164 results on '"Cimmino F"'
Search Results
2. Invited review: Human, cow, and donkey milk comparison: Focus on metabolic effects
- Author
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Cimmino, F., primary, Catapano, A., additional, Villano, I., additional, Di Maio, G., additional, Petrella, L., additional, Traina, G., additional, Pizzella, A., additional, Tudisco, R., additional, and Cavaliere, G., additional
- Published
- 2023
- Full Text
- View/download PDF
3. FGFR1 is a potential therapeutic target in neuroblastoma
- Author
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Cimmino, F., Montella, A., Tirelli, M., Avitabile, M., Lasorsa, V. A., Visconte, F., Cantalupo, S., Maiorino, T., De Angelis, B., Morini, M., Castellano, A., Locatelli, Franco, Capasso, M., Iolascon, A., Locatelli F. (ORCID:0000-0002-7976-3654), Cimmino, F., Montella, A., Tirelli, M., Avitabile, M., Lasorsa, V. A., Visconte, F., Cantalupo, S., Maiorino, T., De Angelis, B., Morini, M., Castellano, A., Locatelli, Franco, Capasso, M., Iolascon, A., and Locatelli F. (ORCID:0000-0002-7976-3654)
- Abstract
Background: FGFR1 regulates cell–cell adhesion and extracellular matrix architecture and acts as oncogene in several cancers. Potential cancer driver mutations of FGFR1 occur in neuroblastoma (NB), a neural crest-derived pediatric tumor arising in sympathetic nervous system, but so far they have not been studied experimentally. We investigated the driver-oncogene role of FGFR1 and the implication of N546K mutation in therapy-resistance in NB cells. Methods: Public datasets were used to predict the correlation of FGFR1 expression with NB clinical outcomes. Whole genome sequencing data of 19 paired diagnostic and relapse NB samples were used to find somatic mutations. In NB cell lines, silencing by short hairpin RNA and transient overexpression of FGFR1 were performed to evaluate the effect of the identified mutation by cell growth, invasion and cologenicity assays. HEK293, SHSY5Y and SKNBE2 were selected to investigate subcellular wild-type and mutated protein localization. FGFR1 inhibitor (AZD4547), alone or in combination with PI3K inhibitor (GDC0941), was used to rescue malignant phenotypes induced by overexpression of FGFR1 wild-type and mutated protein. Results: High FGFR1 expression correlated with low relapse-free survival in two independent NB gene expression datasets. In addition, we found the somatic mutation N546K, the most recurrent point mutation of FGFR1 in all cancers and already reported in NB, in one out of 19 matched primary and recurrent tumors. Loss of FGFR1 function attenuated invasion and cologenicity in NB cells, whereas FGFR1 overexpression enhanced oncogenicity. The overexpression of FGFR1N546K protein showed a higher nuclear localization compared to wild-type protein and increased cellular invasion and cologenicity. Moreover, N546K mutation caused the failure in response to treatment with FGFR1 inhibitor by activation of ERK, STAT3 and AKT pathways. The combination of FGFR1 and PI3K pathway inhibitors was effective in reducing the invasive a
- Published
- 2022
4. Feijoa Sellowiana fruit, an amazing source of anticancer molecules
- Author
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Cimmino, F., primary, Cianciullo, P., additional, Maresca, V., additional, Saggiomo, S., additional, Sorbo, S., additional, Bontempo, P., additional, and Basile, A., additional
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- 2022
- Full Text
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5. 163P Anti-tumor activity of cetuximab plus avelumab in non-small cell lung cancer patients involves innate immunity activation: Findings from the CAVE-lung trial
- Author
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Della Corte, C.M., primary, Fasano, M., additional, Ciaramella, V., additional, Cimmino, F., additional, Cardnell, R., additional, Gay, C.M., additional, Ramkumar, K., additional, Diao, L., additional, Di Liello, R., additional, Viscardi, G., additional, Famiglietti, V., additional, Ciardiello, D., additional, Martini, G., additional, Napolitano, S., additional, Troiani, T., additional, Martinelli, E., additional, Wang, J., additional, Byers, L., additional, Morgillo, F., additional, and Ciardiello, F., additional
- Published
- 2022
- Full Text
- View/download PDF
6. Galectin-1 is a major effector of TrkB-mediated neuroblastoma aggressiveness
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Cimmino, F, Schulte, J H, Zollo, M, Koster, J, Versteeg, R, Iolascon, A, Eggert, A, and Schramm, A
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- 2009
- Full Text
- View/download PDF
7. High Fat Diet Induces Neuroinflammation and Brain Oxidative Stress Affecting Cerebral and Synaptic Mitochondria Function and Efficiency
- Author
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Trinchese G., Cavaliere G., Penna E., Cimmino F., Catapano A., Pirozzi C., Lama A., Annunziata C., Piscopo O., Zammit C., Crispino M., Trinchese, G., Cavaliere, G., Penna, E., Cimmino, F., Catapano, A., Pirozzi, C., Lama, A., Annunziata, C., Piscopo, O., Zammit, C., and Crispino, M.
- Published
- 2019
8. Transcription factors involved in tumorigenesis are over-represented in mutated active DNA binding sites in neuroblastoma
- Author
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Capasso M, Lasorsa VA, Cimmino F, Avitabile M, Cantalupo S, Montella A, De Angelis B, Morini M, de Torres C, Castellano A, Locatelli F, and Iolascon A
- Abstract
The contribution of coding mutations to oncogenesis has been largely clarified whereas little is known about somatic mutations in noncoding DNA and their role in driving tumors remains controversial. Here, we used an alternative approach to interpret the functional significance of noncoding somatic mutations in promoting tumorigenesis. Noncoding somatic mutations of 151 neuroblastomas (NB) were integrated with ENCODE data to locate somatic mutations in regulatory elements specifically active in NB cells, non-specifically active in NB cells, and non-active. Within these types of elements, transcription factors (TFs) were identified whose binding sites (BS) were enriched or depleted in mutations. For these TFs, a gene expression signature was built to assess their implication in NB. DNA and RNA sequencing data were integrated to assess the effects of those mutations on mRNA levels. The pathogenicity of mutations was significantly higher in TFBS of regulatory elements specifically active in NB cells, as compared to the others. Within these elements, they were 18 over-represented TFs involved mainly in cell cycle phase transitions, and 15 under-represented TFs primarily regulating cell differentiation. A gene expression signature based on over-represented TFs correlated with poor survival and unfavourable prognostic markers. Moreover, recurrent mutations in TFBS of over-represented TFs such as EZH2 affected MCF2L and ADPRHL1 expression, among the others. We propose a novel approach to study the involvement of regulatory variants in NB that could be extended to other cancers and provide further evidence that alterations of gene expression may have relevant effects in NB development.
- Published
- 2020
9. Transcription factors involved in tumorigenesis are over-represented in mutated active DNA-binding sites in neuroblastoma A C
- Author
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Capasso, M., Lasorsa, V. A., Cimmino, F., Avitabile, M., Cantalupo, S., Montella, A., De Angelis, B., Morini, M., De Torres, C., Castellano, A., Locatelli, Franco, Iolascon, A., Locatelli F. (ORCID:0000-0002-7976-3654), Capasso, M., Lasorsa, V. A., Cimmino, F., Avitabile, M., Cantalupo, S., Montella, A., De Angelis, B., Morini, M., De Torres, C., Castellano, A., Locatelli, Franco, Iolascon, A., and Locatelli F. (ORCID:0000-0002-7976-3654)
- Abstract
The contribution of coding mutations to oncogenesis has been largely clarified, whereas little is known about somatic mutations in noncoding DNA and their role in driving tumors remains controversial. Here, we used an alternative approach to interpret the functional significance of noncoding somatic mutations in promoting tumorigenesis. Noncoding somatic mutations of 151 neuroblastomas were integrated with ENCODE data to locate somatic mutations in regulatory elements specifically active in neuroblastoma cells, nonspecifically active in neuroblastoma cells, and nonactive. Within these types of elements, transcription factors (TF) were identified whose binding sites were enriched or depleted in mutations. For these TFs, a gene expression signature was built to assess their implication in neuroblastoma. DNA- and RNA-sequencing data were integrated to assess the effects of those mutations on mRNA levels. The pathogenicity of mutations was significantly higher in transcription factor binding site (TFBS) of regulatory elements specifically active in neuroblastoma cells, as compared with the others. Within these elements, there were 18 over-represented TFs involved mainly in cell-cycle phase transitions and 15 under-represented TFs primarily regulating cell differentiation. A gene expression signature based on over-represented TFs correlated with poor survival and unfavorable prognostic markers. Moreover, recurrent mutations in TFBS of over-represented TFs such as EZH2 affected MCF2L and ADP-ribosylhydrolase like 1 expression, among the others. We propose a novel approach to study the involvement of regulatory variants in neuroblastoma that could be extended to other cancers and provide further evidence that alterations of gene expression may have relevant effects in neuroblastoma development.
