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321 results on '"Lollini, P. -L."'

2. Programmable Release of Chemotherapeutics from Ferrocene-based Injectable Hydrogels Slows Melanoma Growth

Author

Rothe, R., Xu, Y., Wodtke, J., Brandt, F., Meister, S., (0000-0003-4916-3794) Laube, M., Lollini, P. L., Zhang, Y., (0000-0002-1610-1493) Pietzsch, J., (0000-0001-8206-6000) Hauser, S., Rothe, R., Xu, Y., Wodtke, J., Brandt, F., Meister, S., (0000-0003-4916-3794) Laube, M., Lollini, P. L., Zhang, Y., (0000-0002-1610-1493) Pietzsch, J., and (0000-0001-8206-6000) Hauser, S.

Abstract

Hydrogel-based injectable drug delivery systems provide temporally and spatially controlled drug release with reduced adverse effects on healthy tissues. Therefore, they represent a promising therapeutic option for unresectable solid tumor entities. In this study, a peptide-starPEG/hyaluronic acid-based physical hydrogel is modified with ferrocene to provide a programmable drug release orchestrated by matrix-drug interaction and local reactive oxygen species (ROS). The injectable ROS-responsive hydrogel (hiROSponse) exhibits adequate biocompatibility and biodegradability, which are important for clinical applications. HiROSponse is loaded with the two cytostatic drugs (hiROSponsedox/ptx) doxorubicin (dox) and paclitaxel (ptx). Dox is a hydrophilic compound and its release is mainly controlled by Fickian diffusion, while the hydrophobic interactions between ptx and ferrocene can control its release and thus be regulated by the oxidation of ferrocene to the more hydrophilic state of ferrocenium. In a syngeneic malignant melanoma-bearing mouse model, hiROSponsedox/ptx slows tumor growth without causing adverse side effects and doubles the relative survival probability. Programmable release is further demonstrated in a tumor model with a low physiological ROS level, where dox release, low dose local irradiation, and the resulting ROS-triggered ptx release lead to tumor growth inhibition and increased survival.

Published
2024

3. Model Deconstruction of an Immunoprevention Vaccine

Author

Pappalardo, F., Lollini, P. -L., Motta, S., Mastriani, E., Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Dough, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Jiao, Licheng, editor, Wang, Lipo, editor, Gao, Xinbo, editor, Liu, Jing, editor, and Wu, Feng, editor

Published
2006
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4. Genetic Algorithm Against Cancer

Author

Pappalardo, F., Mastriani, E., Lollini, P. -L., Motta, S., Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Dough, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Carbonell, Jaime G., editor, Siekmann, Jörg, editor, Bloch, Isabelle, editor, Petrosino, Alfredo, editor, and Tettamanzi, Andrea G. B., editor

Published
2006
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6. A vision of immuno-oncology: the Siena think tank of the Italian network for tumor biotherapy (NIBIT) foundation

