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1. Integrated molecular profiling of patient-derived ovarian cancer models identifies clinically relevant signatures and tumor vulnerabilities

Author

Lupia, M, Melocchi, V, Bizzaro, F, Lo Riso, P, Dama, E, Baronio, M, Ranghiero, A, Barberis, M, Bernard, L, Bertalot, G, Giavazzi, R, Testa, G, Bianchi, F, Cavallaro, U, Lupia M., Melocchi V., Bizzaro F., Lo Riso P., Dama E., Baronio M., Ranghiero A., Barberis M., Bernard L., Bertalot G., Giavazzi R., Testa G., Bianchi F., Cavallaro U., Lupia, M, Melocchi, V, Bizzaro, F, Lo Riso, P, Dama, E, Baronio, M, Ranghiero, A, Barberis, M, Bernard, L, Bertalot, G, Giavazzi, R, Testa, G, Bianchi, F, Cavallaro, U, Lupia M., Melocchi V., Bizzaro F., Lo Riso P., Dama E., Baronio M., Ranghiero A., Barberis M., Bernard L., Bertalot G., Giavazzi R., Testa G., Bianchi F., and Cavallaro U.

Abstract

High-grade serous ovarian carcinoma (HGSOC) is a highly aggressive and intractable neoplasm, mainly because of its rapid dissemination into the abdominal cavity, a process that is favored by tumor-associated peritoneal ascites. The precise molecular alterations involved in HGSOC onset and progression remain largely unknown due to the high biological and genetic heterogeneity of this tumor. We established a set of different tumor samples (termed the As11-set) derived from a single HGSOC patient, consisting of peritoneal ascites, primary tumor cells, ovarian cancer stem cells (OCSC) and serially propagated tumor xenografts. The As11-set was subjected to an integrated RNA-seq and DNA-seq analysis which unveiled molecular alterations that marked the different types of samples. Our profiling strategy yielded a panel of signatures relevant in HGSOC and in OCSC biology. When such signatures were used to interrogate the TCGA dataset from HGSOC patients, they exhibited prognostic and predictive power. The molecular alterations also identified potential vulnerabilities associated with OCSC, which were then tested functionally in stemness-related assays. As a proof of concept, we defined PI3K signaling as a novel druggable target in OCSC.

Published
2022

3. L1CAM promotes ovarian cancer stemness and tumor initiation via FGFR1/SRC/STAT3 signaling

Author

Giordano, M, Decio, A, Battistini, C, Baronio, M, Bianchi, F, Villa, A, Bertalot, G, Freddi, S, Lupia, M, Jodice, M, Ubezio, P, Colombo, N, Giavazzi, R, Cavallaro, U, Giordano M., Decio A., Battistini C., Baronio M., Bianchi F., Villa A., Bertalot G., Freddi S., Lupia M., Jodice M. G., Ubezio P., Colombo N., Giavazzi R., Cavallaro U., Giordano, M, Decio, A, Battistini, C, Baronio, M, Bianchi, F, Villa, A, Bertalot, G, Freddi, S, Lupia, M, Jodice, M, Ubezio, P, Colombo, N, Giavazzi, R, Cavallaro, U, Giordano M., Decio A., Battistini C., Baronio M., Bianchi F., Villa A., Bertalot G., Freddi S., Lupia M., Jodice M. G., Ubezio P., Colombo N., Giavazzi R., and Cavallaro U.

Abstract

Background: Cancer stem cells (CSC) have been implicated in tumor progression. In ovarian carcinoma (OC), CSC drive tumor formation, dissemination and recurrence, as well as drug resistance, thus contributing to the high death-to-incidence ratio of this disease. However, the molecular basis of such a pathogenic role of ovarian CSC (OCSC) has been elucidated only to a limited extent. In this context, the functional contribution of the L1 cell adhesion molecule (L1CAM) to OC stemness remains elusive. Methods: The expression of L1CAM was investigated in patient-derived OCSC. The genetic manipulation of L1CAM in OC cells provided gain and loss-of-function models that were then employed in cell biological assays as well as in vivo tumorigenesis experiments to assess the role of L1CAM in OC cell stemness and in OCSC-driven tumor initiation. We applied antibody-mediated neutralization to investigate L1CAM druggability. Biochemical approaches were then combined with functional in vitro assays to study the molecular mechanisms underlying the functional role of L1CAM in OCSC. Results: We report that L1CAM is upregulated in patient-derived OCSC. Functional studies showed that L1CAM promotes several stemness-related properties in OC cells, including sphere formation, tumor initiation and chemoresistance. These activities were repressed by an L1CAM-neutralizing antibody, pointing to L1CAM as a druggable target. Mechanistically, L1CAM interacted with and activated fibroblast growth factor receptor-1 (FGFR1), which in turn induced the SRC-mediated activation of STAT3. The inhibition of STAT3 prevented L1CAM-dependent OC stemness and tumor initiation. Conclusions: Our study implicate L1CAM in the tumorigenic function of OCSC and point to the L1CAM/FGFR1/SRC/STAT3 signaling pathway as a novel driver of OC stemness. We also provide evidence that targeting this pathway can contribute to OC eradication.

