Malignant Odontogenic Tumors: A Multicentric Latin American Study Of 25 Cases

Objective: The aim of this study was to show the epidemiological features of 25 malignant odontogenic tumors (MOT) in Latin America. Materials and Methods: We retrieved 25 cases of MOT out of 2142 odontogenic tumors, from four oral diagnostic centers in Latin America, and described the main clinical and pathological characteristics. Results: A total of 19 cases were carcinomas, including eight ameloblastic carcinomas, five primary intra-osseous squamous cell carcinomas, three clear cell odontogenic carcinomas and three ghost cell odontogenic carcinomas. All six sarcomas corresponded to ameloblastic fibrosarcoma. Thirteen cases occurred in men and 12 in women, age ranged from 7 to 77 years old, with a mean of 41.4 years. The average age of patients with carcinomas and sarcomas were 48.53 and 19 years old, respectively. Conclusion: As malignant odontogenic tumors are very rare, this series helps to better clarify their relative frequency, predominant subtypes, and clinical characteristics in Latin America. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.204380385Adebayo, E.T., Ajike, S.O., Adekeye, E.O., A review of 318 odontogenic tumors in Kaduna, Nigeria (2005) J Oral Maxillofac Surg, 63, pp. 811-819Akrish, S., Buchner, A., Shoshani, Y., Vered, M., Dayan, D., Ameloblastic carcinoma: report of a new case, literature review, and comparison to ameloblastoma (2007) J Oral Maxillofac Surg, 65, pp. 777-783Arashiyama, T., Kodama, Y., Kobayashi, T., Ghost cell odontogenic carcinoma arising in the background of a benign calcifying cystic odontogenic tumor of the mandible (2012) Oral Surg Oral Med Oral Pathol Oral Radiol, 114, pp. e35-e40Arotiba, J.T., Ogunbiyi, J.O., Obiechina, A.E., Odontogenic tumors: a 15-year review from Ibadan, Nigeria (1997) Br J Oral Maxillofac Surg, 35, pp. 363-367Avelar, R.L., Antunes, A.A., Santos Tde, S., Andrade, E.S., Dourado, E., Odontogenic tumors: clinical and pathology study of 238 cases (2008) Braz J Otorhinolaryngol, 74, pp. 668-673Barnes, L., Eveson, J.W., Reichart, P.A., Sidransky, D., (2005) World health organization classification of tumours: pathology and genetics of tumours of the head and neck, , eds IARC: LyonBello, I.O., Alanen, K., Slootweg, P.J., Salo, T., Alpha-smooth muscle actin within epithelial islands is predictive of ameloblastic carcinoma (2009) Oral Oncol, 45, pp. 760-765Bilodeau, E.A., Hoschar, A.P., Barnes, E.L., Hunt, J.L., Seethala, R.R., Clear cell carcinoma and clear cell odontogenic carcinoma: a comparative clinicopathologic and immunohistochemical study (2011) Head Neck Pathol, 5, pp. 101-107Bodner, L., Manor, E., Shear, M., van der Waal, I., Primary intraosseous squamous cell carcinoma arising in an odontogenic cyst: a clinicopathologic analysis of 116 reported cases (2011) J Oral Pathol Med, 40, pp. 733-738Bologna-Molina, R., Mosqueda-Taylor, A., Lopez-Corella, E., Comparative expression of syndecan-1 and Ki-67 in peripheral and desmoplastic ameloblastomas and ameloblastic carcinoma (2009) Pathol Int, 59, pp. 229-233Bregni, R.C., Taylor, A.M., García, A.M., Ameloblastic fibrosarcoma of the mandible: report of two cases and review of the literature (2001) J Oral Pathol Med, 30, pp. 316-320Buchner, A., Merrell, P.W., Carpenter, W.M., Relative frequency of central odontogenic tumors: a study of 1,088 cases from Northern California and comparison to studies from other parts of the world (2006) J Oral Maxillofac Surg, 64, pp. 1343-1352Chaisuparat, R., Sawangarun, W., Scheper, M.A., A clinicopathological study of malignant odontogenic tumours (2012) Histopathology, 61, pp. 