Author

Maio M., Lahn M., Di Giacomo A. M., Covre A., Calabro L., Ibrahim R., Fox B., Abrignani S., Paola A., Anichini A., Ardizzoni A., Gregorio A., Azab M., Ballas M., Barberis M., Bayless N. L., Bell B., Bifarini A., Blank C., Brodin P., Camerini R., Ennio C., Ceccarelli M., Francesca C., Connolly J., Sandra C., Cornelissen R., Eggermont A., Eid J., Fajgenbaum D., Ferretti E., Ferrone S., Finotello F., Flaherty K., Ester F., Elisabetta F., Fridman C. S., Fridman W. H., Garcia P., Gherardini P. F., Goonewardene A., Hacking G., Heller K., Hulett T. W., Michael I., Jacobson D., Janek M., Joho S., Keer H., Kleif S., Kotecha N., Kotter M., Krogan N., Lanzavecchia A., Locatelli F., Lollini P. -L., Mantovani A., Melacarne A., Melillo G., Menden M., Minerva D., Moretta L., Namouni F., Natali P. G., Necchi A., Nistico P., Cosimo P., Giuseppe P., Pardoll D., Paz-Ares L., Plessala K., Peters S., Prins R. M., Provendier O., Rappuoli R., Rescigno M., Ruettinger D., Seliger B., Sette A., Luca S., Spasic M., Tortora G., Trajanoski Z., Tunici P., Vitale C., Wigginton J., Yadav M., Yu H., Maio, Michele, Lahn, Michael, Di Giacomo, Anna Maria, Covre, Alessia, Calabrò, Luana, Ibrahim, Ramy, Fox, Bernard, Siena Think Tank, Lollini, Pier-Luigi, Pulmonary Medicine, Maio, M., Lahn, M., Di Giacomo, A. M., Covre, A., Calabro, L., Ibrahim, R., Fox, B., Abrignani, S., Paola, A., Anichini, A., Ardizzoni, A., Gregorio, A., Azab, M., Ballas, M., Barberis, M., Bayless, N. L., Bell, B., Bifarini, A., Blank, C., Brodin, P., Camerini, R., Ennio, C., Ceccarelli, M., Francesca, C., Connolly, J., Sandra, C., Cornelissen, R., Eggermont, A., Eid, J., Fajgenbaum, D., Ferretti, E., Ferrone, S., Finotello, F., Flaherty, K., Ester, F., Elisabetta, F., Fridman, C. S., Fridman, W. H., Garcia, P., Gherardini, P. F., Goonewardene, A., Hacking, G., Heller, K., Hulett, T. W., Michael, I., Jacobson, D., Janek, M., Joho, S., Keer, H., Kleif, S., Kotecha, N., Kotter, M., Krogan, N., Lanzavecchia, A., Locatelli, F., Lollini, P. -L., Mantovani, A., Melacarne, A., Melillo, G., Menden, M., Minerva, D., Moretta, L., Namouni, F., Natali, P. G., Necchi, A., Nistico, P., Cosimo, P., Giuseppe, P., Pardoll, D., Paz-Ares, L., Plessala, K., Peters, S., Prins, R. M., Provendier, O., Rappuoli, R., Rescigno, M., Ruettinger, D., Seliger, B., Sette, A., Luca, S., Spasic, M., Tortora, G., Trajanoski, Z., Tunici, P., Vitale, C., Wigginton, J., Yadav, M., and Yu, H.

Subjects
0301 basic medicine, Oncology, Mesothelioma, Cancer Research, Artificial intelligence, Research areas, medicine.medical_treatment, Corona virus disease 19 (COVID-19), Glioblastoma, Immunotherapy, Melanoma, Novel treatments, PD-L1, PD1, Antibodies, Monoclonal, COVID-19, Humans, Immunity, Italy, Medical Oncology, Neoplasms, Meeting Report, 0302 clinical medicine, Monoclonal, RC254-282, Foundation (evidence), Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Immunotherapy, Novel treatments, PD1, PD-L1, Melanoma, Mesothelioma, Artificial intelligence, Glioblastoma, Corona virus disease 19 (COVID-19), 030220 oncology & carcinogenesis, Non small cell, medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), Antibodies, NO, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Internal medicine, medicine, Novel treatment, Tumor microenvironment, business.industry, Cancer, medicine.disease, 030104 developmental biology, business
Abstract

Background The yearly Think Tank Meeting of the Italian Network for Tumor Biotherapy (NIBIT) Foundation, brings together in Siena, Tuscany (Italy), experts in immuno-oncology to review the learnings from current immunotherapy treatments, and to propose new pre-clinical and clinical investigations in selected research areas. Main While immunotherapies in non-small cell lung cancer and melanoma led to practice changing therapies, the same therapies had only modest benefit for patients with other malignancies, such as mesothelioma and glioblastoma. One way to improve on current immunotherapies is to alter the sequence of each combination agent. Matching the immunotherapy to the host’s immune response may thus improve the activity of the current treatments. A second approach is to combine current immunotherapies with novel agents targeting complementary mechanisms. Identifying the appropriate novel agents may require different approaches than the traditional laboratory-based discovery work. For example, artificial intelligence-based research may help focusing the search for innovative and most promising combination partners. Conclusion Novel immunotherapies are needed in cancer patients with resistance to or relapse after current immunotherapeutic drugs. Such new treatments may include targeted agents or monoclonal antibodies to overcome the immune-suppressive tumor microenvironment. The mode of combining the novel treatments, including vaccines, needs to be matched to the patient’s immune status for achieving the maximum benefit. In this scenario, specific attention should be also paid nowadays to the immune intersection between COVID-19 and cancer.