Published
2021

4. The Italian Registry for Primary Immunodeficiencies (Italian Primary Immunodeficiency Network; IPINet): Twenty Years of Experience (1999–2019)

Author

Lougaris, V, Pession, A, Baronio, M, Soresina, A, Rondelli, R, Gazzurelli, L, Benvenuto, A, Martino, S, Gattorno, M, Biondi, A, Zecca, M, Marinoni, M, Fabio, G, Aiuti, A, Marseglia, G, Putti, M, Agostini, C, Lunardi, C, Tommasini, A, Bertolini, P, Gambineri, E, Consolini, R, Matucci, A, Azzari, C, Danieli, M, Paganelli, R, Duse, M, Cancrini, C, Moschese, V, Chessa, L, Spadaro, G, Civino, A, Vacca, A, Cardinale, F, Martire, B, Carpino, L, Trizzino, A, Russo, G, Cossu, F, Badolato, R, Pietrogrande, M, Quinti, I, Rossi, P, Ugazio, A, Pignata, C, Plebani, A, Lougaris V., Pession A., Baronio M., Soresina A., Rondelli R., Gazzurelli L., Benvenuto A., Martino S., Gattorno M., Biondi A., Zecca M., Marinoni M., Fabio G., Aiuti A., Marseglia G., Putti M. C., Agostini C., Lunardi C., Tommasini A., Bertolini P., Gambineri E., Consolini R., Matucci A., Azzari C., Danieli M. G., Paganelli R., Duse M., Cancrini C., Moschese V., Chessa L., Spadaro G., Civino A., Vacca A., Cardinale F., Martire B., Carpino L., Trizzino A., Russo G., Cossu F., Badolato R., Pietrogrande M. C., Quinti I., Rossi P., Ugazio A., Pignata C., Plebani A., Lougaris, V, Pession, A, Baronio, M, Soresina, A, Rondelli, R, Gazzurelli, L, Benvenuto, A, Martino, S, Gattorno, M, Biondi, A, Zecca, M, Marinoni, M, Fabio, G, Aiuti, A, Marseglia, G, Putti, M, Agostini, C, Lunardi, C, Tommasini, A, Bertolini, P, Gambineri, E, Consolini, R, Matucci, A, Azzari, C, Danieli, M, Paganelli, R, Duse, M, Cancrini, C, Moschese, V, Chessa, L, Spadaro, G, Civino, A, Vacca, A, Cardinale, F, Martire, B, Carpino, L, Trizzino, A, Russo, G, Cossu, F, Badolato, R, Pietrogrande, M, Quinti, I, Rossi, P, Ugazio, A, Pignata, C, Plebani, A, Lougaris V., Pession A., Baronio M., Soresina A., Rondelli R., Gazzurelli L., Benvenuto A., Martino S., Gattorno M., Biondi A., Zecca M., Marinoni M., Fabio G., Aiuti A., Marseglia G., Putti M. C., Agostini C., Lunardi C., Tommasini A., Bertolini P., Gambineri E., Consolini R., Matucci A., Azzari C., Danieli M. G., Paganelli R., Duse M., Cancrini C., Moschese V., Chessa L., Spadaro G., Civino A., Vacca A., Cardinale F., Martire B., Carpino L., Trizzino A., Russo G., Cossu F., Badolato R., Pietrogrande M. C., Quinti I., Rossi P., Ugazio A., Pignata C., and Plebani A.