- Published
- 2020
10. 1335P Anti-tumour efficacy of cetuximab plus avelumab in NSCLC through induction of ADCC: Final data from CAVE-lung trial
- Author
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Fasano, M., primary, Della Corte, C.M., additional, Di Liello, R., additional, Barra, G., additional, Cimmino, F., additional, Sparano, F., additional, Viscardi, G., additional, Iacovino, M.L., additional, Paragliola, F., additional, Famiglietti, V., additional, Ciaramella, V., additional, Sforza, V., additional, Morabito, A., additional, Maiello, E., additional, Ciardiello, F., additional, and Morgillo, F., additional
- Published
- 2020
- Full Text
- View/download PDF
11. Fine mapping of 2q35 high-risk neuroblastoma locus reveals independent functional risk variants and suggests full-length BARD1 as tumor-suppressor
- Author
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Cimmino F, Avitabile M, Diskin SJ, Vaksman Z, Pignataro P, Formicola D, Cardinale A, Testori A, Koster J, de Torres C, Devoto M, Maris JM, Iolascon A, and Capasso M
- Subjects
SNP ,neuroblastoma ,BARD1 ,GWAS ,fine mapping - Abstract
A previous genome-wide association study (GWAS) identified common variation at the BARD1 locus as being highly associated with susceptibility to high-risk neuroblastoma, but the mechanisms underlying this association have been not extensively investigated. Here, we performed a fine mapping analysis of BARD1 locus (2q35) using GWAS data from 556 high-risk neuroblastoma patients and 2,575 controls of European-American ancestry, and identified two independent genome-wide neuroblastoma-associated loci. Functional single-nucleotide polymorphism (SNP) prioritization identified two causative variants that independently contributed to neuroblastoma risk, and each replicated robustly in multiple independent cohorts comprising 445 high-risk cases and 3,170 controls (rs17489363: combined p = 1.07 × 10(-31) , OR:1.79, 95% CI:1.62-1.98 and rs1048108: combined p = 7.27 × 10(-14) , OR:0.65, 95% CI:0.58-0.73). Particularly, the T risk allele of rs17489363 in the canonical promoter region of full-length BARD1 altered binding site of the transcription factor HSF1 and correlated with low expression of full-length BARD1 mRNA and protein. Low-level expression of full-length BARD1 associated with advanced neuroblastoma. In human neuroblastoma cells, attenuating full-length BARD1 increased proliferation and invasion capacity. In conclusion, we have identified two potentially causative SNPs at the BARD1 locus associated with predisposition to high-risk neuroblastoma, and have shown that full-length BARD1 may act as tumor suppressor.
- Published
- 2018
12. Search for leptophobic Z ' bosons decaying into four-lepton final states in proton-proton collisions at root s=8 TeV
- Author
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Khachatryan, and Sirunyan, V., and Tumasyan, A. M., and Adam, A., and Asilar, W., and Bergauer, E., and Brandstetter, T., and Brondolin, J., and Dragicevic, E., and Eroe, M., and Flechl, J., and Friedl, M., and Fruehwirth, M., and Ghete, R., and Hartl, V. M., and Hoermann, C., and Hrubec, N., and Jeitler, J., and Koenig, M., and Kraetschmer, A., and Liko, I., and Matsushita, D., and Mikulec, T., and Rabady, I., and Rad, D., and Rahbaran, N., and Rohringer, B., and Schieck, H., and Strauss, J., and Treberer-Treberspurg, J., and Waltenberger, W., and Wulz, W., and Mossolov, C. -E., and Shumeiko, V., and Gonzalez, N., Suarez and Alderweireldt, J., and De Wolf, S., and Janssen, E. A., and Lauwers, X., and Van de Klundert, J., and Van Haevermaet, M., and Van Mechelen, H., and Van Remortel, P., and Van Spilbeeck, N., and Abu Zeid, A., and Blekman, S., and D'Hondt, F., and Daci, J., and De Bruyn, N., and Deroover, I., and Heracleous, K., and Lowette, N., and Moortgat, S., and Moreels, S., and Olbrechts, L., and Python, A., and Tavernier, Q., and Van Doninck, S., and Van Mulders, W., and Van Parijs, P., and Brun, I., and Caillol, H., and Clerbaux, C., and De Lentdecker, B., and Delannoy, G., and Fasanella, H., and Favart, G., and Goldouzian, L., and Grebenyuk, R., and Karapostoli, A., and Lenzi, G., and Leonard, T., and Luetic, A., and Maerschalk, J., and Marinov, T., and Randle-Conde, A., and Seva, A., and Vander Velde, T., and Vanlaer, C., and Yonamine, P., and Zenoni, R., and Zhang, F., and Cimmino, F., and Cornelis, A., and Dobur, T., and Fagot, D., and Garcia, A., and Gul, G., and Poyraz, M., and Salva, D., and Schofbeck, S., and Sharma, R., and Tytgat, A., and Van Driessche, M., and Yazgan, W., and Zaganidis, E., and Bakhshiansohi, N., and Beluffi, H., and Bondu, C., and Brochet, O., and Bruno, S., and Caudron, G., and De Visscher, A., and Delaere, S., and Delcourt, C., and Francois, M., and Giammanco, B., and Jafari, A., and Jez, A., and Komm, P., and Lemaitre, M., and Magitteri, V., and Mertens, A., and Musich, A., and Nuttens, M., and Piotrzkowski, C., and Quertenmont, K., and Selvaggi, L., and Marono, M., Vidal and Wertz, M., and Beliy, S., and Alda Junior, N., and Alves, W. L., and Alves, F. L., and Brito, G. A., and Hensel, L., and Moraes, C., and Pol, A., and Rebello Teles, M. E., and Belchior Batista Das Chagas, P., and Carvalho, E., and Chinellato, W., and Custodio, J., and Da Costa, A., and Da Silveira, E. M., and De Jesus Damiao, G. G., and De Oliveira Martins, D., and Fonseca De Souza, C., and Huertas Guativa, S., and Malbouisson, L. M., and Matos Figueiredo, H., and Mora Herrera, D., and Mundim, C., and Nogima, L., and Prado Da Silva, H., and Santoro, W. L., and Sznajder, A., and Tonelli Manganote, A., and Vilela Pereira, E. J., and Ahuja, A., and Bernardes, S., and Dogra, C. A., and Fernandez Perez Tomei, S., and Gregores, T. R., and Mercadante, E. M., and Moon, P. G., and Novaes, C. S., and Padula, S. F., and Romero Abad, Sandra S., and Ruiz Vargas, D., and Aleksandrov, J. C., and Hadjiiska, A., and Iaydjiev, R., and Rodozov, P., and Stoykova, M., and Sultanov, S., and Vutova, G., and Dimitrov, M., and Glushkov, A., and Litov, I., and Pavlov, L., and Petkov, B., and Fang, P., and Ahmad, W., and Bian, M., and Chen, J. G., and Chen, G. M., and Chen, H. S., and Chen, M., and Cheng, Y., and Jiang, T., and Leggat, C. H., and Liu, D., and Romeo, Z., and Shaheen, F., and Spiezia, S. M., and Tao, A., and Wang, J., and Wang, C., and Zhang, Z., and Zhao, H., and Ban, J., and Chen, Y., and Li, G., and Liu, Q., and Mao, S., and Qian, Y., and Wang, S. J., and Xu, D., and Avila, Z., and Cabrera, C., and Chaparro Sierra, A., and Florez, L. F., and Gomez, C., and Gonzalez Hernandez, J. P., and Ruiz Alvarez, C. F., and Sanabria, J. D., and Godinovic, J. C., and Lelas, N., and Puljak, D., and Ribeiro Cipriano, I., and Sculac, P. M., and Antunovic, T., and Kovac, Z., and Brigljevic, M., and