Published
2021

22. Pathobiological implications of the d16HER2 splice variant for stemness and aggressiveness of HER2-positive breast cancer

Author

Castagnoli, L, primary, Ghedini, G C, additional, Koschorke, A, additional, Triulzi, T, additional, Dugo, M, additional, Gasparini, P, additional, Casalini, P, additional, Palladini, A, additional, Iezzi, M, additional, Lamolinara, A, additional, Lollini, P L, additional, Nanni, P, additional, Chiodoni, C, additional, Tagliabue, E, additional, and Pupa, S M, additional

Published
2016
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23. 45th Annual Meeting of the Italian Cancer Society

Author

GIAVAZZI R., AGLIETTA M., ASTOLFI A., FALANGA A., LABIANCA R., LOLLINI P. L., LOMBARDO C., NATALI P. G., PIEROTTI M. A., PRESTA M., TARABOLETTI G., ZUPI G., FUSCO, ALFREDO, SANTORO, MASSIMO, VECCHIO, GIANCARLO, Giavazzi, R., Aglietta, M., Astolfi, A., Falanga, A., Fusco, Alfredo, Labianca, R., Lollini, P. L., Lombardo, C., Natali, P. G., Pierotti, M. A., Presta, M., Santoro, Massimo, Taraboletti, G., Zupi, G., and Vecchio, Giancarlo

Abstract

The 45th Annual Meeting of the Italian Cancer Society (SIC), held at the Centro Congressi Giovanni XXIII in Bergamo, Italy on 9-12 November, 2003, attracted almost 400 participants. The Scientific Committee chaired by R Giavazzi (Mario Negri Institute, Bergamo) and the board of the Italian Cancer Society produced a packed and varied program. Plenary sessions with keynote speakers (24 lectures) were combined with oral proffered papers (20 selected presentations), providing a platform from laboratory science to clinical interventions. Two hundred and sixty-one abstracts were submitted to the conference and presented in poster and poster discussion sessions, providing a stimulating ground for discussion and a network of interactive collaboration among young investigators. The venue of Bergamo offered exceptional hospitality with social events in the beautiful old town and at the Modern Art Museum. We hope that the following report gives an idea of the event and will encourage the reader to attend the 46th meeting of the SIC, 24-26 October, 2004 in Pisa.

