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11. Meeting abstracts

Author

Agnifili A., Gola P., Guadagni S., Verzaro R., Carducci G., Gianfelice F., Ibi I., Marino M., Mancini E., De Bernardinis G., Allegri C., Spoletini F., Mariotti V., Vari A., Polinari U., Altomare D. F., Brienza E., Rinaldi M., Vicente-Prieta R., Memeo V., Bertolino F., Ceccopieri B., Nasi P. G., Porcellana V., Mattio R., Forconi S., Dellepiane M., Biccari V., Tedesco M., Matrone A. M., Sirovich I., Nicolanti V., Stipa S., Bonalumi U., Galleano R., Baiardi A., Balbi P., Simoni G., Calleri G., Casaldi, V., Cosimelli, M., Giannarelli, D., Botti, C., Mannella, E., Wappner, G., Cavaliere, R., Casale, V., Fracasso, P., Grassi, A., Lapenta, R., Stigliano, V., Nasi P. G., Cianciulli A. M., Antonaci S., Casale V., Greco C., Gandolfo G. M., Coco, C., Giordano, A., Roncolini, G., Mattana, C., Coppola, R., Magistrelli, P., Crespi C., De Giorgio A. M., Giuliani A., Galasso V., Truglia S., De Ligio F., De Ligio S., Serafino L., Limiti R., Arrabito G., Guadagni S., Palumbo G., Pantaleoni G., D'Alessandro V., Agnifili A., Carducci G., Mancini E., Marino M., Gola P., Gianfelice F., Verzaro R., Ibi I., Ranalletta D., Fanini R., De Bernardinis G., Huscher, C., Chiodini, S., Zamboni, F., Montorsi, M., Marchese C., Bertolino F., Ceccopieri B., Locatelli L., Mareni C., Mattio R., Scaglione D., Vanzetti M., Mascagni, D., Di Matteo, G., Hojo, K., Moriya, Y., Sugihara, K., Massidda, B., Nicolosi, A., Tarquini, A., Natalini, G., Borgognoni, F., Ranieri, S., Menculini, M., Carioni, G., Botti C., Cosimelli M., Casaldi V., Cavaliere R., Caporossi M., Huguet C., Chiavellati L., Cavallaro A., Pietroletti, R., Cianca, G., Barnabei, R., Simi, M., Romano G., Di Carlo A., Mariano A., D'Alessandro V., Rotondano G., Macchia V., Secco, G. B., Fardelli, R., Zoli, S., Lapini, C., Cariati, A., Prior, C., Sironi, I., Mietti, G., Arisi, B. A., Ferrari, G. C., Gasbacortat, M., Brusamolino, R., Bauer, D., Russo, A., Spinelli C., Berti P., Gori L., Materazzi G., Mucci M., Pierallini S., Miccoli P., Cosimeili M., Mannella E., Valabrega, S., Pozzi, G., De Angelis, R., D'Angelo, F., Indinnimeo, M., Aurello, P., Tabbi, P., Fegiz, G., Venezia, P., Colella, R., Pitzalis, M. V., Pitzalis, M., Vuolo, G., Di Cosmo, L., Grimaldi, L., Maglio, C., Masellis, D., and Carli, A.

Published
1994
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14. A Specific Mutational Signature Associated with DNA 8-Oxoguanine Persistence in MUTYH-defective Colorectal Cancer.

Author

Viel, A, Bruselles, A, Meccia, E, Fornasarig, M, Quaia, M, Canzonieri, V, Policicchio, E, Urso, Ed, Agostini, M, Genuardi, Maurizio, Lucci Cordisco, Emanuela, Venesio, T, Martayan, Aline, Diodoro, Mg, Sanchez-Mete, L, Stigliano, V, Mazzei, Francesca, Grasso, F, Giuliani, Alessandro, Baiocchi, M, Maestro, R, Giannini, G, Tartaglia, Marco, Alexandrov, Lb, Bignami, M., Genuardi M (ORCID:0000-0002-7410-8351), Lucci-Cordisco E (ORCID:0000-0002-6279-7604), Martayan A, Tartaglia M, Viel, A, Bruselles, A, Meccia, E, Fornasarig, M, Quaia, M, Canzonieri, V, Policicchio, E, Urso, Ed, Agostini, M, Genuardi, Maurizio, Lucci Cordisco, Emanuela, Venesio, T, Martayan, Aline, Diodoro, Mg, Sanchez-Mete, L, Stigliano, V, Mazzei, Francesca, Grasso, F, Giuliani, Alessandro, Baiocchi, M, Maestro, R, Giannini, G, Tartaglia, Marco, Alexandrov, Lb, Bignami, M., Genuardi M (ORCID:0000-0002-7410-8351), Lucci-Cordisco E (ORCID:0000-0002-6279-7604), Martayan A, and Tartaglia M