Ferencek, V., and Kadija, D., and Micanovic, K., and Sudic, S., and Susa, L., and Attikis, T., and Mavromanolakis, A., and Mousa, G., and Nicolaou, J., and Ptochos, C., and Razis, F., and Rykaczewski, P. A., and Finger, H., and Finger, M., J, R., and Carrera Jarrin, M., and Abdelalim, E., and Mohammed, A. A., and Salama, Y., and Calpas, E., and Kadastik, B., and Murumaa, M., and Perrini, M., and Raidal, L., and Tiko, M., and Veelken, A., and Eerola, C., and Pekkanen, P., and Voutilainen, J., and Harkonen, M., and Karimaki, J., and Kinnunen, V., and Lampen, R., and Lassila-Perini, T., and Lehti, K., and Linden, S., and Luukka, T., and Tuominiemi, P., and Tuovinen, J., and Wendland, E., and Talvitie, L., and Tuuva, J., and Besancon, T., and Couderc, M., and Dejardin, F., and Denegri, M., and Fabbro, D., and Faure, B., and Favaro, J. L., and Ferri, C., and Ganjour, F., and Ghosh, S., and Givernaud, S., and Gras, A., and de Monchenault, P., Hamel and Jarry, G., and Kucher, P., and Locci, I., and Machet, E., and Malcles, M., and Rander, J., and Rosowsky, J., and Titov, A., and Zghiche, M., and Abdulsalam, A., and Antropov, A., and Baffioni, I., and Beaudette, S., and Busson, F., and Cadamuro, P., and Chapon, L., and Charlot, E., and Davignon, C., and de Cassagnac, O., Granier and Jo, R., and Lisniak, M., and Mine, S., and Nguyen, P., and Ochando, M., and Ortona, C., and Paganini, G., and Pigard, P., and Regnard, P., and Salerno, S., and Sirois, R., and Strebler, Y., and Yilmaz, T., and Zabi, Y., and Agram, A., and Andrea, J. -L., and Aubin, J., and Bloch, A., and Brom, D., and Buttignol, J. -M., and Chabert, M., and Chanon, E. C., and Collard, N., and Conte, C., and Coubez, E., and Fontaine, X., and Gele, J. -C., and Goerlach, D., and Le Bihan, U., and Skovpen, A. -C., and Van Hove, K., and Gadrat, P., and Beauceron, S., and Bernet, S., and Boudoul, C., and Bouvier, G., and Montoya, E., Carrillo and Chierici, C. A., and Contardo, R., and Courbon, D., and Depasse, B., and El Mamouni, P., and Fan, H., and Fay, J., and Gascon, J., and Gouzevitch, S., and Grenier, M., and Ille, G., and Lagarde, B., and Laktineh, F., and Lethuillier, I. B., and Mirabito, M., and Pequegnot, L., and Perries, A. L., and Popov, S., and Sabes, A., and Sordini, D., and Vander Donckt, V. i., and Verdier, M., and Viret, P., and Toriashvili, S., and Tsamalaidze, T., and Autermann, Z., and Beranek, C., and Feld, S., and Heister, L., and Kiesel, A., and Klein, M. K., and Lipinski, K., and Ostapchuk, M., and Preuten, A., and Raupach, M., and Schael, F., and Schomakers, S., and Schulte, C., and Schulz, J. F., and Verlage, J., and Weber, T., and Zhukov, H., and Albert, V., and Brodski, A., and Dietz-Laursonn, M., and Duchardt, E., and Endres, D., and Erdmann, M., and Erdweg, M., and Esch, S., and Fischer, T., and Gueth, R., and Hamer, A., and Hebbeker, M., and Heidemann, T., and Hoepfner, C., and Knutzen, K., and Merschmeyer, S., and Meyer, M., and Millet, A., and Mukherjee, P., and Olschewski, S., and Padeken, M., and Pook, K., and Radziej, T., and Reithler, M., and Rieger, H., and Scheuch, M., and Sonnenschein, F., and Teyssier, L., and Thueer, D., and Cherepanov, S., and Fluegge, V., and Ahmad, G., Haj and Hoehle, W., and Kargoll, F., and Kress, B., and Kuensken, T., and Lingemann, A., and Mueller, J., and Nehrkorn, T., and Nowack, A., and Nugent, A., and Pistone, I. M., and Pooth, C., and Stahl, O., and Martin, A., Aldaya and Asawatangtrakuldee, M., and Beernaert, C., and Behnke, K., and Behrens, O., and Bin Anuar, U., and Borras, A. A., and Campbell, K., and Connor, A., and Contreras-Campana, P., and Costanza, C., and Pardos, F., Diez and Dolinska, C., and Eckerlin, G., and Eckstein, G., and Eichhorn, D., and Eren, T., and Gallo, E., and Garcia, E., Garay and Geiser, J., and Gizhko, A., and Luyando, A., Grados and Gunnellini, J. M., and Harb, P., and Hauk, A., and Hempel, J., and Jung, M., and Kalogeropoulos, H., and Karacheban, A., and Kasemann, O., and Keaveney, M., and Kleinwort, J., and Korol, C., and Kruecker, I., and Lange, D., and Lelek, W., and Leonard, A., and Lipka, J., and Lobanov, K., and Lohmann, A., and Mankel, W., and Melzer-Pellmann, R., and Meyer, I. -A., and Mittag, A. B., and Mnich, G., and Mussgiller, J., and Ntomari, A., and Pitzl, E., and Placakyte, D., and Raspereza, R., and Roland, A., and Sahin, B., and Saxena, M. Oe., and Schoerner-Sadenius, P., and Seitz, T., and Spannagel, C., and Stefaniuk, S., and Van Onsem, N., and Walsh, G. P., and Wissing, R., and Blobel, C., and Vignali, V., Centis and Draeger, M., and Dreyer, A. R., and Garutti, T., and Gonzalez, E., and Haller, D., and Hoffmann, J., and Junkes, M., and Klanner, A., and Kogler, R., and Kovalchuk, R., and Lapsien, N., and Lenz, T., and Marchesini, T., and Marconi, I., and Meyer, D., and Niedziela, M., and Nowatschin, M., and Pantaleo, D., and Peiffer, F., and Perieanu, T., and Poehlsen, A., and Sander, J., and Scharf, C., and Schleper, C., and Schmidt, P., and Schumann, A., and Schwandt, S., and Stadie, J., and Steinbrueck, H., and Stober, G., and Stoever, F. M., and Tholen, M., and Troendle, H., and Usai, D., and Vanelderen, E., and Vanhoefer, L., and Vormwald, A., and Barth, B., and Baus, C., and Berger, C., and Butz, J., and Chwalek, E., and Colombo, T., and De Boer, F., and Dierlamm, W., and Fink, A., and Friese, S., and Giffels, R., and Gilbert, M., and Goldenzweig, A., and Haitz, P., and Hartmann, D., and Heindl, F., and Husemann, S. M., and Katkov, U., and Pardo, I., Lobelle and Maier, P., and Mildner, B., and Mozer, H., and Mueller, M. U., and Plagge, Th., and Quast, M., and Rabbertz, G., and Roecker, K., and Roscher, S., and Schroeder, F., and Shvetsov, M., and Sieber, I., and Simonis, G., and Ulrich, H. J., and Wagner-Kuhr, R., and Wayand, J., and Weber, S., and Weiler, M., and Williamson, T., and Woehrmann, S., and Wolf, C., and Anagnostou, R., and Daskalakis, G., and Geralis, G., and Giakoumopoulou, T., and Kyriakis, V. A., and Loukas, A., and Topsis-Giotis, D., and Kesisoglou, I., and Panagiotou, S., and Saoulidou, A., and Tziaferi, N., and Evangelou, E., and Flouris, I., and Foudas, G., and Kokkas, C., and Loukas, P., and Manthos, N., and Papadopoulos, N., and Paradas, I., and Filipovic, E., and Bencze, N., and Hajdu, G., and Hidas, C., and Horvath, P., and Sikler, D., and Veszpremi, F., and Vesztergombi, V., and Zsigmond, G., and Beni, A. J., and Czellar, N., and Karancsi, S., and Makovec, J., and Molnar, A., and Szillasi, J., and Bartok, Z., and Raics, M., and Trocsanyi, P., and Ujvari, Z. L., and Bahinipati, B., and Choudhury, S., and Mal, S., and Mandal, P., and Nayak, K., and Sahoo, A., and Sahoo, D. K., and Swain, N., and Bansal, S. K., and Beri, S., and Bhatnagar, S. B., and Chawla, V., and Bhawandeep, R., and