Abstract

Primary immunodeficiencies (PIDs) are heterogeneous disorders, characterized by variable clinical and immunological features. National PID registries offer useful insights on the epidemiology, diagnosis, and natural history of these disorders. In 1999, the Italian network for primary immunodeficiencies (IPINet) was established. We report on data collected from the IPINet registry after 20 years of activity. A total of 3352 pediatric and adult patients affected with PIDs are registered in the database. In Italy, a regional distribution trend of PID diagnosis was observed. Based on the updated IUIS classification of 2019, PID distribution in Italy showed that predominantly antibody deficiencies account for the majority of cases (63%), followed by combined immunodeficiencies with associated or syndromic features (22.5%). The overall age at diagnosis was younger for male patients. The minimal prevalence of PIDs in Italy resulted in 5.1 per 100.000 habitants. Mortality was similar to other European registries (4.2%). Immunoglobulin replacement treatment was prescribed to less than one third of the patient cohort. Collectively, this is the first comprehensive description of the PID epidemiology in Italy.

Published
2020

5. Two siblings presenting with novel ADA2 variants, lymphoproliferation, persistence of large granular lymphocytes, and T-cell perturbations

Author

Saettini, F, Fazio, G, Corti, P, Quadri, M, Bugarin, C, Gaipa, G, Penco, F, Moratto, D, Chiarini, M, Baronio, M, Gazzurelli, L, Imberti, L, Paghera, S, Giliani, S, Cazzaniga, G, Plebani, A, Badolato, R, Lougaris, V, Gattorno, M, Biondi, A, Saettini F., Fazio G., Corti P., Quadri M., Bugarin C., Gaipa G., Penco F., Moratto D., Chiarini M., Baronio M., Gazzurelli L., Imberti L., Paghera S., Giliani S., Cazzaniga G., Plebani A., Badolato R., Lougaris V., Gattorno M., Biondi A., Saettini, F, Fazio, G, Corti, P, Quadri, M, Bugarin, C, Gaipa, G, Penco, F, Moratto, D, Chiarini, M, Baronio, M, Gazzurelli, L, Imberti, L, Paghera, S, Giliani, S, Cazzaniga, G, Plebani, A, Badolato, R, Lougaris, V, Gattorno, M, Biondi, A, Saettini F., Fazio G., Corti P., Quadri M., Bugarin C., Gaipa G., Penco F., Moratto D., Chiarini M., Baronio M., Gazzurelli L., Imberti L., Paghera S., Giliani S., Cazzaniga G., Plebani A., Badolato R., Lougaris V., Gattorno M., and Biondi A.

Abstract

The presence of large granular lymphocytes has been reported in patients with ADA2 deficiency and T-LGL leukemia. Here we describe two siblings with novel ADA2 variants, expanding the mutational spectrum of ADA2 deficiency. We show that lymphoproliferation, persistence of large granular lymphocytes, T-cell perturbations, and activation of PI3K pathway, measured by means of phosphorylation levels of S6, are detectable in DADA2 patients without T-LGL leukemia.

Published
2020

12. Italian SARS-CoV-2 patients in intensive care: towards an identikit for subjects at risk?

Author

BARONIO, M., FRENI-STERRANTINO, A., PINELLI, M., NATALINI, G., TONINI, G., MARRI, M., BAGLIVO, M., SABATINI, T., MALTESE, P. E., CHIURAZZI, P., MICHELINI, S., MORREALE, G., ASCIONE, A., NOTARO, P., and BERTELLI, M.