Abstract

8-Oxoguanine, a common mutagenic DNA lesion, generates G:C>T:A transversions via mispairing with adenine during DNA replication. When operating normally, the MUTYH DNA glycosylase prevents 8-oxoguanine-related mutagenesis by excising the incorporated adenine. Biallelic MUTYH mutations impair this enzymatic function and are associated with colorectal cancer (CRC) in MUTYH-Associated Polyposis (MAP) syndrome. Here, we perform whole-exome sequencing that reveals a modest mutator phenotype in MAP CRCs compared to sporadic CRC stem cell lines or bulk tumours. The excess G:C>T:A transversion mutations in MAP CRCs exhibits a novel mutational signature, termed Signature 36, with a strong sequence dependence. The MUTYH mutational signature reflecting persistent 8-oxoG:A mismatches occurs frequently in the APC, KRAS, PIK3CA, FAT4, TP53, FAT1, AMER1, KDM6A, SMAD4 and SMAD2 genes that are associated with CRC. The occurrence of Signature 36 in other types of human cancer indicates that DNA 8-oxoguanine-related mutations might contribute to the development of cancer in other organs.

Published
2017

16. Clinical, dermoscopic and reflectance confocal microscopy features of sebaceous neoplasms in Muir-Torre syndrome

Author

Moscarella, Elvira, Argenziano, Giuseppe, Longo, Caterina, Cota, C., Ardigò, M., Stigliano, V., Mete, L. S., Donati, P., Piana, S., Silipo, V., Catricalà, C., Albertini, G., Zalaudek, I., Moscarella, E, Argenziano, G, Longo, C, Cota, C, Ardigò, M, Stigliano, V, Mete, L S, Donati, P, Piana, S, Silipo, V, Catricalà, C, Albertini, G, Zalaudek, I, Argenziano, Giuseppe, Ardigo, M, Mete, L, and Zalaudek, I.

Subjects
Adenoma, Male, Microscopy, Microscopy, Confocal, Dermoscopy, Middle Aged, Aged, Female, Humans, Muir-Torre Syndrome, Retrospective Studies, Sebaceous Gland Neoplasms, Infectious Diseases, Sebaceous Gland Neoplasm, Retrospective Studie, Confocal, Human
Abstract

Muir-Torre syndrome (MTS) is an autosomal-dominant disorder characterized by the association of sebaceous tumors or keratoacanthomas with an early onset visceral cancer in the spectrum of Lynch syndrome.A total of 20 sebaceous tumors including 18 sebaceous adenoma and two sebaceomas of six patients with MTS were analysed. Two main clinico-dermoscopic features were observed: (1) clinically pink to white papules/nodules with a central crater, dermoscopically characterized by radially arranged, elongated crown vessels surrounding opaque structureless yellow areas at times covered by blood crusts (n = 13) and (2), clinically pink to yellow papules/nodules without a central crater, dermoscopically exhibiting a few, loosely arranged yellow comedo-like globules and branching arborizing vessels (n = 7). Confocal microscopy was available in three sebaceous adenomas and revealed a good histopathologic correlation; sebaceous lobules were composed by clusters of ovoid cells with dark nuclei and bright, highly refractile glistening cytoplasm. They were delimited by a rim of epithelial cells, corresponding to basaloid cells.A better characterization of clinical, dermoscopic and confocal microscopy features of sebaceous tumors may improve their recognition and consequently, aid to rise the suspect for MTS.