107-112da-Costa, D.O., Maurício, A.S., de-Faria, P.A., Odontogenic tumors: a retrospective study of four Brazilian diagnostic pathology centers (2012) Med Oral Patol Oral Cir Bucal, 17, pp. e389-e394Daley, T.D., Wysocki, G.P., Pringle, G.A., Relative incidence of odontogenic tumors and jaw cysts in a Canadian population (1994) Oral Surg Oral Med Oral Pathol, 77, pp. 276-280Demoor-Goldschmidt, C., Minard-Colin, V., Cassagneau, E., Ameloblastic fibrosarcoma of the mandible: report of 2 chemosensitive pediatric cases (2012) J Pediatr Hematol Oncol, 34, pp. e72-e76Dissanayake, R.K., Jayasooriya, P.R., Siriwardena, D.J., Tilakaratne, W.M., Review of metastasizing (malignant) ameloblastoma (METAM): pattern of metastasis and treatment (2011) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 111, pp. 734-741El-Gehani, R., Orafi, M., Elarbi, M., Subhashraj, K., Benign tumours of orofacial region at Benghazi, Libya: a study of 405 cases (2009) J Craniomaxillofac Surg, 37, pp. 370-375Ellis, G.L., Shmookler, B.M., Aggressive (malignant?) epithelial odontogenic ghost cell tumor (1986) Oral Surg Oral Med Oral Pathol, 61, pp. 471-478Fernandes, A.M., Duarte, E.C., Pimenta, F.J., Odontogenic tumors: a study of 340 cases in a Brazilian population (2005) J Oral Pathol Med, 34, pp. 583-587Gallego, L., Junquera, L., Villarreal, P., Fresno, M.F., Primary de novo intraosseous carcinoma: report of a new case (2010) Med Oral Patol Oral Cir Bucal, 15, pp. e48-e51Goldenberg, D., Sciubba, J., Koch, W., Tufano, R.P., Malignant odontogenic tumors: a 22-year experience (2004) Laryngoscope, 114, pp. 1770-1774Grodjesk, J.E., Dolinsky, H.B., Schneider, L.C., Dolinsky, E.H., Doyle, J.L., Odontogenic ghost cell carcinoma (1987) Oral Surg Oral Med Oral Pathol, 63, pp. 576-581Günhan, O., Erseven, G., Ruacan, S., Odontogenic tumors. A series of 409 cases (1990) Aust Dent J, 35, pp. 518-522Huang, J.W., Luo, H.Y., Li, Q., Li, T.J., Primary intraosseous squamous cell carcinoma of the jaws Clinicopathologic presentation and prognostic factors (2009) Arch Pathol Lab Med, 133, pp. 1834-1840Jing, W., Xuan, M., Lin, Y., Odontogenic tumors: a retrospective study of 1642 cases in a Chinese population (2007) Int J Oral Maxillofac Surg, 36, pp. 20-25Karakida, K., Aoki, T., Sakamoto, H., Ameloblastic carcinoma, secondary type: a case report (2010) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 110, pp. e33-e37Kobayashi, K., Murakami, R., Fujii, T., Hirano, A., Malignant transformation of ameloblastic fibroma to ameloblastic fibrosarcoma: case report and review of the literature (2005) J Craniomaxillofac Surg, 33, pp. 352-355Kousar, A., Hosein, M.M., Ahmed, Z., Minhas, K., Rapid sarcomatous transformation of an ameloblastic fibroma of the mandible: case report and literature review (2009) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 108, pp. e80-e85Ladeinde, A.L., Ajayi, O.F., Ogunlewe, M.O., Odontogenic tumors: a review of 319 cases in a Nigeriam teaching hospital (2005) Oral Surg Oral Med Oral Pathol Osal Radiol Endod, 99, pp. 191-195Lai, J., Blanas, N., Higgins, K., Klieb, H., Ameloblastic fibrosarcoma: report of a case, study of immunophenotype, and comprehensive review of the literature (2012) J Oral Maxillofac Surg, 70, pp. 2007-2012Li, B.H., Cho, Y.A., Kim, S.M., Recurrent odontogenic ghost cell carcinoma (OGCC) at a reconstructed fibular flap: a case report with immunohistochemical findings (2011) Med Oral Patol Oral Cir Bucal, 16, pp. e651-e656Lu, Y., Xuan, M., Takata, T., Odontogenic tumors. A demographic study of 759 cases in a Chinese population (1998) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 86, pp. 