Published
2004

24. Late abstracts 186–187

Author

Jaehne, J., Meyer, H. -J., Wittekind, Ch., Maschek, H., Pichlmayr, R., Jacobi, G., Weiermann, G., Vitzthum, H. Gräfin, Schwabe, D., Manegold, Ch., Krempien, B., Kaufmann, M., Bailly, M., Doré, J. -F., Fodstad, Ø., Kjønniksen, I., Brøgger, A., Flørenes, V. A., Pihl, A., Aamdal, S., Nesland, J. M., Geldof, A. A., Rao, B. R., De Giovanni, C., Lollini, P. -L., Del Re, B., Scotlandi, K., Nicoletti, G., Nanni, P., Van Muijen, G. N. P., Van Der Wiel-Miezenbeek, J. M., Cornelissen, L. M. H. A., Jansen, C. F. J., Ruiter, D. J., Kieler, J., Oda, Y., Tokuriki, Y., Tenang, E. M., Lamb, J. F., Galante, E., Zanoni, F., Galluzzi, D., Cerrotta, A., Martelli, G., Guzzon, A., Reduzzi, D., Barberá-Guillem, E., Barceló, J. R., Urcelay, B., Alonso-Varona, A. I., Vidal-Vanaclocha, F., Bassukas, I. D., Maurer-Schultze, B., Storeng, R., Manzotti, C., Pratesi, G., Schachert, G., Fidler, I. J., Grimstad, I. A., Rutt, G. Th., Riesinger, P., Frank, J., Neumann, G., Wissler, J. H., Bastert, G., Liebrich, W., Lehner, B., Gonzer, S., Schlag, P., Vehmeyer, K., Hajto, T., Gabius, H. -J., Funke, I., Schlimok, G., Bock, B., Dreps, A., Schweiberer, B., Riethmüller, G., Nicolai, U., Vykoupil, K. -F., Wolf, M., Havemann, K., Georgii, A., Bertrand, S., N'Guyen, M. -J., Siracky, J., Kysela, B., Siracka, E., Pflüger, E., Schirrmacher, V., Boyano, M. D., Hanania, N., Poupon, M. F., Sherbet, G. V., Lakshmi, M. S., Van Roy, F., Vleminckx, K., Fiers, W., Dragonetti, C., De Bruyne, G., Messiaen, L., Mareel, M., Kuhn, S., Choritz, H., Schmid, U., Bihl, H., Griesbach, A., Matzku, S., Eccles, S. A., Purvies, H. P., Miller, F. R., McEachern, D., Ponton, A., Waghorne, C., Coulombe, B., Kerbel, R. S., Breitman, M., Skup, D., Gingras, M. C., Jarolim, L., Wright, J. A., Greenberg, A. H., N'Guyen, M. J., Allavena, G., Melchiori, A., Aresu, O., Percario, M., Parodi, S., Schmidt, J., Kars, P., Chader, G., Albini, A., Zöller, M., Lissitzky, J. C., Bouzon, M., Martin, P. M., Grossi, I. M., Taylor, J. D., Honn, K. V., Koch, B., Baum, W., Giedl, J., Gabius, H. J., Kalden, J. R., Hakim, A. A., LadÁnyi, A., Timár, J., Moczar, E., Lapis, K., Müller, K., Wolf, M. F., Benz, B., Schumacher, K., Kemmner, W., Morgenthaler, J., Brossmer, R., Hagmar, B., Burns, G., Erkell§, L. J., Ryd, W., Paku, S., Rot, A., Hilario, E., Unda, F., Simón, J., Aliño, S. F., Sargent, N. S. E., Burger, M. M., Altevogt, P., Kowitz, A., Chopra, H., Bandlow, G., Nagel, G. A., Lotan, R., Carralero, D., Lotan, D., Raz, A., Skubitz, A. P. N., Koliakos, G. G., Furcht, L. T., Charonis, A. S., Hamann, A., Jablonski-Westrich, D., Jonas, P., Harder, R., Butcher, E. C., Thiele, H. G., Breillout, F., Antoine, E., Lascaux, V., Boxberger, H. -J., Paweletz, N., Bracke, M., Vyncke, B., Opdenakker, G., Castronovo, V., Foidart, J. -M., Camacho, M., Fras, A. Fabra, Llorens, A., Rutllant, M. L., Erkell, L. J., Brunner, G., Heredia, A., Imhoff, J. M., Burtin, P., Nakajima, M., Lunec, J., Parker, C., Fennelly, J. A., Smith, K., Roossien, F. F., La Rivière, G., Roos, E., Erdel, M., Trefz, G., Spiess, E., Ebert, W., Verhaegen, S., Remels, L., Verschueren, H., Dekegel, D., De Baetselier, P., Van Hecke, D., Hannecart-Pokorni, E., Falkvoll, K. H., Alonso, A., Baroja, A., Sebbag, U., Barbera-Guillem, E., Behrens, J., Mareel, M. M., Birchmeier, W., Waterhouse, P., Khokha, R., Chambers, A., Yagel, S., Lala, P. K., Denhardt, D. T., Hennes, R., Frantzen, F., Keller, R., Schwartz-Albiez, R., Fondaneche, M. C., Mignatti, P., Tsuboi, R., Robbins, E., Rifkin, D. B., Overall, C. M., Sacchi, A., Falcioni, R., Piaggio, G., Rizzo, M. G., Perrotti, N., Kennel, S. J., Girschick, H., Müller-Hermelink, H. K., Vollmers, H. P., Wenzel, A., Liu, S., Günthert, U., Wesch, V., Giles, M., Ponta, H., Herrlich, P., Stade, B., Hupke, U., Holzmann, B., Johnson, J. P., Sauer, A., Roller, E., Klumpp, B., Güttler, N., Lison, A., Walk, A., Redini, F., Moczar, M., Leoni, F., Da