Published
2012

20. Escissione locale in pazienti con risposta completa dopo radiochemiotera¬pia neoadiuvante per carcinoma rettale localmente avanzato: incidenza e risultati a lungo termine

Author

Palmieri, A., Mancini, R., Pattaro, G., Sperduti, I., Ambesi Impiombato, F., Garufi, C., Zeuli, M., Diodoro, M. G., Stigliano, V., Assisi, D., Caterino, M., Grazi, G. L., Perri, P., D’annibale, M., Oddi, A., Di Filippo, S., Scarinci, A., Police, A., Andrea Sagnotta, Daniele Crocetti, and Cosimelli, M.

Published
2013

21. Erratum: Prognostic relevance of MLH1 and MSH2 mutations in hereditary non-polyposis colorectal cancer patients (Tumori (2009) 95:6 (731-738))

Author

Russo, A., De Leon, M. P., Lucci-Cordisco, E., Genuardi, M., Messerini, L., Stigliano, V., Cama, A., Curia, M. C., De Lellis, L., Signoroni, S., Pierotti, M. A., Pedroni, M., Benatti, P., Sala, P., Alberici, P., Gazzoli, I., Radice, P., Montefusco, C., Torrini, M., Mareni, C., Fornasarig, M., Santarosa, M., Viel, A., and Bertario, L.

Published
2010

22. Rabeprazole is equivalent to omeprazole in the treatment of erosive gastro-oesophageal reflux disease. A randomised, double-blind, comparative study of rabeprazole and omeprazole 20 mg in acute treatment of reflux oesophagitis, followed by a maintenance open-label, low-dose therapy with rabeprazole

Author

Pace, F., Annese, V., Prada, A., Zambelli, A., Casalini, S., Nardini, P., Bianchi Porro, G., Rossi, Z., Fenderico, P., Molinari, F., Molinari, A., Poletti, M., Benedetti, A., Bolognini, L., Cercamondi, P., Piergallini, S., Pieroni, N., Ridolfi, F., Palazzi, A., Agnolucci, A., Ceccatelli, P., Laurenzi, F., Grassini, M., Iaquinto, G., D'Onofrio, V., Giardullo, N., Pasquale, L., Sedici, A., Moschetta, R., Maurogiovanni, G., Costan, F., Germana, B., Lecis, P., Negrini, F., Signorelli, S., Landi, P., Malaguti, P., Roda, E., De, E., Gandolfi, L., Torresan, F., Chilovi, F., Benvenuti, S., Grasso, T., Adamo, S., Azzurro, M., Carrara, M., Rubbiani, C., P. V., Di, Di, M., Belvedere, F., Di, A., Giglio, A., De Medici, A., Rodino, S., Sacca, N., Neri, M., Carbone, F., Laterza, F., Trimboli, V., Accattatis, G. C., Rizzuti, L. F., Sabatino, A., Lupinacci, G., Faleo, D., De Francesco, V., Lombardi, L. P, Minenna, M., Nocchiero, M. C., Tonti, P., Bocchini, R., D'Imperio, N., Giaccari, S., Tronci, S., Dall'Acqua, S., Berrini, E., Garatti, S., Putignano, R., Sferrazzo, A., Giacosa, A., Blanchi, S., Munizzi, F., Morlando, L., Bruno, G., Guardascione, F., Benedetti, E., Orzes, N., Pincione, F., Dell'Amico, I., Vannucci, P., Maurano, A., Calabrese, A., Napoli, G., Quagliariello, G., Sabarese, G., Pracanica, G., Gullotti, G., Princiotta, A., Rando, L., Anderloni, A., Pallotta, S., Fesce, E., Abbiati, D., Crippa, C., Ideo, G. M., Mannucci, P. M., Abbiati, C., De Franchis, R., Fazzini, L., Rossi, A., Bini, M., Chahin, N. J., Testoni, P. A., Fossati, D., Frego, R., Passaretti, S., Catanzano, C., Siciliano, S., Sivero, L., Cattaneo, D., Di Martino, V., Inzirillo, A., Lavelli, M., Del Genio, A., Maffettone, V., Napolitano, V., Del Piano, M., Ballare, M., Garello, E., Orsello, M., Capezzuto, E., Amuso, M., Marino, M., Reina, G., Craxi, A., Arini, A., Di Pisa, M., Peralta, S., Ficano, L., Miceli, D., Tarantello, M., Orlando, A., Perego, M., Alvisi, C., Pozzi, L., Torello Viera, F., Marchi, S., Arpe, P., Bellini, M., Costa, F., Da Massa Carrara, P., Manghetti, M., Meletis, P., Romano, A., Torelli, E., Garcea, M. R., Lombardi, M., Tristaino, B., Farroni, F., Di Cicco, M., Proietti, M., Tanzilli, A., Benedetti, G., Guido, E., Lacchin, T., Sablich, R., Vitalba, A., Casetti, T., Cantoni, F., Salzetta, A., Polimeni, F., Bortoli, A., Buono, M., Gozzini, C., Barberani, F., Boschetto, S., Giovannone, M., Casale, V., Assisi, D., Grassi, A., Lapenta, R., Stigliano, V., Fedeli, G., Pirozzi, G. A., Pippa, G., Bazuro, M. E., Romano, M., Borgheresi, P., Andriulli, A., Fiorella, S., De Rocco, R., Greco, G., Meloni, M., Fina, G., Frosini, G., Macchiarelli, R., Virgilio, C., Borina, E., Lauria, M., Cappelletti, F., Puglisi, F., Ravizza, M., Emanuelli, G., Battaglia, E., Dughera, L., Navino, M., Ferrari, A., Martinoglio, P., Turco, D., Pera, A., Daperno, M., Lombardo, L., Gusmaroli, R., Milesi, F., Zilli, M., Brosolo, P., De, G., Zoratti, L., Curzio, M., Amato, A., Bisso, G., Feliziani, M., Gianfrate, L., Natale, C., Petillo, A., Spadaccini, A., Meddi, P., Sciampa, G., and Ubalducci, G. M.