Kalsi, U., and Kaur, A. K., and Kaur, A., and Kumar, M., and Kumari, R., and Mehta, P., and Mittal, A., and Singh, M., and Walia, J. B., and Kumar, G., Ashok and Bhardwaj, and Choudhary, A., and Garg, B. C., and Keshri, R. B., and Malhotra, S., and Naimuddin, S., and Nishu, M., and Ranjan, N., and Sharma, K., and Bhattacharya, V., and Bhattacharya, R., and Chatterjee, S., and Dey, K., and Dutt, S., and Dutta, S., and Majumdar, S., and Modak, N., and Mondal, A., and Mukhopadhyay, K., and Nandan, S., and Purohit, S., and Roy, A., and Chowdhury, D., Roy and Sarkar, S., and Sharan, S., and Thakur, M., and Behera, S., and Chudasama, P. K., and Dutta, R., and Jha, D., and Kumar, V., and Mohanty, V., and Netrakanti, A. K., and Pant, P. K., and Shukla, L. M., and Topkar, P., and Aziz, A., and Dugad, T., and Kole, S., and Mahakud, G., and Mitra, B., and Mohanty, S., and Parida, G. B., and Sur, B., and Sutar, N., and Banerjee, B., and Bhowmik, S., and Dewanjee, S., and Ganguly, R. K., and Guchait, S., and Jain, M., and Kumar, Sa., and Maity, S., and Majumder, M., and Mazumdar, G., and Sarkar, K., and Wickramage, T., and Chauhan, N., and Dube, S., and Hegde, S., and Kapoor, V., and Kothekar, A., and Rane, K., and Sharma, A., and Behnamian, S., and Chenarani, H., and Tadavani, S., Eskandari and Etesami, E., and Fahim, S. 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- Subjects
DIMENSIONS ,Science & Technology ,CMS ,Physics ,High Energy Physics::Phenomenology ,STANDARD MODEL ,ATLAS DETECTOR ,Astronomy & Astrophysics ,MASS ,LHC ,Exotica ,Z ' ,Four leptons ,PHYSICS ,RESONANCES ,Nuclear & Particles Physics ,Physics, Particles & Fields ,Physics, Nuclear ,0202 Atomic, Molecular, Nuclear, Particle And Plasma Physics ,Physical Sciences ,High Energy Physics::Experiment - Abstract
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No. of bitstreams: 0 Previous issue date: 2017-10-10 BMWFW (Austria) FWF (Austria) FNRS (Belgium) FWO (Belgium) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) MES (Bulgaria) CERN CAS (China) MOST (China) NSFC (China) COLCIENCIAS (Colombia) MSES (Croatia) CSF (Croatia) RPF (Cyprus) SENESCYT (Ecuador) MoER (Estonia) ERC (Estonia) IUT (Estonia) ERDF (Estonia) Academy of Finland (Finland) MEC (Finland) HIP (Finland) CEA (France) CNRS/IN2P3 (France) BMBF (Germany) DFG (Germany) HGF (Germany) GSRT (Greece) OTKA (Hungary) NIH (Hungary) DAE (India) DST (India) IPM (Iran) SFI (Ireland) INFN (Italy) MSIP (Republic of Korea) NRF (Republic of Korea) LAS (Lithuania) MOE (Malaysia) UM (Malaysia) BUAP (Mexico) CINVESTAV (Mexico) CONACYT (Mexico) LNS (Mexico) SEP (Mexico) UASLP-FAI (Mexico) MBIE (New Zealand) PAEC (Pakistan) MSHE (Poland) NSC (Poland) FCT (Portugal) JINR (Dubna) MON (Russia) RosAtom (Russia) RAS (Russia) RFBR (Russia) RAEP (Russia) MESTD (Serbia) SEIDI (Spain) CPAN (Spain) Swiss Funding Agencies (Switzerland) MST (Taipei) ThEPCenter (Thailand) IPST (Thailand) STAR (Thailand) NSTDA (Thailand) TUBITAK (Turkey) TAEK (Turkey) NASU (Ukraine) SFFR (Ukraine) STFC (United Kingdom) DOE (USA) NSF (USA) Marie-Curie programme European Research Council EPLANET (European Union) Leventis Foundation A.P. Sloan Foundation Alexander von Humboldt Foundation Belgian Federal Science Policy Office Fonds pour la Formation a la Recherche dans l'Industrie et dans l'Agriculture (FRIA-Belgium) Agentschap voor Innovatie door Wetenschap en Technologie (IWT-Belgium) Ministry of Education, Youth and Sports (MEYS) of the Czech Republic Council of Science and Industrial Research, India HOMING PLUS programme of the Foundation for Polish Science European Union, Regional Development Fund Mobility Plus programme of the Ministry of Science and Higher Education National Science Center (Poland) Thalis programme - EU-ESF Aristeia programme - EU-ESF Greek NSRF National Priorities Research Program by Qatar National Research Fund Programa Clarin-COFUND del Principado de Asturias Rachadapisek Sompot Fund for Postdoctoral Fellowship, Chulalongkorn University (Thailand) Chulalongkorn Academic into Its 2nd Century Project Advancement Project (Thailand) Welch Foundation A search for heavy narrow resonances decaying into four-lepton final states has been performed using proton-proton collision data at root s= 8 TeVcollected by the CMS experiment, corresponding to an integrated luminosity of 19.7fb(-1). No excess of events over the standard model background expectation is observed. Upper limits for a benchmark model on the product of cross section and branching fraction for the production of these heavy narrow resonances are presented. The limit excludes leptophobic Z' bosons with masses below 2.5 TeV within the benchmark model. This is the first result to constrain a leptophobic Z' resonance in the four-lepton channel. (C) 2017 The Author(s). Published by Elsevier B.V. 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Middle East Tech Univ, Phys Dept, Ankara, Turkey Bogazici Univ, Istanbul, Turkey Istanbul Tech Univ, Istanbul, Turkey Natl Acad Sci Ukraine, Inst Scintillat Mat, Kharkov, Ukraine Kharkov Inst Phys & Technol, Natl Sci Ctr, Kharkov, Ukraine Univ Bristol, Bristol, Avon, England Rutherford Appleton Lab, Didcot, Oxon, England Imperial Coll, London, England Brunel Univ, Uxbridge, Middx, England Baylor Univ, Waco, TX 76798 USA Univ Alabama, Tuscaloosa, AL USA Boston Univ, Boston, MA 02215 USA Brown Univ, Providence, RI 02912 USA Univ Calif Davis, Davis, CA 95616 USA Univ Calif Los Angeles, Los Angeles, CA USA Univ Calif Riverside, Riverside, CA 92521 USA Univ Calif San Diego, La Jolla, CA 92093 USA Univ Calif Santa Barbara, Dept Phys, Santa Barbara, CA 93106 USA CALTECH, Pasadena, CA 91125 USA Carnegie Mellon Univ, Pittsburgh, PA 15213 USA Univ Colorado, Boulder, CO 80309 USA Cornell Univ, Ithaca, NY USA Fairfield Univ, Fairfield, CT 06430 USA Fermilab Natl Accelerator Lab, POB 500, Batavia, IL 60510 USA Univ Florida, Gainesville, FL USA Florida Int Univ, Miami, FL 33199 USA Florida State Univ, Tallahassee, FL 32306 USA Florida Inst Technol, Melbourne, FL USA Univ Illinois, Chicago, IL USA Univ Iowa, Iowa City, IA USA Johns Hopkins Univ, Baltimore, MD USA Univ Kansas, Lawrence, KS 66045 USA Kansas State Univ, Manhattan, KS USA Lawrence Livermore Natl Lab, Livermore, CA USA Univ Maryland, College Pk, MD 20742 USA MIT, Cambridge, MA 02139 USA Univ Minnesota, Minneapolis, MN USA Univ Mississippi, University, MS 38677 USA Univ Nebraska, Lincoln, NE 68583 USA SUNY Buffalo, Buffalo, NY USA Northeastern Univ, Boston, MA 02115 USA Northwestern Univ, Evanston, IL USA Univ Notre Dame, Notre Dame, IN 46556 USA Ohio State Univ, Columbus, OH 43210 USA Princeton Univ, Princeton, NJ 08544 USA Univ Puerto Rico, Mayaguez, PR USA Purdue Univ, W Lafayette, IN 47907 USA Purdue Univ Calumet, Hammond, LA USA Rice