Dalt, M. G., Ménard, S., Canevari, S., Miotti, S., Tagliabue, E., Colnaghi, M. I., Ostmeier, H., Suter, L., Possati, L., Rosciani, C., Recanatini, E., Beatrici, V., Diambrini, M., Polito, M., Rothbächer, U., Eisenbach, L., Plaksin, D., Gelber, C., Kushtai, G., Gubbay, J., Feldman, M., Benke, R., Benedetto, A., Elia, G., Sala, A., Belardelli, F., Lehmann, J. M., Ladanyi, A., Hanisch, F. -G., Sölter, J., Jansen, V., Böhmer, G., Peter-Katalinic, J., Uhlenbruck, G., O'Connor, R., Müller, J., Kirchner, T., Bover, B., Tucker, G., Valles, A. M., Gavrilovic, J., Thiery, J. P., Kaufmann, A. M., Volm, M., Edel, G., Zühlsdorf, M., Voss, H., Wörmann, B., Hiddemann, W., De Neve, W., Van Den Berge, D., Van Loon, R., Storme, G., Zacharski, L. R., Wojtukiewicz, M. Z., Memoli, V., Kisiel, W., Kudryk, B. J., Stump, D., Piñol, G., Gonzalez-Garrigues, M., Fabra, A., Marti, F., Rueda, F., Lichtner, R. B., Khazaie, K., Timar, J., Greenzhevskaya, S. N., Shmalko, Yu. P., Hill, S. E., Rees, R. C., MacNeil, S., Millon, R., Muller, D., Eber, M., Abecassis, J., Betzler, M., Bahtsky, K. P., Umansky, V. Yu., Krivorotov, A. A., Balitskaya, E. K., Pridatko, O. E., Smelkova, M. I., Smirnov, I. M., Korczak, B., Fisher, C., Thody, A. J., Young, S. D., Hill, R. P., Frixen, U., Gopas, J., Segal, S., Hammerling, G., Bar-Eli, M., Rager-Zisman, B., Har-Vardi, I., Alon, Y., Hämmerling, G. J., Perez, M., Algarra, I., Collado, Ma. D., Peran, E., Caballero, A., Garrido, F., Turner, G. A., Blackmore, M., Stern, P. L., Thompson, S., Levin, I., Kuperman, O., Eyal, A., Kaneti, J., Notter, M., Knuth, A., Martin, M., Chauffert, B., Caignard, A., Hammann, A., Martin, F., Dearden, M. T., Pelletier, H., Dransfield, I., Jacob, G., Rogers, K., Pérez-Yarza, G., Cañavate, M. L., Lucas, R., Bouwens, L., Mantovani, G., Serri, F. G., Macciò, A., Zucca, M. V., Del Giacco, G. S., Pérez, M., Kärre, K., Apt, D., Traversari, C., Sensi, M., Carbone, G., Parmiani, G., Hainaut, P., Weynants, P., Degiovanni, G., Boon, T., Marquardt, P., Stulle, K., Wölfel, T., Herin, M., Van den Eynde, B., Klehmann, E., Büschenfelde, K. -H. Meyer zum, Samija, M., Gerenčer, M., Eljuga, D., Bašić, I., Heacock, C. S., Blake, A. M., D'Aleo, C. J., Alvarez, V. L., Gresser, I., Maury, C., Moss, J., Woodrow, D., von Ardenne, M., Krüger, W., Möller, P., Schachert, H. K., Itaya, T., Frost, P., Rodolfo, M., Salvi, C., Bassi, C., Huland, E., Huland, H., Sersa, G., Willingham, V., Hunter, N., Milas, L., Schild, H., von Hoegen, P., Mentges, B., Bätz, W., Suzuki, N., Mizukoshi, T., Sava, G., Ceschia, V., Zabucchi, G., Farkas-Himsley, H., Schaal, O., Klenner, T., Keppler, B., Alvarez-Diaz, A., Bizzari, J. P., Barbera-Guillem, F., Osterloh, B., Bartkowski, R., LÖhrke, H., Schwahn, E., Schafmayer, A., Goerttler, K., Cillo, C., Ling, V., Giavazzi, R., Vecchi, A., Luini, W., Garofalo, A., Iwakawa, M., Arundel, C., Tofilon, P., Giraldi, T., Perissin, L., Zorzet, S., Piccini, P., Pacor, S., Rapozzi, V., Fink, U., Zeuner, H., Dancygier, H., Classen, M., Lersch, C., Reuter, M., Hammer, C., Brendel, W., Mathé, G., Bourut, C., Chenu, E., Kidani, Y., Mauvernay, Y., Schally, A. V., Reizenstein, P., Gastiaburu, J., Comaru-Schally, A. M., Cupissol, D., Jasmin, C., Missot, J. L., Wingen, F., Schmähl, D., Pauwels-Vergely, C., Poupon, M. -F., Gasic, T. B., Ewaskiewicz, J. I., Gasic, G. J., Pápay, J., Mauvernay, R., Schally, A., Keiling, R., Hagipantelli, R., Busuttil, M., VoVan, M. L., Misset, J. L., Lévi, F., Musset, M., Ribaud, P., Hilgard, P., Reissmann, T., Stekar, J., Voegeli, R., Den Otter, W., Maas, H. A., Dullens, H. F. J., Merriman, R. L., Tanzer, L. R., Shackelford, K. A., Bemis, K. G., Campbell, J. B., and Matsumoto, K.