707-714Lu, Y., Mock, D., Takata, T., Jordan, R.C., Odontogenic ghost cell carcinoma: report of four new cases and review of the literature (1999) J Oral Pathol Med, 28, pp. 323-329Luo, H.Y., Li, T.J., Odontogenic tumors: a study of 1309 cases in a Chinese population (2009) Oral Oncol, 45, pp. 706-711Mainenti, P., Oliveira, G.S., Valério, J.B., Ameloblastic fibro-odontosarcoma: a case report (2009) Int J Oral Maxillofac Surg, 38, pp. 289-292McCoy, B.P., Carroll, O., Hall, M.K.J.M., Carcinoma arising in a dentinogenic ghost cell tumor (1992) Oral Surg Oral Med Oral Pathol, 74, pp. 371-378Mosqueda-Taylor, A., Meneses-García, A., Ruíz-Godoy Rivera, L.M., Suárez-Roa, M.d.L., Clear cell odontogenic carcinoma of the mandible (2002) J Oral Pathol Med, 31, pp. 439-441Mosqueda Taylor, A., Meneses García, A., Ruíz-Godoy Rivera, L.M., Suárez Roa Mde, L., Luna Ortiz, K., Malignant odontogenic tumors. A retrospective and collaborative study of seven cases (2003) Med Oral, 8, pp. 110-121Mosqueda-Taylor, A., New findings and controversies in odontogenic tumors (2008) Med Oral Patol Cir Bucal, 13, pp. e555-e558Mosqueda-Taylor, A., Ledesma-Montes, C., Caballero Sandoval, S., Portilla Robertson, J., Ruíz-Godoy Rivera, L.M., Meneses-García, A., Odontogenic tumors in Mexico: a collaborative retrospective study of 349 cases (1997) Oral Surg Oral Med Oral Pathol Oral Radiol, 84, pp. 672-675Noordhoek, R., Pizer, M.E., Laskin, D.M., Ameloblastic fibrosarcoma of the mandible: treatment, long-term follow-up, and subsequent reconstruction of a case (2012) J Oral Maxillofac Surg, 70, pp. 2930-2935Ochsenius, G., Ortega, A., Godoy, L., Peñafiel, C., Escobar, E., Odontogenic tumors in Chile: a study of 362 cases (2002) J Oral Pathol Med, 31, pp. 415-420Odukoya, O., Odontogenic tumors: analysis of 289 Nigerian cases (1995) J Oral Pathol Med, 24, pp. 454-457Ogunsalu, C.O., Odontogenic tumors from two centres in Jamaica. A 15-year review (2003) West Indian Med J, 52, pp. 285-289Okada, H., Yamamoto, H., Tilakaratne, W.M., Odontogenic tumors in Sri Lanka: analysis of 226 cases (2007) J Oral Maxillofac Surg, 65, pp. 875-882Olgac, V., Koseoglu, B.G., Aksakalli, N., Odontogenic tumors in Istanbul: 527 cases (2006) Br J Oral Maxillofac Surg, 44, pp. 386-388Osterne, R.L., Brito, R.G., Alves, A.P., Cavalcante, R.B., Sousa, F.B., Odontogenic tumors: a 5-year retrospective study in a Brazilian population and analysis of 3406 cases reported in the literature (2011) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 111, pp. 474-481Otero, D., Lourenço, S.Q., Ruiz-Ávila, I., Expression of proliferative markers in ameloblastomas and malignant odontogenic tumors (2013) Oral Dis, 19, pp. 360-365Pontes, H.A., Pontes, F.S., Silva, B.S., Immunoexpression of Ki67, proliferative cell nuclear antigen, and Bcl-2 proteins in a case of ameloblastic fibrosarcoma (2010) Ann Diagn Pathol, 14, pp. 447-452Regezi, J.A., Kerr, D.A., Courtney, R.M., Odontogenic tumors: analysis of 706 cases (1978) J Oral Surg, 36, pp. 771-778Saghravanian, N., Jafarzadeh, H., Bashardoost, N., Pahlavan, N., Shirinbak, I., Odontogenic tumors in an Iranian population: a 30-year evaluation (2010) J Oral Sci, 52, pp. 391-396Santos, J.N., Pinto, L.P., de Figueredo, C.R., de Souza, L.B., Odontogenic tumors: analysis of 127 cases (2001) Pesqui Odontol Bras, 15, pp. 308-313Servato, J.P., Prieto-Oliveira, P., de Faria, P.R., Loyola, A.M., Cardoso, S.V., Odontogenic tumours: 240 cases diagnosed over 31 years at a Brazilian university and a review of international literature (2012) Int J Oral Maxillofac Surg, 42, pp. 288-293Simon, E.N., Stoelinga, P.J., Vuhahula, E., Ngassapa, D., Odontogenic tumours and tumour-like