Univ, Houston, TX USA Univ Rochester, Rochester, NY 14627 USA Rutgers State Univ, Piscataway, NJ USA Univ Tennessee, Knoxville, TN USA Texas A&M Univ, College Stn, TX USA Texas Tech Univ, Lubbock, TX 79409 USA Vanderbilt Univ, 221 Kirkland Hall, Nashville, TN 37235 USA Univ Virginia, Charlottesville, VA USA Wayne State Univ, Detroit, MI USA Univ Wisconsin, Madison, WI USA Vienna Univ Technol, Vienna, Austria Univ Strasbourg, CNRS, IN2P3, IPHC, Strasbourg, France Univ Estadual Campinas, Campinas, SP, Brazil Univ Fed Pelotas, Pelotas, Brazil Helwan Univ, Cairo, Egypt Zewail City Sci & Technol, Zewail, Egypt Fayoum Univ, Al Fayyum, Egypt British Univ Egypt, Cairo, Egypt Ain Shams Univ, Cairo, Egypt Univ Haute Alsace, Mulhouse, France European Org Nucl Res, CERN, Geneva, Switzerland Rhein Westfal TH Aachen, Phys Inst A 3, Aachen, Germany Brandenburg Tech Univ Cottbus, Cottbus, Germany Eotvos Lorand Univ, MTA ELTE Lendalet CMS Particle & Nucl Phys Grp, Budapest, Hungary Indian Inst Sci Educ & Res, Bhopal, India Inst Phys, Bhubaneswar, Orissa, India Univ Visva Bharati, Santini Ketan, W Bengal, India Univ Ruhuna, Matara, Sri Lanka Isfahan Univ Technol, Esfahan, Iran Univ Tehran, Dept Engn Sci, Tehran, Iran Yazd Univ, Yazd, Iran Islamic Azad Univ, Sci & Res Branch, Plasma Phys Res Ctr, Tehran, Iran Univ Siena, Siena, Italy Purdue Univ, W Lafayette, IN USA Int Islamic Univ Malaysia, Kuala Lumpur, Malaysia MOSTI, Malaysian Nucl Agcy, Kajang, Malaysia Consejo Nacl Ciencia & Technol, Mexico City, DF, Mexico Warsaw Univ Technol, Inst Elect Syst, Warsaw, Poland St Petersburg State Polytech Univ, St Petersburg, Russia PN Lebedev Phys Inst, Moscow, Russia Budker Inst Nucl Phys, Novosibirsk, Russia Univ Roma, INFN, Sez Roma, Rome, Italy Scuola Normale & Sez INFN, Pisa, Italy Riga Tech Univ, Riga, Latvia Albert Einstein Ctr Fundamental Phys, Bern, Switzerland Adiyaman Univ, Adiyaman, Turkey Mersin Univ, Mersin, Turkey Cag Univ, Mersin, Turkey Piri Reis Univ, Istanbul, Turkey Gaziosmanpasa Univ, Tokat, Turkey Ozyegin Univ, Istanbul, Turkey Izmir Inst Technol, Izmir, Turkey Marmara Univ, Istanbul, Turkey Kafkas Univ, Kars, Turkey Istanbul Bilgi Univ, Istanbul, Turkey Yildiz Tech Univ, Istanbul, Turkey Hacettepe Univ, Ankara, Turkey Univ Southampton, Sch Phys & Astron, Southampton, Hants, England Inst Astrofis Canarias, San Cristobal la Laguna, Spain Utah Valley Univ, Orem, UT USA Vinca Inst Nucl Sci, Belgrade, Serbia Univ Roma, Fac Ingn, Rome, Italy Argonne Natl Lab, 9700 S Cass Ave, Argonne, IL 60439 USA Erzincan Univ, Erzincan, Turkey Mimar Sinan Univ, Istanbul, Turkey Texas A&M Univ Qatar, Doha, Qatar Univ Estadual Paulista, Sao Paulo, Brazil National Science Center (Poland): Harmonia 2014/14/M/ST2/00428 National Science Center (Poland): Opus 2014/13/B/ST2/02543 National Science Center (Poland): 2014/15/B/ST2/03998 National Science Center (Poland): 2015/19/B/ST2/02861 National Science Center (Poland): Sonata-bis 2012/07/E/ST2/01406 Welch Foundation: C-1845
- Published
- 2017
13. Exome and deep sequencing of clinically aggressive neuroblastoma reveal somatic mutations that affect key pathways involved in cancer progression
- Author
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Lasorsa VA, Formicola D, Pignataro P, Cimmino F, Calabrese FM, Mora J, Esposito MR, Pantile M, Zanon C, De Mariano M, Longo L, Hogarty MD, de Torres C, Tonini GP, Iolascon A, and Capasso M
- Subjects
neuroblastoma ,NGS ,somatic mutation ,high risk ,cancer driver genes - Abstract
The spectrum of somatic mutation of the most aggressive forms of neuroblastoma is not completely determined. We sought to identify potential cancer drivers in clinically aggressive neuroblastoma.Whole exome sequencing was conducted on 17 germline and tumor DNA samples from high-risk patients with adverse events within 36 months from diagnosis (HR-Event3) to identify somatic mutations and deep targeted sequencing of 134 genes selected from the initial screening in additional 48 germline and tumor pairs (62.5% HR-Event3 and high-risk patients), 17 HR-Event3 tumors and 17 human-derived neuroblastoma cell lines.We revealed 22 significantly mutated genes, many of which implicated in cancer progression. Fifteen genes (68.2%) were highly expressed in neuroblastoma supporting their involvement in the disease. CHD9, a cancer driver gene, was the most significantly altered (4.0% of cases) after ALK.Other genes (PTK2, NAV3, NAV1, FZD1 and ATRX), expressed in neuroblastoma and involved in cell invasion and migration were mutated at frequency ranged from 4% to 2%.Focal adhesion and regulation of actin cytoskeleton pathways, were frequently disrupted (14.1% of cases) thus suggesting potential novel therapeutic strategies to prevent disease progression.Notably BARD1, CHEK2 and AXIN2 were enriched in rare, potentially pathogenic, germline variants.In summary, whole exome and deep targeted sequencing identified novel cancer genes of clinically aggressive neuroblastoma. Our analyses show pathway-level implications of infrequently mutated genes in leading neuroblastoma progression.
- Published
- 2016
14. Disturbi d’ansia, qualità della vita ed obesità in pazienti oncologici affetti da linfedema secondario dell’arto superiore o inferiore
- Author
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PINTO M, MOLESE M, CIMMINO F, DE FALCO F, IAZZETTA F, GIMIGLIANO, Raffaele, IOLASCON, Giovanni, GIMIGLIANO, Francesca, Pinto, M, Gimigliano, Francesca, Molese, M, Cimmino, F, DE FALCO, F, Iazzetta, F, Gimigliano, Raffaele, and Iolascon, Giovanni
- Published
- 2009
15. CD55 is a HIF-2α marker with anti-adhesive and pro-invading properties in neuroblastoma
- Author
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Cimmino, F, primary, Avitabile, M, additional, Pezone, L, additional, Scalia, G, additional, Montanaro, D, additional, Andreozzi, M, additional, Terracciano, L, additional, Iolascon, A, additional, and Capasso, M, additional
- Published
- 2016
- Full Text
- View/download PDF
16. PATOLOGIE OSTEOMUSCOLARI E FATTORI DI RISCHIO: RISULTATI DI INDAGINI STATISTICHE SU LAVORATORI DI DIFFERENTI SETTORI
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CARBONE, UMBERTO, PUCA G., CIMMINO F., FUSCO S., MAISTO A., SANZULLO A., VELLUTINO S., FARINARO E., GRIECO, LUIGI, Carbone, Umberto, Grieco, Luigi, Puca, G., Cimmino, F., Fusco, S., Maisto, A., Sanzullo, A., Vellutino, S., and Farinaro, E.
- Published
- 2003
17. La dissezione ascellare con tecnica miniinvasiva
- Author
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Procaccini E, RUGGIERO, Roberto, Falco P, DOCIMO, Giovanni, GUBITOSI, Adelmo, Cimmino F, Perrotta S, Piazza P, Lo Schiavo F., Procaccini, E, Ruggiero, Roberto, Falco, P, Docimo, Giovanni, Gubitosi, Adelmo, Cimmino, F, Perrotta, S, Piazza, P, and Lo Schiavo, F.