Published
1988
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26. Expression of an IGF-I receptor dominant negative mutant induces apoptosis, inhibits tumorigenesis and enhances chemosensitivity in Ewing's sarcoma cells

Author

Scotlandi K., Avnet S., Benini S., Manara M. C., Serra M., Cerisano V., Perdichizzi S., Lollini P. -L., De Giovanni C., Landuzzi L., Picci P., Scotlandi K., Avnet S., Benini S., Manara M.C., Serra M., Cerisano V., Perdichizzi S., Lollini P.-L., De Giovanni C., Landuzzi L., and Picci P.

Subjects
Time Factors, Time Factor, Cell Survival, Blotting, Western, Mice, Nude, Apoptosis, Sarcoma, Ewing, Transfection, Receptor, IGF Type 1, Mice, Tumor Cells, Cultured, Animals, Insulin-like growth factor-I, Chemosensitivity, Tumorigenesi, Animal, Apoptosi, Ewing's sarcoma, Gene Expression Regulation, Neoplastic, Survival Rate, Doxorubicin, Dominant negative mutant, Mutation, Nude mice, Cell Division, Neoplasm Transplantation
Abstract

IGF-IR plays an essential role in the establishment and maintenance of the transformed phenotype of ES cells and interference with the IGF-IR pathways causes reversal of the malignant potential of this neoplasm. In this report, we stably transfected a dominant negative IGF-IR expression plasmid in an ES cell line to determine the effectiveness of this strategy against the in vitro and in vivo growth of ES cells. DXR sensitivity of TC-71 cells expressing dominant negative mutants of IGF-IR was also examined. The mutated IGF-IR that we used carries a mutation in the ATP-binding domain of the intracellular β subunit, while the extracellular, ligand-binding α subunit remains unchanged. Cells carrying the dominant mutant IGF-IR had a marked decrease in proliferation, a significant increase in anoikis-induced apoptosis and a severely reduced ability to form colonies in soft agar. In vivo, when cells carrying dominant negative IGF-IR were injected into nude mice, the tumor formation and metastatic abilities of ES cells were reduced and survival increased. Furthermore, transfected clones showed significantly higher sensitivity to DXR, a major drug in the treatment of ES. These results indicate that the IGF/IGF-IR stimulation of ES cells may be inhibited by expression of mutated IGF-IR on their surfaces and that this strategy may be considered a possible alternative to impair this important target of ES cells, whose therapeutic potential was further confirmed. © 2002 Wiley-Liss, Inc.