Abstract

OBJECTIVE: To investigate patient characteristics and factors that increase the risk of being admitted to intensive care and that influence survival in cases of SARS-CoV-2 pneumonia. PATIENTS AND METHODS: One-hundred and ninety-one SARS-CoV-2 patients were admitted to the “Fondazione Poliambulanza di Brescia” Hospital (Brescia, Lombardy, Italy) in the period 1st March 2020 to 11th April 2020. Data on demographics, clinical presentation at admission, co-morbidities, pharmacological treatment, admission to intensive care and death was recorded. Logistic regression and survival analysis were carried out to investigate the risk of being admitted to intensive care and the risk of death. RESULTS: The mean age of the study cohort was 64.6±9.9 years (range 20-88). Median BMI was 28.5±5 kg/m². Fever (81%) and dyspnea (65%) were the most common symptoms on admission. Most of patients (63%) had at least one co-existing disease. The 157 (82%) patients admitted to intensive care were more likely to be of intermediate age (60-69 years; OR 3.23, 95% CI 1.32-8.38), overweight (OR 2.66, 95% CI 1.02- 7.07) or obese (OR 5.63, 95% CI 1.73-21.09) and with lymphocytopenia (OR 2.75, 95% CI 1.17- 6.89) than the 34 patients admitted to the ordinary ward. During intensive care, 50% of patients died and their death was associated with older age (HR 2.06, 95% CI 1.07-3.97), obesity (HR 2.23, 95% CI 1.15-4.35) and male gender (HR 1.9, 95% CI 1.02-3.57). CONCLUSIONS: We found that admission to intensive care and poor survival were associated with advanced age and higher body mass index, albeit with differences in statistical significance. Pre-existing diseases and symptoms on admission were not associated with different clinical outcomes. Interestingly, male gender was more prevalent among SARS-CoV-2 patients and was related negatively to survival, but it was not associated with more frequent admission to intensive care. [ABSTRACT FROM AUTHOR]

Published
2020

14. Myeloid microvesicles in cerebrospinal fluid are associated with myelin damage and neuronal loss in mild cognitive impairment and Alzheimer disease

Author

Agosta F, Dalla Libera D, Spinelli EG, Finardi A, Canu E, Bergami A, Chiavetto L, Baronio M, Comi G, Martino G, Matteoli M, Magnani G, Verderio C, Furlan R, Agosta, F, Dalla Libera, D, Spinelli, Eg, Finardi, A, Canu, E, Bergami, A, Chiavetto, L, Baronio, M, Comi, G, Martino, G, Matteoli, M, Magnani, G, Verderio, C, and Furlan, R

Subjects
Aged, 80 and over, Male, Neurons, Alzheimer Disease, Humans, Cell Count, Cognitive Dysfunction, Female, Myeloid Cells, Middle Aged, Biomarkers, Myelin Sheath, Aged
Abstract

We have described cerebrospinal fluid (CSF) myeloid microvesicles (MVs) as a marker of microglia activation during neuroinflammation in Alzheimer disease (AD), and characterized their ability to produce toxic amyloid β1-42 (Aβ1-42 ) oligomers from aggregated or soluble substrate. The aim of this study is to investigate the association of CSF myeloid MVs with neuroimaging, clinical, and paraclinical data in AD and mild cognitive impairment (MCI).We collected CSF from 106 AD patients, 51 MCI patients, and 29 neurologically healthy controls. We examined CSF myeloid MV content and AD markers. A subgroup of 34 AD and 21 MCI patients underwent structural and diffusion tensor MRI.Higher levels of myeloid MVs were found in the CSF of AD patients and MCI patients converting within 3 years relative to controls, but also, at a lower level, in MCI patients not converting to AD. CSF myeloid MVs were associated with Tau but not with Aβ1-42 CSF levels. CSF MVs levels correlated with white matter (WM) tract damage in MCI, and with hippocampal atrophy in AD.Microglial MVs are neurotoxic and myelinotoxic in the presence of Aβ1-42 . CSF myeloid MVs, mirroring microglia activation and MV release, are associated with WM damage in MCI and hippocampal atrophy in AD. This suggests that hippocampal microglia activation, in the presence of Aβ1-42 in excess, produces neurotoxic and oligodendrotoxic oligomers that, through WM tract damage, spread disease to neighboring and connected areas, causing local microglia activation and propagation of disease through the same sequence of events. Ann Neurol 2014;76:813-825.

Published
2014

15. DELETERIOUS LRBA MUTATIONS IN A NOVEL SYNDROME OF IMMUNE DEFICIENCY AND AUTOIMMUNITY

Author

Lopez-Herrera, G, Tampella, G, Pan-Hammarstrom, Q, Herholz, P, Trujillo-Vargas, C, Phadwal, K, Simon, A, Moutschen, M, Etzioni, A, Mory, A, Srugo, I, Melamed, D, Hultenby, K, Liu, C, Baronio, M, Vitali, M, Philippet, P, Dideberg, V, Aghamohammadi, A, Rezai, N, Enright, V, Du, L, Salzer, U, Eibel, H, and Pfeifer, D