- Published
- 2003
18. IL CONTRIBUTO DEI FATTORI DI RISCHIO LAVORATIVO E DI QUELLI INDIVIDUALI NELLE PATOLOGIE CARDIOCIRCOLATORIE
- Author
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CARBONE, UMBERTO, PUCA G., CIMMINO F., FUSCO S., MAISTO A., SANZULLO A., VELLUTINO S., FARINARO E., GRIECO, LUIGI, Carbone, Umberto, Grieco, Luigi, Puca, G., Cimmino, F., Fusco, S., Maisto, A., Sanzullo, A., Vellutino, S., and Farinaro, E.
- Published
- 2003
19. LO STATO DI SALUTE NEL SETTORE TERZIARIO
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CARBONE, UMBERTO, VELLUTINO S., CIMMINO F., FUSCO S., GRIECO, LUIGI, Carbone, Umberto, Grieco, Luigi, Vellutino, S., Cimmino, F., and Fusco, S.
- Published
- 2002
20. INCIDENZA DI INFORTUNI SUL LAVORO IN DIFFERENTI SETTORI LAVORATIVI NELLA REGIONE CAMPANIA:ANALISI DEI DATI DERIVATI DA INDICATORI INDIRETTI
- Author
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CARBONE, UMBERTO, CIMMINO F., DE PASCALE G., FUSCO S., MAISTO A., PUCA G., VELLUTINO S., FARINARO E., GRIECO, LUIGI, Carbone, Umberto, Grieco, Luigi, Cimmino, F., DE PASCALE, G., Fusco, S., Maisto, A., Puca, G., Vellutino, S., and Farinaro, E.
- Published
- 2002
21. CONFRONTO TRA GLI INDICATORI DIRETTI ED INDIRETTI DI RIDOTTA FERTILITA' IN LAVORATORI MASCHI ESPOSTI A RISCHI
- Author
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CARBONE, UMBERTO, CIMMINO F., MAISTO A., FUSCO S., PUCA G., VELLUTINO S., FARINARO E., GRIECO, LUIGI, Carbone, Umberto, Grieco, Luigi, Cimmino, F., Maisto, A., Fusco, S., Puca, G., Vellutino, S., and Farinaro, E.
- Published
- 2002
22. Per una stima del rischio
- Author
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TRIASSI, MARIA, CARBONE, UMBERTO, FUSCO S, DI MATTEO R, CIMMINO F, RICCARDI S., Triassi, Maria, Carbone, Umberto, Fusco, S, DI MATTEO, R, Cimmino, F, and Riccardi, S.
- Published
- 2002
23. ATTUALITA' DEL RISCHIO DA AMIANTO DOPO L'EMANAZIONE DEL DECRETO LEGISLATIVO 257/94
- Author
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VELLUTINO S., CIMMINO F., MAISTO A., PUCA G., VEROPALUMBO E., CARBONE, UMBERTO, GRIECO, LUIGI, Vellutino, S., Cimmino, F., Maisto, A., Puca, G., Veropalumbo, E., Carbone, Umberto, and Grieco, Luigi
- Published
- 2001
24. EFFETTI STIMA DEL DISPENDIO ENERGETICO UMANO NELLE ATTIVITA' LAVORATIVE VALUTATO IN TELEMETRIA
- Author
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GRIECO, LUIGI, CARBONE, UMBERTO, BASILE M. L., CIMMINO F., SANZULLO A., Grieco, Luigi, Carbone, Umberto, Basile, M. L., Cimmino, F., and Sanzullo, A.
- Published
- 2000
25. Effects of environnemental pollution on semen
- Author
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DE ROSA M, PAESANO L, CIMMINO F, ZARRILLI, STEFANO, CARBONE, UMBERTO, DE ROSA, M, Carbone, Umberto, Paesano, L, Cimmino, F, and Zarrilli, Stefano
- Published
- 2000
26. [The integrated radiosurgical treatment of rectal cancer]
- Author
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LO SCHIAVO F, IOVINO, Francesco, LOJODICE F, CIMMINO F, DOCIMO, Giovanni, LO SCHIAVO, F, Iovino, Francesco, Lojodice, F, Cimmino, F, and Docimo, Giovanni
- Subjects
Adult ,Male ,Rectal Neoplasms ,Rectum ,Radiotherapy Dosage ,Radio-surgical treatment ,Middle Aged ,Combined Modality Therapy ,Postoperative Complications ,Humans ,Female ,Advanced rectal cancer ,Aged ,Follow-Up Studies ,Neoplasm Staging ,Retrospective Studies - Abstract
The value of radio-surgical protocols in the treatment of advanced rectal cancer has been studied retrospectively. 21 patients operated between 1986 and 1990 fulfilling some criteria were considered for this study. They were 9 men and 12 women with rectal cancer Duke's stage B2-C; 16 were treated with preoperative radiotherapy (30-35 Gy), 5 were treated with postoperative radiotherapy (40-60 Gy). The operative procedures were 12 anterior resections and 9 Miles operations. The 5 years results were: a) cancer free survival 52%; 2 patients alive with relapse; 2 patients with non cancer related death (DIC, radiation enteritis); d) cancer related deaths 28%; e) local recurrence was observed (3 pts) only in association with metastatic disease; f) no isolated local recurrence was observed. Preoperative radiotherapy with 30-35 Gy is judged the preferred protocol for decreasing the rate of isolated local recurrence and for increasing the survival rate. Omental flap transposition plays an important role in the radio-surgical treatment of advanced rectal cancer. The value of radio-surgical protocols in the treatment of advanced rectal cancer has been studied retrospectively. 21 patients operated between 1986 and 1990 fulfilling some criteria were considered fior this study. They were 9 men and 12 women with rectal cancer Duke's stage B2-C; 16 were treated with preoperative radiotherapy (30-35 Gy), 5 were treated with postoperative radiotherapy (40-60 Gy). The operative procedures were 12 anterior resections and 9 Miles operations. The 5 years results were: a) cancer free survival 52%; 2 patients alive with rebipse; 2 patients with non cancer related death (DIC, radiation enteritis); d) cancer related deaths 28%; e) local recurrence was observed (3 pts) only in association with metastatic disease; f) no isolated local recurrence was observed. Preoperative radiotherapy with 30-35 Gy is judjed the preferred protocol for decreasing the rate of isolated local recurrence and for increasing the survival rate. Omental flap trasposition plays an important role in the radio-surgical treatment of advanced rectal cancer. Copyright © 1999 GEM s.r.l.
- Published
- 1999
27. LA SOLUZIONE MATEMATICA DEL PROBLEMA DI CALCOLO DEL RISCHIO RESIDUO: APPLICAZIONE NELL'AUP 'FEDERICO II'
- Author
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TRIASSI M., CARBONE, UMBERTO, GALDI A., CIMMINO F., MIRISOLA C., RICCARDI S., GRIECO, LUIGI, Triassi, M., Carbone, Umberto, Grieco, Luigi, Galdi, A., Cimmino, F., Mirisola, C., and Riccardi, S.
- Published
- 1999
28. Valutazione della spermiogenesi come indicatore precoce di effetto nei protocolli di indagine sperimentale
- Author
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CARBONE, UMBERTO, VEROPALUMBO E., CIMMINO F., MIRISOLA C., DE ROSA M., Carbone, Umberto, Veropalumbo, E., Cimmino, F., Mirisola, C., and DE ROSA, M.
- Published
- 1999
29. Idoneità lavorativa degli operatori del Ser.T. dell’A.S.L'Av2
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PERNA L., CIMMINO F., MIRISOLA C., CARBONE, UMBERTO, Perna, L., Carbone, Umberto, Cimmino, F., and Mirisola, C.
- Published
- 1998
30. DONNE ED UOMINI A CONFRONTO IN DUE SETTORI LAVORATIVI DIFFERENTI: VALUTAZIONI DELLE PATOLOGIE EMERSE
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CARBONE, UMBERTO, BILANCIO G., CIMMINO F., DI MAIO S., GALDI A., GRIECO, LUIGI, Carbone, Umberto, Grieco, Luigi, Bilancio, G., Cimmino, F., DI MAIO, S., and Galdi, A.