Published
2002

33. Prevention by delay: nonspecific immunity elicited by IL-12 hinders Her-2/neu mammary carcinogenesis in transgenic mice

Author

Federica Cavallo, Di Carlo, E., Quaglino, E., Jezzi, M., Strasly, M., Bussolino, F., Colombo, M. P., Nanni, P., Lollini, P. -L, Musiani, P., and Forni, G.

Subjects
Interferon-gamma, Mice, Mice, Inbred BALB C, Neovascularization, Pathologic, Receptor, ErbB-2, Animals, Humans, Female, Mammary Neoplasms, Animal, Interleukin-12, Models, Biological, Cells, Cultured
Abstract

As a natural consequence of the expression of the activated transforming rat Her-2/neu oncogene all mammary glands of female transgenic BALB/c (BALB-neuT) mice develop atypical epithelial hyperplasia which progresses to invasive carcinoma. A lobular carcinoma is palpable in all mammary glands of 33-week-old BALB-neuT mice. This progression is markedly delayed by systemic administration of IL-12. In a series of studies the best administration schedule, the lowest dose and the most effective administration time have been defined. The cellular and molecular mechanisms resulting in the delay of carcinogenesis have been established. By means of a series of downstream mediators IL-12 inhibits the angiogenic burst that goes along with the passage from preneoplastic to neoplastic and invasive lesions; it also recruits lymphoid cells in the mammary pad and activates their cytotoxicity towards neoplastic cells and newly formed vessels; and furthermore, it induces lymphoid cells to trigger antiangiogenic activities in neoplastic epithelial cells. Effective, low-dose and non-toxic IL-12 treatments may thus be envisaged as a possible option in the management of preneoplastic mammary lesions and in mammary cancer prevention.

Published
2001

37. Human responses against HER-2-positive cancer cells in human immune system-engrafted mice

Author

De Giovanni, C, primary, Nicoletti, G, additional, Landuzzi, L, additional, Romani, F, additional, Croci, S, additional, Palladini, A, additional, Murgo, A, additional, Antognoli, A, additional, Ianzano, M L, additional, Stivani, V, additional, Grosso, V, additional, Iezzi, M, additional, Stramucci, L, additional, Barbieri, E, additional, Lemoli, R M, additional, Nanni, P, additional, and Lollini, P-L, additional

Published
2012
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38. Pathobiological implications of the d16HER2 splice variant for stemness and aggressiveness of HER2-positive breast cancer

Author

Castagnoli, L, Ghedini, G C, Koschorke, A, Triulzi, T, Dugo, M, Gasparini, P, Casalini, P, Palladini, A, Iezzi, M, Lamolinara, A, Lollini, P L, Nanni, P, Chiodoni, C, Tagliabue, E, and Pupa, S M

Abstract

We have previously shown that the d16HER2 splice variant is linked to HER2-positive breast cancer (BC) tumorigenesis, progression and response to Trastuzumab. However, the mechanisms by which d16HER2 contributes to HER2-driven aggressiveness and targeted therapy susceptibility remain uncertain. Here, we report that the d16HER2-positive mammary tumor cell lines MI6 and MI7, derived from spontaneous lesions of d16HER2 transgenic (tg) mice and resembling the aggressive features of primary lesions, are enriched in the expression of Wnt, Notch and epithelial–mesenchymal transition pathways related genes compared with full-length wild-type (WT) HER2-positive cells (WTHER2_1 and WTHER2_2) derived from spontaneous tumors arising in WTHER2 tg mice. MI6 cells exhibited increased resistance to anoikis and significantly higher mammosphere-forming efficiency (MFE) and self-renewal capability than the WTHER2-positive counterpart. Furthermore, d16HER2-positive tumor cells expressed a higher fraction of CD29High/CD24+/SCA1Lowcells and displayed greater in vivo tumor engraftment in serial dilution conditions than WTHER2_1 cells. Accordingly, NOTCH inhibitors impaired mammosphere formation only in MI6 cells. A comparative analysis of stemness-related features driven by d16HER2 and WTHER2 in ad hoc engineered human BC cells (MCF7 and T47D) revealed a higher MFE and aldehyde dehydrogenase-positive staining in d16HER2- vs WTHER2-infected cells, sustaining consistent BC-initiating cell enrichment in the human setting. Moreover, marked CD44 expression was found in MCF7_d16 and T47D_d16 cells vs their WTHER2 and Mock counterparts. Clinically, BC cases from two distinct HER2-positive cohorts characterized by high levels of expression of the activated-d16HER2 metagene were significantly enriched in the Notch family and signal transducer genes vs those with low levels of the metagene.