Subjects
Adult, Male, Gastrointestinal, Time Factors, Severity of Illness Index, 2-Pyridinylmethylsulfinylbenzimidazoles, Endoscopy, Gastrointestinal, Helicobacter Infections, Dose-Response Relationship, Gastro-oesophageal reflux disease, Double-Blind Method, Heartburn, Esophagitis, Humans, Esophagitis, Peptic, Curative/maintenance therapy, Peptic, Hepatology, Dose-Response Relationship, Drug, Helicobacter pylori, Rabeprazole, Antacids, Anti-Ulcer Agents, Benzimidazoles, Female, Gastroesophageal Reflux, Middle Aged, Omeprazole, Patient Satisfaction, Treatment Outcome, Gastroenterology, Endoscopy, Drug
Abstract

Previous studies have shown similar effects of rabeprazole and omeprazole, when used at the same dose in the treatment of reflux oesophagitis. However, such studies have been conducted as superiority studies but interpreted as equivalence ones.To properly assess the comparative efficacy of rabeprazole and omeprazole in inducing complete endoscopic healing and symptom relief in patients with reflux oesophagitis.Patients (n=560) with Savary-Miller grade I-III reflux oesophagitis were randomised in a double-blind, double-dummy fashion to rabeprazole or omeprazole 20 mg once daily for 4-8 weeks. Then, patients endoscopically healed and symptomatically relieved were openly maintained with rabeprazole 10 mg or 2x10 mg once daily (in the event of clinical and/or endoscopic relapse) for a maximum of 48 weeks.After 4-8 weeks of treatment, healing (primary end-point) was observed in 228/233 (97.9%) patients in the rabeprazole group and in 231/237 (97.5%) in the omeprazole one (equivalence effect demonstrated by p0.0001 at Blackwelder test and an upper confidence limit at 97.5% of 0.023). However, rabeprazole was faster in inducing heartburn relief than omeprazole (2.8+/-0.2 versus 4.7+/-0.5 days of therapy to reach the first day with satisfactory heartburn relief, p=0.0045 at log-rank test). In the maintenance phase, 15.2% of patients had an endoscopic and/or clinical relapse.Rabeprazole is equivalent to omeprazole in healing reflux oesophagitis, but shows a faster activity on reflux symptoms in the early treatment phase.