- Abstract
FOLIA MEDICA
- Published
- 1998
31. Spermiogenesi e tossici ubiquitari
- Author
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CARBONE, UMBERTO, CIMMINO F., MIRISOLA C., PENNACCHIO P. C., RUSSO N., Carbone, Umberto, Cimmino, F., Mirisola, C., Pennacchio, P. C., and Russo, N.
- Published
- 1998
32. K-Cl cotransport (KCC) plays an important role in normal and b thalassemic erythropoiesis
- Author
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DE FRANCESCHI, Lucia, Ronzoni, L, Cappellini, Md, Cimmino, F, Siciliano, Angela, Alper, Sl, Servedio, V, Pozzobon, Christian, and Iolascon, A.
- Published
- 2007
33. Pharmacological inhibition of K-Cl cotransport alters in vivo the maturation of normal and b thalassemic human erythroid progenitors
- Author
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DE FRANCESCHI, Lucia, Ronzoni, L, Iolascon, A, and Cimmino, F.
- Published
- 2005
34. Georisorse e Beni Culturali Lapidei: le Arenarie di M. Gottero; quadro preliminare tecnico-scientifico e storico-architettonico su un materiale lapideo arenaceo largamente utilizzato nelle pavimentazioni dei centri storici liguri
- Author
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Cimmino, F, Faccini, Francesco, and Robbiano, A.
- Published
- 2005
35. Stones and coloured marbles of Liguria in historical monuments
- Author
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Cimmino, F., FRANCESCO FACCINI, and Robbiano, A.
- Published
- 2004
36. Il Calcare a Calpionelle, una tipica georisorsa ligure
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Campi, G, Cimmino, F, Faccini, Francesco, and Robbiano, A.
- Published
- 2004
37. L’utilizzo delle Arenarie di M. Zatta nelle pavimentazioni dei centri storici delle zone di provenienza (Appennino Ligure-Emiliano)
- Author
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Cimmino, F, Faccini, Francesco, and Robbiano, A.
- Published
- 2003
38. Caratteristiche fisico-meccaniche di un materiale lapideo ligure (calcare marnoso di M. Antola) utilizzato come pietra da costruzione in un manufatto emergente di pregio monumentale
- Author
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Cimmino, F, Faccini, Francesco, and Robbiano, A.
- Published
- 2002
39. The P/T boundary in the Tesero section, Western Dolomites (Trento)
- Author
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Beretta, C, Cimmino, F, Cirilli, S, Neri, C, Nicora, A, Perri, C, PIRINI RADRIZZANI, C, Posenato, Renato, and Radrizzani, S.
- Published
- 1999
40. Upper mantle evolution of ophiolitic peridotites from the Northern Apennine: petrological constraints to the geodynamic processes
- Author
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Piccardo, GIOVANNI BATTISTA, Rampone, Elisabetta, Vannucci, R., and Cimmino, F.
- Published
- 1994
41. PA.96 TRANSGASTRIC EUS-GUIDED BILIARY DRAINAGE OF POSTOPERATIVE BILOMA
- Author
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Di Bella, S., primary, Cimmino, F., additional, D'Amore, E., additional, and De Luca, L., additional
- Published
- 2008
- Full Text
- View/download PDF
42. Le peridotiti di mantello e i processi evolutivi del sistema litosfera-astenosfera: esempi da rift passivi fossili (Ba¬cino Giurassico Ligure-Piemontese) ed attuali (Mar Rosso Settentrionale)
- Author
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Piccardo, GIOVANNI BATTISTA, Rampone, Elisabetta, Vannucci, R., and Cimmino, F.
- Published
- 1992
43. K-CL co-transport plays an important role in normal and thalassemic erythropoiesis
- Author
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De Franceschi, L., primary, Ronzoni, L., additional, Cappellini, M. D., additional, Cimmino, F., additional, Siciliano, A., additional, Alper, S. L., additional, Servedio, V., additional, Pozzobon, C., additional, and Iolascon, A., additional
- Published
- 2007
- Full Text
- View/download PDF
44. Clinopyroxene-orthopiroxene major and REE partitioning in spinel peridotite xenoliths from Assab (Ethiopia)
- Author
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Ottonello, GIULIO ARMANDO, Piccardo, G. B., Mazzuccotelli, A., and Cimmino, F.
- Subjects
rare earths - Published
- 1978
45. Clinopyroxene-orthopyroxene major and rare earth elements partitioning in spinel peridotite xenoliths from Assab (Ethiopia)
- Author
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Ottonello, G, primary, Piccardo, G.B, additional, Mazzucotelli, A, additional, and Cimmino, F, additional
- Published
- 1978
- Full Text
- View/download PDF
46. High-Fat Diet Induces Neuroinflammation and Mitochondrial Impairment in Mice Cerebral Cortex and Synaptic Fraction
- Author
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Gina Cavaliere, Giovanna Trinchese, Eduardo Penna, Fabiano Cimmino, Claudio Pirozzi, Adriano Lama, Chiara Annunziata, Angela Catapano, Giuseppina Mattace Raso, Rosaria Meli, Marcellino Monda, Giovanni Messina, Christian Zammit, Marianna Crispino, Maria Pina Mollica, Cavaliere, G., Trinchese, G., Penna, E., Cimmino, F., Pirozzi, C., Lama, A., Annunziata, C., Catapano, A., Mattace Raso, G., Meli, R., Monda, M., Messina, G., Zammit, C., Crispino, M., Mollica, M. P., Cavaliere, G, Trinchese, G, Penna, E, Cimmino, F, Pirozzi, C, Lama, A, Annunziata, C, Catapano, A, Mattace Raso, G, Meli, R, Monda, M, Messina, G, Zammit, C, Crispino, M, and Mollica, Mp.
- Subjects
0301 basic medicine ,medicine.medical_specialty ,Inflammation ,Biology ,Mitochondrion ,medicine.disease_cause ,lcsh:RC321-571 ,neuroinflammation ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,high fat diet, neuroinflammation, mitochondria, synaptic plasticity, bdnf ,0302 clinical medicine ,Neurotrophic factors ,Internal medicine ,Neuroplasticity ,medicine ,BDNF, high-fat diet, mitochondria, neuroinflammation, synaptic plasticity ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Neuroinflammation ,Original Research ,synaptic plasticity ,mitochondria ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,BDNF ,high-fat diet ,Cerebral cortex ,Cellular Neuroscience ,Synaptic plasticity ,medicine.symptom ,030217 neurology & neurosurgery ,Oxidative stress - Abstract
Brain mitochondrial dysfunction is involved in the development of neurological and neurodegenerative diseases. Mitochondria specifically located at synapses play a key role in providing energy to support synaptic functions and plasticity, thus their defects may lead to synaptic failure, which is a common hallmark of neurodegenerative diseases. High-Fat Diet (HFD) consumption increases brain oxidative stress and impairs brain mitochondrial functions, although the underlying mechanisms are not completely understood. The aim of our study is to analyze neuroinflammation and mitochondrial dysfunctions in brain cortex and synaptosomal fraction isolated from a mouse model of diet-induced obesity. Male C57Bl/6 mice were divided into two groups fed a standard diet or HFD for 18 weeks. At the end of the treatment, inflammation (detected by ELISA), antioxidant state (measured by enzymatic activity), mitochondrial functions and efficiency (detected by oxidative capacity and Seahorse analysis), and brain-derived neurotrophic factor (BDNF) pathway (analyzed by western blot) were determined in brain cortex and synaptosomal fraction. In HFD animals, we observed an increase in inflammatory parameters and oxidative stress and a decrease in mitochondrial oxidative capacity both in the brain cortex and synaptosomal fraction. These alterations parallel with modulation of BDNF, a brain key signaling molecule that is linking synaptic plasticity and energy metabolism. Neuroinflammation HFD-dependent negatively affects BDNF pathway and mitochondrial activity in the brain cortex. The effect is even more pronounced in the synaptic region, where the impaired energy supply may have a negative impact on neuronal plasticity.