Published
2017
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39. Immunizing and curative potential of replicating and nonreplicating murine mammary adenocarcinoma cells engineered with interleukin (IL)-2, IL-4, IL-6, IL-7, IL-10, tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor, and gamma-interferon gene or admixed with conventional adjuvants

Author

Allione, A., Consalvo, M., Nanni, P., Lollini, P. L., Cavallo, F., Giovarelli, M., Forni, M., Gulino, A., Colombo, M. P., Dellabona, P., Hock, H., Blankenstein, T., Rosenthal, F. M., Gansbacher, B., Musso, T., Gusella, L., and Forni, G.

Subjects
Mice, Inbred BALB C, Tumor Necrosis Factor-alpha, Interleukins, Granulocyte-Macrophage Colony-Stimulating Factor, Mammary Neoplasms, Experimental, Adenocarcinoma, Transfection, Interferon-gamma, Mice, Adjuvants, Immunologic, Animals, Cytokines, Female, Immunization, Neoplasm Transplantation
Abstract

To evaluate the efficacy of vaccinations with cytokine-gene-transduced tumor cells, BALB/c mice were challenged with 1 x 10(5) parental cells of a syngeneic adenocarcinoma cell line (TSA-pc). No protection was observed in mice immunized 30 days earlier with 1 x 10(5) nonreplicating mitomycin-C-treated TSA-pc alone, or with Corynebacterium parvum or Complete Freund Adjuvant (CFA). Ten to 30% of mice immunized with nonreplicating cells engineered to produce interleukin (IL)-2, IL-4, IL-6, IL-7, IL-10, tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor, and gamma-interferon gene were protected. Fifty % of mice immunized with replicating TSA-pc admixed with C. parvum and 80-100% of mice immunized with replicating tumor cells transduced with IL-2, IL-4, IL-7, IL-10, or gamma-interferon gene were protected. No cure was afforded by TSA cells admixed with C. parvum or CFA, nor by TSA cells engineered with IL-6, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha gene injected starting 1 day after TSA-pc challenge. Complete tumor regression, however, was obtained in 10-20% of mice treated with TSA cells transduced with IL-2, IL-4, IL-7, or IL-10 and in 30% of those treated with TSA cells transduced with gamma-interferon gene.

Published
1994

43. A Multi-DNA Preventive Vaccine for p53/Neu-Driven Cancer Syndrome

Author

De Giovanni, C., primary, Nicoletti, G., additional, Palladini, A., additional, Croci, S., additional, Landuzzi, L., additional, Antognoli, A., additional, Murgo, A., additional, Astolfi, A., additional, Ferrini, S., additional, Fabbi, M., additional, Orengo, A.M., additional, Amici, A., additional, Penichet, M.L., additional, Aurisicchio, L., additional, Iezzi, M., additional, Musiani, P., additional, Nanni, P., additional, and Lollini, P.-L., additional

Published
2009
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44. ImmunoGrid, an integrative environment for large-scale simulation of the immune system for vaccine discovery, design and optimization

Author

Pappalardo, F., primary, Halling-Brown, M. D., additional, Rapin, N., additional, Zhang, P., additional, Alemani, D., additional, Emerson, A., additional, Paci, P., additional, Duroux, P., additional, Pennisi, M., additional, Palladini, A., additional, Miotto, O., additional, Churchill, D., additional, Rossi, E., additional, Shepherd, A. J., additional, Moss, D. S., additional, Castiglione, F., additional, Bernaschi, M., additional, Lefranc, M.-P., additional, Brunak, S., additional, Motta, S., additional, Lollini, P.-L., additional, Basford, K. E., additional, and Brusic, V., additional

Published
2008
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