Published
2005

24. Cancer risk associated with STK11/LKB1 germline mutations in Peutz-Jeghers syndrome patients: Results of an Italian multicenter study

Author

Resta, N, Pierannunzio, D, Lenato, Gm, Stella, A, Capocaccia, R, Bagnulo, R, Lastella, P, Susca, Fc, Bozzao, C, Loconte, Dc, Sabbà, C, Urso, E, Sala, P, Fornasarig, M, Grammatico, P, Piepoli, A, Host, C, Turchetti, D, Viel, A, Memo, L, Giunti, L, Stigliano, V, Varesco, L, Bertario, L, Genuardi, Maurizio, Lucci Cordisco, Emanuela, Tibiletti, Mg, Di Gregorio, C, Andriulli, A, Ponz De Leon, M., Genuardi, Maurizio (ORCID:0000-0002-7410-8351), Lucci Cordisco, Emanuela (ORCID:0000-0002-6279-7604), Resta, N, Pierannunzio, D, Lenato, Gm, Stella, A, Capocaccia, R, Bagnulo, R, Lastella, P, Susca, Fc, Bozzao, C, Loconte, Dc, Sabbà, C, Urso, E, Sala, P, Fornasarig, M, Grammatico, P, Piepoli, A, Host, C, Turchetti, D, Viel, A, Memo, L, Giunti, L, Stigliano, V, Varesco, L, Bertario, L, Genuardi, Maurizio, Lucci Cordisco, Emanuela, Tibiletti, Mg, Di Gregorio, C, Andriulli, A, Ponz De Leon, M., Genuardi, Maurizio (ORCID:0000-0002-7410-8351), and Lucci Cordisco, Emanuela (ORCID:0000-0002-6279-7604)

Abstract

BACKGROUND: Germline mutations in the STK11/LKB1 gene cause Peutz-Jeghers syndrome, an autosomal-dominantly inherited condition characterized by mucocutaneous pigmentation, hamartomatous gastrointestinal polyposis, and an increased risk for various malignancies. We here report the results of the first Italian collaborative study on Peutz-Jeghers syndrome. AIMS: To assess cancer risks in a large homogenous cohort of patients with Peutz-Jeghers syndrome, carrying, in large majority, an identified STK11/LKB1 mutation. METHODS: One-hundred and nineteen patients with Peutz-Jeghers syndrome, ascertained in sixteen different Italian centres, were enrolled in a retrospective cohort study. Relative and cumulative cancer risks and genotype-phenotype correlations were evaluated. RESULTS: 36 malignant tumours were found in 31/119 (29 STK11/LKB1 mutation carriers) patients. The mean age at first cancer diagnosis was 41 years. The relative overall cancer risk was 15.1 with a significantly higher risk (p<0.001) in females (22.0) than in males (8.6). Highly increased relative risks were present for gastrointestinal (126.2) and gynaecological cancers (27.7), in particular for pancreatic (139.7) and cervical cancer (55.6). The Kaplan-Meier estimates for overall cumulative cancer risks were 20%, 43%, 71%, and 89%, at age 40, 50, 60 and 65 years, respectively. CONCLUSION: Peutz-Jeghers syndrome entails markedly elevated cancer risks, mainly for pancreatic and cervical cancers. This study provides a helpful reference for improving current surveillance protocols.

Published
2013

30. Prognostic relevance of MLH1 and MSH2 mutations in hereditary non-polyposis colorectal cancer patients

Author

Russo, A, Sala, P, Alberici, P, Gazzoli, I, Radice, P, Montefusco, C, Torrini, M, Mareni, C, Fornasarig, M, Santarosa, M, Viel, A, Benatti, P, Pedroni, M, De Leon, M, Lucci Cordisco, E, Genuardi, Maurizio, Messerini, L, Stigliano, V, Cama, A, Curia, M, De Lellis, L, Signoroni, S, Pierotti, M, Bertario, L., Lucci Cordisco, E (ORCID:0000-0002-6279-7604), Genuardi, Maurizio (ORCID:0000-0002-7410-8351), Russo, A, Sala, P, Alberici, P, Gazzoli, I, Radice, P, Montefusco, C, Torrini, M, Mareni, C, Fornasarig, M, Santarosa, M, Viel, A, Benatti, P, Pedroni, M, De Leon, M, Lucci Cordisco, E, Genuardi, Maurizio, Messerini, L, Stigliano, V, Cama, A, Curia, M, De Lellis, L, Signoroni, S, Pierotti, M, Bertario, L., Lucci Cordisco, E (ORCID:0000-0002-6279-7604), and Genuardi, Maurizio (ORCID:0000-0002-7410-8351)

