Oncogene Proteins B-raf genetics, Colorectal Neoplasms genetics
Abstract

The p38 inhibitor SB202190 is a necessary component of the medium used for normal colorectal mucosa cultures. Sato et al. suggested that the primary activity of SB202190 may be EGFR signaling stabilization, causing an increased phosphorylation of Erk1-2 sustaining organoid proliferation. However, the growth of some colorectal cancer (CRC)-derived organoid cultures is inhibited by this molecule via an unknown mechanism. We biochemically investigated SB202190 activity on a collection of 25 primary human CRC organoids, evaluating EGFR, Akt and Erk1-2 activation using Western blot. We found that Erk1-2 phosphorylation was induced by SB202190 in 20 organoid cultures and inhibited in 5 organoid cultures. A next-generation sequencing (NGS) analysis revealed that the inhibition of p-Erk1-2 signaling corresponded to the cultures with BRAF mutations (with four different hits, one being undescribed), while p-Erk1-2 induction was apparently unrelated to other mutations involving the EGFR pathway (Her2, KRAS and NRAS). We found that SB202190 mirrored the biochemical activity of the BRAF inhibitor Dabrafenib, known to induce the paradoxical activation of p-Erk1-2 signaling in BRAF wild-type cells. SB202190 was a more effective inhibitor of BRAF-mutated organoid growth in the long term than the specific BRAF inhibitors Dabrafenib and PLX8394. Overall, SB202190 can predict BRAF-activating mutations in patient-derived organoids, as well as allowing for the identification of new BRAF variants, preceding and enforcing NGS data.

Published
2023
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