Published
2016

16. Mutations in LRBA are Associated with a Syndrome of Immune Deficiency and Autoimmunity

Author

Lopez-Herrera, G, Tampella, G, Baronio, M, Vitali, M, Lougaris, V, Plebani, A, Pan-Hammarstroem, Q, Hammarstroem, L, Du, L, Hultenby, K, Trujillo-Vargas, C, Phadwal, K, Simon, A, Moutschen, M, Etzioni, A, Srugo, A, Melamed, D, Liu, C, Philippet, P, Dideberg, V, Aghamohammadi, A, Rezai, N, Enright, V, Stauss, H, and Herholz, P

Published
2016

19. NFKB1 regulates human NK cell maturation and effector functions

Author

Lougaris, V., Patrizi, O., Baronio, M., Tabellini, G., Tampella, G., Damiati, E., Frede, N., Meer, J.W.M. van der, Fliegauf, M., Grimbacher, B., Parolini, S., Plebani, A., Lougaris, V., Patrizi, O., Baronio, M., Tabellini, G., Tampella, G., Damiati, E., Frede, N., Meer, J.W.M. van der, Fliegauf, M., Grimbacher, B., Parolini, S., and Plebani, A.

Abstract

Contains fulltext : 169759.pdf (publisher's version ) (Closed access), NFKB1, a component of the canonical NF-kappaB pathway, was recently reported to be mutated in a limited number of CVID patients. CVID-associated mutations in NFKB2 (non-canonical pathway) have previously been shown to impair NK cell cytotoxic activity. Although a biological function of NFKB1 in non-human NK cells has been reported, the role of NFKB1 mutations for human NK cell biology and disease has not been investigated yet. We decided therefore to evaluate the role of monoallelic NFKB1 mutations in human NK cell maturation and functions. We show that NFKB1 mutated NK cells present impaired maturation, defective cytotoxicity and reduced IFN-gamma production upon in vitro stimulation. Furthermore, human IL-2 activated NFKB1 mutated NK cells fail to up-regulate the expression of the activating marker NKp44 and show reduced proliferative capacity. These data suggest that NFKB1 plays an essential novel role for human NK cell maturation and effector functions.

Published
2017

21. DELETERIOUS LRBA MUTATIONS IN A NOVEL SYNDROME OF IMMUNE DEFICIENCY AND AUTOIMMUNITY

Author

GABRIELA LOPEZ HERRERA, Tampella, G., Pan-Hammarstrom, Q., Herholz, P., Trujillo-Vargas, C. M., Phadwal, K., Simon, A. K., Moutschen, M., Etzioni, A., Mory, A., Srugo, I., Melamed, D., Hultenby, K., Liu, C., Baronio, M., Vitali, M., Philippet, P., Dideberg, V., Aghamohammadi, A., Rezai, N., Enright, V., Du, L., Salzer, U., Eibel, H., Pfeifer, D., Veelken, H., Stauss, H., Lougaris, V., Plebani, A., Gertz, E. M., Schaeffer, A. A., Hammarstrom, L., and Grimbacher, B.

Published
2012

28. Characterization of polar membrane lipids of the extremely halophilic bacterium Salinibacter ruber and possible role of cardiolipin

Author

Lattanzio V.M., Baronio M, Oren A, Russell NJ, and Corcelli A.

Subjects
lipids (amino acids, peptides, and proteins)
Abstract

The lipid composition of the extremely halophilic bacterium Salinibacter ruber (Bacteroidetes) was investigated by thin layer chromatography, gas chromatography, high performance liquid chromatography and electrospray ionization-mass spectrometry. Polar lipids represent about 80% of the total lipid extract. The main polar lipids are a sulfonic acid analogue of ceramide (or capnine analogue), phosphatidylcholine, phosphatidylserine, dimethylphosphatidylethanolamine, phosphatidylglycerol, cardiolipin or bisphosphatidylglycerol, and a glycolipid. The major acyl chains in the phospholipids are C16:1 Delta9cis and C18:1 Delta11cis, while the sulfonolipid contains an amide-bound iso C15:0 fatty acid. On changing the salinity of the culture medium, no significant differences were found in the lipid profile or the unsaturation of the lipid fatty acyl chains. The structure of the cardiolipin, which represents 20% of polar lipids, has been elucidated by gas chromatography and electrospray ionization mass spectrometry analysis.