Abstract

Aims and background. Colorectal carcinoma patients from hereditary non-polyposis colorectal cancer families are suggested to have a better prognosis than sporadic colorectal carcinoma cases. Since the majority of hereditary non-polyposis colorectal cancer-related colorectal carcinomas are characterized by microsatellite instability due to germline mutations in DNA mismatch repair genes, this is consistent with the prolonged survival observed in sporadic microsatellite instability-positive colorectal carcinoma compared to microsatellite stable cases. However, a fraction of colorectal carcinoma cases belongs to families that, despite fulfilling the clinical criteria for hereditary non-polyposis colorectal cancer, do not carry mismatch repair gene mutations. Our aim was to verify to what extent the genotypic heterogeneity influences the prognosis of hereditary non-polyposis colorectal cancer patients. Methods. A survival analysis was performed on 526 colorectal carcinoma cases from 204 Amsterdam Criteria-positive hereditary non-polyposis colorectal cancer families. Enrolled cases were classified as MLITH-positive, MSH2-positive and mutation-negative, according to the results of genetic testing in each family. Results. Five-year survival rates were 0.73 (95% Cl, 0.66-0.80), 0.75 (95% CI, 0.66-0.84) and 0.62 (95% Cl, 0.55-0.68) for MLH1-positive, MSH2-positive and mutation-negative groups, respectively (logrank test, P= 0.01). Hazard ratio, computed using Cox regression analysis and adjusted for age, sex, tumor site and stage, was 0.71 (95% Cl, 0.51-0.981 for the mutation-positive compared to the mutation-negative group. Moreover, in the latter group, patients with microsatellite instability-positive colorectal carcinomas showed a better outcome than microsatellite stable cases (5-year survival rates, 0.81 and 0.60, respectively; logrank test, P = 0.006). Conclusions. Our results suggest that the prognosis of hereditary non-polyposis colorectal cancer-related colorectal, AIMS AND BACKGROUND: Colorectal carcinoma patients from hereditary non-polyposis colorectal cancer families are suggested to have a better prognosis than sporadic colorectal carcinoma cases. Since the majority of hereditary non-polyposis colorectal cancer-related colorectal carcinomas are characterized by microsatellite instability due to germline mutations in DNA mismatch repair genes, this is consistent with the prolonged survival observed in sporadic microsatellite instability-positive colorectal carcinoma compared to microsatellite stable cases. However, a fraction of colorectal carcinoma cases belongs to families that, despite fulfilling the clinical criteria for hereditary non-polyposis colorectal cancer, do not carry mismatch repair gene mutations. Our aim was to verify to what extent the genotypic heterogeneity influences the prognosis of hereditary non-polyposis colorectal cancer patients. METHODS: A survival analysis was performed on 526 colorectal carcinoma cases from 204 Amsterdam Criteria-positive hereditary non-polyposis colorectal cancer families. Enrolled cases were classified as MLH1-positive, MSH2-positive and mutation-negative, according to the results of genetic testing in each family. RESULTS: Five-year survival rates were 0.73 (95% CI, 0.66-0.80), 0.75 (95% CI, 0.66-0.84) and 0.62 (95% CI, 0.55-0.68) for MLH1-positive, MSH2-positive and mutation-negative groups, respectively (logrank test, P = 0.01). Hazard ratio, computed using Cox regression analysis and adjusted for age, sex, tumor site and stage, was 0.71 (95% CI, 0.51-0.98) for the mutation-positive compared to the mutation-negative group. Moreover, in the latter group, patients with microsatellite instability-positive colorectal carcinomas showed a better outcome than microsatellite stable cases (5-year survival rates, 0.81 and 0.60, respectively; logrank test, P = 0.006). CONCLUSIONS: Our results suggest that the prognosis of hereditary non-polyposis colorectal cancer-related co

Published
2009

49. Ascorbic acid levels in patients with chronic atrophic gastritis

Author

Citarda, F, primary, Caperle, M, additional, Casale, V, additional, Conti, E M S, additional, Fracasso, P, additional, Apenta, R L, additional, Marcucci, M, additional, Ramazzotti, V, additional, Schorah, C J, additional, Sciarretta, F, additional, Stigliano, V, additional, White, K, additional, and Crespi, M, additional

Published
1996
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