- Published
- 2019
47. Invited review: Human, cow, and donkey milk comparison: Focus on metabolic effects
- Author
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F. Cimmino, A. Catapano, I. Villano, G. Di Maio, L. Petrella, G. Traina, A. Pizzella, R. Tudisco, G. Cavaliere, Cimmino, F, Catapano, A, Villano, I, Di Maio, G, Petrella, L, Traina, G, Pizzella, A, Tudisco, R, and Cavaliere, G
- Subjects
cow milk ,metabolic effects ,Genetics ,human milk ,Animal Science and Zoology ,donkey milk ,Food Science - Abstract
Milk is an important food of the daily diet. Many countries include it in their dietary recommendations due to its content in several important nutrients that exert beneficial effects on human health. Human milk is a newborn's first food and plays an important role in the growth, development, and future health of every individual. Cow milk is the type of milk most consumed in the world. However, its relatively high content of saturated fats raises concerns about potential adverse effects on human health, although epidemiological studies have disproved this association. Indeed, dairy consumption appear to be linked to a lower risk of mortality and major cardiovascular disease events. In the last few years many researchers have begun to focus their attention on both the production and quality of cow milk as well as the analysis of milk from other animal species to evaluate their effect on human health. The need to investigate the composition and metabolic effects of milk from other animal species arises from the adverse reactions of individuals in several groups to certain components of cow milk. It has emerged that donkey milk compared with that of other animal species, is the nearest to human milk and an excellent substitute for it. Milk from various animal species shows substantial differences in nutritional composition and distinct metabolic effects. In this review, we discussed the main compositional features and metabolic effects of 3 types of milk: human, cow, and donkey milk.
- Published
- 2023
48. Crosstalk between Adipose Tissue and Hepatic Mitochondria in the Development of the Inflammation and Liver Injury during Ageing in High-Fat Diet Fed Rats
- Author
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Gina Cavaliere, Angela Catapano, Giovanna Trinchese, Fabiano Cimmino, Ciro Menale, Lidia Petrella, Maria Pina Mollica, Cavaliere, G., Catapano, A., Trinchese, G., Cimmino, F., Menale, C., Petrella, L., and Mollica, M. P.
- Subjects
liver diseases ,Organic Chemistry ,adipocyte size ,General Medicine ,Catalysis ,Computer Science Applications ,adipose tissue ,Inorganic Chemistry ,mitochondrial function ,inflammation ,Physical and Theoretical Chemistry ,liver disease ,Molecular Biology ,Spectroscopy - Abstract
Obesity is considered an epidemic disorder, due to an imbalance between energy consumption and metabolizable energy intake. This balance is increasingly disrupted during normal aging processes due to the progressive impairment of mechanisms that normally control energy homeostasis. Obesity is triggered by an excessive lipid depots but reflects systemic inflammation along with large adipocytes secreting proinflammatory adipokines, an increase of the free fatty acids levels in the bloodstream, and ectopic lipid accumulation. Hepatic fat accumulation is the most common cause of chronic liver disease, characterized by mitochondrial dysfunction with a consequent impaired fat metabolism and increased oxidative stress. Therefore, mitochondrial dysfunction is associated to hepatic lipid accumulation and related complications. In this study, we assessed the crosstalk between adipose tissue and liver, analyzing the time-course of changes in hepatic mitochondrial fatty acid oxidation capacity versus fatty acid storage, focusing on the contribution of adipose tissue inflammation to hepatic lipid accumulation, using a rodent model of high fat diet-induced obesity. Our results demonstrate that both high-fat diet-induced obesity and aging induce dysregulation of adipose tissue function and similar metabolic alterations mediated by mitochondrial function impairment and altered inflammatory profile. The high fat diet-induced obesity anticipates and exacerbates liver mitochondrial dysfunction that occurs with aging processes.
- Published
- 2023
49. Microcytic anemia and hepatic iron overload in a child with compound heterozygous mutations in DMT1 (SLC11A2)
- Author
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Maria D'Apolito, Flora Cimmino, Veronica Servedio, Antonio Piga, Clara Camaschella, Achille Iolascon, Iolascon, Achille, D'Apolito, M., Servedio, V., Cimmino, F., Piga, A., Camaschella, C., Iolascon, A, D'Apolito, M, Servedio, V, Cimmino, F, Piga, A, and Camaschella, Clara
- Subjects
medicine.medical_specialty ,Heterozygote ,Iron Overload ,metabolismo del ferro ,Anemia ,Microcytic anemia ,Immunology ,Transferrin receptor ,Compound heterozygosity ,medicine.disease_cause ,Biochemistry ,Internal medicine ,Iron-Binding Proteins ,medicine ,Humans ,Point Mutation ,Erythropoiesis ,Cation Transport Proteins ,Erythropoietin ,Sequence Deletion ,Mutation ,biology ,digestive, oral, and skin physiology ,Cell Biology ,Hematology ,DMT1 ,medicine.disease ,anemia ,Endocrinology ,globulo rosso ,Child, Preschool ,biology.protein ,medicine.drug - Abstract
Divalent metal transporter 1 (DMT1) mediates apical iron uptake in duodenal enterocytes and iron transfer from the transferrin receptor endosomal cycle into the cytosol in erythroid cells. Both mk mice and Belgrade rats, which carry an identical DMT1 mutation, exhibit severe microcytic anemia at birth and defective intestinal iron use and erythroid iron use. We report the hematologic phenotype of a child, compound heterozygote for 2 DMT1 mutations, who was affected by severe anemia since birth and showed hepatic iron overload. The novel mutations were a 3-bp deletion in intron 4 (c.310-3_5del CTT) resulting in a splicing abnormality and a C>T transition at nucleotide 1246(p. R416C). A striking reduction of DMT1 protein in peripheral blood mononuclear cells was demonstrated by Western blot analysis. The proband required blood transfusions until erythropoietin treatment allowed transfusion independence when hemoglobin levels between 75 and 95 g/L (7.5 and 9.5 g/dL) were achieved. Hematologic data of this patient at birth and in the first years of life strengthen the essential role of DMT1 in erythropoiesis. The early onset of iron overload indicates that, as in animal models, DMT1 is dispensable for liver iron uptake, whereas its deficiency in the gut is likely bypassed by the up-regulation of other pathways of iron use.
- Published
- 2006
50. 19p loss is significantly enriched in older age neuroblastoma patients and correlates with poor prognosis
- Author
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Giovanni Erminio, Annalisa Pezzolo, Vito Alessandro Lasorsa, Martina Morini, Flora Cimmino, Mario Capasso, Achille Iolascon, Marzia Ognibene, Katia Mazzocco, Massimo Conte, Lasorsa, V. A., Cimmino, F., Ognibene, M., Mazzocco, K., Erminio, G., Morini, M., Conte, M., Iolascon, A., Pezzolo, A., and Capasso, M.
- Subjects
0301 basic medicine ,Oncology ,medicine.medical_specialty ,Poor prognosis ,lcsh:QH426-470 ,Age at diagnosis ,lcsh:Medicine ,Cancer genomic ,Article ,Prognostic markers ,03 medical and health sciences ,symbols.namesake ,0302 clinical medicine ,Internal medicine ,Neuroblastoma ,Cancer genomics ,Genetics ,medicine ,In patient ,CDKN2D ,Molecular Biology ,Genetics (clinical) ,business.industry ,lcsh:R ,medicine.disease ,Genomic Biomarker ,DNM2 ,lcsh:Genetics ,030104 developmental biology ,Bonferroni correction ,030220 oncology & carcinogenesis ,symbols ,business - Abstract
Genomic aberrations of neuroblastoma occurring in late childhood and adolescence are still understudied. Publicly available DNA copy number profiles of 556 tumors (discovery set) and of 208 tumors obtained by array-CGH assay (validation set) were used to test if 19p loss is significantly over-represented in children and adolescents with neuroblastoma. The 19p loss occurrence was separately tested within different age groups in the discovery and validation set and the resulting P values were combined by meta-analysis and corrected by Bonferroni’s method. In both sets, 19p loss was associated with older age at diagnosis. Particularly, the lowest age group significantly associated with 19p loss (discovery set: 20%; validation set: 35%) was 6 years. The 19p loss correlated with inferior overall survival in patients over 6 years of age. Relevant tumor suppressor genes (KEAP1, DNM2, SMARCA4, SLC44A2 and CDKN2D) and microRNAs (miR-181c, miR-27a, and mirR-199a-1) are located in the genomic region involved in 19p loss. Downregulation of DNM2, SLC44A2 and CDKN2D was associated with poor patient outcome and older age. Among the recurrent NB chromosomal aberrations, only 1q gain was enriched in patients older than 6, and its presence was mutually exclusive with respect to 19p loss. Our data demonstrate that 19p loss is a genomic biomarker of NB diagnosed in older children that can predict clinical outcome.
- Published
- 2020
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