Published
2009

50. Posters * Safety & Quality (I.E. Guidelines, Multiple Pregnancy, Outcome, Follow-Up etc.)

Author

Ocal, P., primary, Sahmay, S., additional, Irez, T., additional, Senol, H., additional, Cepni, I., additional, Purisa, S., additional, Lin, W., additional, Liu, X., additional, Donjacour, A., additional, Maltepe, E., additional, Rinaudo, P., additional, Baumgarten, M. N., additional, Stoop, D., additional, Haentjes, P., additional, Verheyen, G., additional, De Schrijver, F., additional, Liebaers, I., additional, Camus, M., additional, Bonduelle, M., additional, Devroey, P., additional, Nelissen, E. C. M., additional, Van Montfoort, A. P. A., additional, Coonen, E., additional, Derhaag, J. G., additional, Evers, J. L. H., additional, Dumoulin, J. C. M., additional, Costa Lopes, J. R., additional, Mendes dos Santos, J., additional, Portugal Silva Lima, S., additional, Portugal Silva Souza, S., additional, Rodrigues Pereira, T., additional, Barguil Brasileiro, J. P., additional, Pina, H., additional, Lessa, M. L., additional, Genovese Soares, M., additional, Medina Lopes, V., additional, Ribeiro, C. G., additional, Adami, K., additional, Hughes, C., additional, Emerson, G., additional, Grundy, K., additional, Kelly, P., additional, Mocanu, E., additional, Coelho Cafe, T., additional, de Souza Costa, J. B. M., additional, Zavattiero Tierno, N. I., additional, Singh, S., additional, Vitthala, S., additional, Zosmer, A., additional, Sabatini, L., additional, Tozer, A., additional, Davis, C., additional, Al-Shawaf, T., additional, Neri, Q. V., additional, Monahan, D., additional, Rosenwaks, Z., additional, Palermo, G. D., additional, Kalu, E., additional, Thum, M. Y., additional, Abdalla, H. A., additional, Sazonova, A., additional, Bergh, C., additional, Kallen, K., additional, Thurin-Kjellberg, A., additional, Wennerholm, U. B., additional, Griesinger, G., additional, Doody, K., additional, Witjes, H., additional, Mannaerts, B., additional, Tarlatzis, B., additional, Rombauts, L., additional, Heijnen, E., additional, Marintcheva-Petrova, M., additional, Elbers, J., additional, Koning, A., additional, Mutsaerts, M. A. Q., additional, Hoek, A., additional, Mol, B. W., additional, Fadini, R., additional, Guarnieri, T., additional, Mignini Renzini, M., additional, Comi, R., additional, Mastrolilli, M., additional, Villa, A., additional, Colpi, E., additional, Coticchio, G., additional, Dal Canto, M., additional, Dolleman, M., additional, Broer, S. L., additional, Opmeer, B. C., additional, Fauser, B. C., additional, Broekmans, F. J. M., additional, Alama, P., additional, Requena, A., additional, Crespo, J., additional, Munoz, M., additional, Ballesteros, A., additional, Munoz, E., additional, Fernandez, M., additional, Meseguer, M., additional, Garcia-Velasco, J. A., additional, Pellicer, A., additional, Munk, M., additional, Smidt-Jensen, S., additional, Blaabjerg, J., additional, Christoffersen, C., additional, Lenz, S., additional, Lindenberg, S., additional, Bosch, E., additional, Labarta, E., additional, Cruz, F., additional, Simon, C., additional, Remohi, J., additional, Esler, J., additional, Osborn, J., additional, Boissonnas Chalas, C., additional, Marszalek, A., additional, Fauque, P., additional, Wolf, J. P., additional, De Ziegler, D., additional, Cabanes, L., additional, Jouannet, P., additional, Han, A. R., additional, Park, C. W., additional, Cha, S. W., additional, Kim, H. O., additional, Yang, K. M., additional, Kim, J. Y., additional, Song, I. O., additional, Koong, M. K., additional, Kang, I. S., additional, Roszaman, R., additional, Omar, M. H., additional, Nazri, Y., additional, Azantee, Y. W., additional, Murad, A. Z., additional, Zainulrashid, M. R., additional, Wang, N., additional, Le, F., additional, Wang, L. Y., additional, Ding, G. L., additional, Sheng, J. Z., additional, Huang, H. F., additional, Jin, F., additional, Reinblatt, S., additional, Holzer, H., additional, Son, W. Y., additional, Shalom-Paz, E., additional, Chian, R. C., additional, Buckett, W., additional, Dahan, M., additional, Demirtas, E., additional, Tan, S. L., additional, Revel, A., additional, Schejter-Dinur, Y., additional, Revel-Vilk, S., additional, Hermens, R. P. M. G., additional, van den Boogaard, E., additional, Leschot, N. J., additional, Vollebergh, J. H. A., additional, Bernardus, R., additional, Kremer, J. A. M., additional, van der Veen, F., additional, Goddijn, M., additional, Nahuis, M. J., additional, Kose, N., additional, Bayram, N., additional, Hompes, P. G. A., additional, Mol, B. W. J., additional, van der veen, F., additional, van Wely, M., additional, Van Disseldorp, J., additional, Dolleman, M. D., additional, Broeze, K., additional, De Rycke, M., additional, Petrussa, L., additional, Van de Velde, H., additional, Cerrillo, M., additional, Pacheco, A., additional, Rodriguez, S., additional, Gomez, R., additional, Delagado, F., additional, Garcia Velasco, J. A., additional, Desmyttere, S., additional, Verpoest, W., additional, Staessen, C., additional, De Vos, A., additional, Kohls, G., additional, Ruiz, F. J., additional, De la Fuente, G., additional, Toribio, M., additional, Martinez, M., additional, Soderstrom - Anttila, V., additional, Salevaara, M., additional, Suikkari, A. M., additional, Clua, E., additional, Tur, R., additional, Alcaniz, N., additional, Boada, M., additional, Rodriguez, I., additional, Barri, P. N., additional, Veiga, A., additional, Nelen, W. L. D. M., additional, Van Empel, I. W. H., additional, Cohlen, B. J., additional, Laven, J. S., additional, Aarts, J. W. M., additional, Ricciarelli, E., additional, Gomez-Palomares, J. L., additional, Andres-Criado, L., additional, Hernandez, E. R., additional, Courbiere, B., additional, Aye, M., additional, Perrin, J., additional, Di Giorgio, C., additional, De Meo, M., additional, Botta, A., additional, Castilla Alcala, J., additional, Luceno Maestre, F., additional, Cabello, Y., additional, Hernandez, J., additional, Marqueta, J., additional, Pareja, A., additional, Hernandez, E., additional, Coroleu, B., additional, Helmgaard, L., additional, Klein, B. M., additional, Arce, J. C., additional, van Empel, I. W. H., additional, Boivin, J., additional, Verhaak, C. M., additional, Ding, G., additional, Yin, R., additional, Sheng, J., additional, Huang, H., additional, Mancini, F., additional, Gomez, M. J., additional, van den Boogaard, N. M., additional, van der Steeg, J. W., additional, Hompes, P., additional, Boyer, P., additional, Gervoise-Boyer, M., additional, Meddeb, L., additional, Rossin, B., additional, Audibert, F., additional, Sakian, S., additional, Chan Wong, E., additional, Ma, S., additional, Pathak, R., additional, Mustafa, M. D., additional, Ahmed, R. S., additional, Tripathi, A. K., additional, Guleria, K., additional, Banerjee, B. D., additional, Vela, G., additional, Luna, M., additional, Flisser, E. D., additional, Sandler, B., additional, Brodman, M., additional, Grunfeld, L., additional, Copperman, A. B., additional, Baronio, M., additional, Carrascosa, P., additional, Capunay, C., additional, Vallejos, J., additional, Papier, S., additional, Borghi, M., additional, Sueldo, C., additional, Carrascosa, J., additional, Martin Lopez, E., additional, Marcucci, A., additional, Marcucci, I., additional, Salacone, P., additional, Sebastianelli, A., additional, Caponecchia, L., additional, Pacini, N., additional, Rago, R., additional, Alvarez, M., additional, Carreras, O., additional, Arnoldi, M., additional, Diaferia, D., additional, Corbucci, M. G., additional, De Lauretis, L., additional, Kook, M. J., additional, Jung, J. Y., additional, Lee, J. H., additional, Jung, Y. J., additional, Hwang, H. K., additional, Kang, A., additional, An, S. J., additional, Kim, H. M., additional, Kwon, H. C., additional, Lee, S. 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2010
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