lesions in Tanzania (2002) East Afr Med J, 79, pp. 3-7Simon, E.N., Merkx, M.A., Vuhahula, E., Ngassapa, D., Stoelinga, P.J., A 4-year prospective study on epidemiology and clinicopathological presentation of odontogenic tumors in Tanzania (2005) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 99, pp. 598-602Slater, L.J., Odontogenic malignancies (2004) Oral Maxillofac Surg Clin North Am, 16, pp. 409-424Sriram, G., Shetty, R.P., Odontogenic tumors: a study of 250 cases in an Indian teaching hospital (2008) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 105, pp. e14-e21Tamme, T., Soots, M., Kulla, A., Odontogenic tumors, a collaborative retrospective study of 75 cases covering more than 25 years from Estonia (2004) J Craniomaxillofac Surg, 32, pp. 161-165Tawfik, M.A., Zyada, M.M., Odontogenic tumors in Dakahlia, Egypt: analysis of 82 cases (2010) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 109, pp. e67-e73Werle, H., Blake, F.A., Reichelt, U., Schmelzle, R., Heiland, M., Clear-cell odontogenic carcinoma: a new case and long-term follow-up of an old case, and review of the literature (2009) J Oral Maxillofac Surg, 67, pp. 1342-1348Xavier, F.C., Rodini, C.O., Ramalho, L.M., Sarmento, V.A., Nunes, F.D., de Sousa, S.C., Clear cell odontogenic carcinoma: case report with immunohistochemical findings adding support to the challenging diagnosis (2008) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 106, pp. 403-410Yoon, H.J., Hong, S.P., Lee, J.I., Lee, S.S., Hong, S.D., Ameloblastic carcinoma: an analysis of 6 cases with review of the literature (2009) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 108, pp. 904-913Zabolinejad, N., Hiradfar, M., Anvari, K., Razavi, A.S., Ameloblastic fibrosarcoma of the maxillary sinus in an infant: a case report with long-term follow-up (2008) J Pediatr Surg, 43, pp. e5-e

Lingual cyst with respiratory epithelium: a histopathological and immunohistochemical analysis of two cases

Cysts of the tongue are rare, usually derived from epithelia of the embryonic gastrointestinal and respiratory tracts, and classified according to the predominant epithelium lining. These cysts are usually discovered during infancy, more frequently in males, but they may not appear until well into adulthood. The authors report two lingual cysts lined mainly with respiratory, and focally by squamous, epithelium. Periodic acid-Schiff and mucicarmine staining revealed focal positivity in intracystic mucoid material and goblet cells. Immunohistochemical analysis with vimentin, cytokeratins (AE1/AE3, 34 beta E12, CK1, CK5, CK6, CK7, CK8, CK10, CK13, CK14, CK16, CK18, and CK19), E-cadherin, P-catenin, and epithelial membrane antigen showed a similar profile of normal respiratory epithelium, Suggesting well-differentiated states. Owing to their controversial origin, these cysts should be named descriptively, as Suggested by Manor et al., as lingual cysts with respiratory epithelium.38438839

Malignant odontogenic tumors: a multicentric latin american study of 25 cases

The aim of this study was to show the epidemiological features of 25 malignant odontogenic tumors (MOT) in Latin America. We retrieved 25 cases of MOT out of 2142 odontogenic tumors, from four oral diagnostic centers in Latin America, and described the main clinical and pathological characteristics. A total of 19 cases were carcinomas, including eight ameloblastic carcinomas, five primary intra-osseous squamous cell carcinomas, three clear cell odontogenic carcinomas and three ghost cell odontogenic carcinomas. All six sarcomas corresponded to ameloblastic fibrosarcoma. Thirteen cases occurred in men and 12 in women, age ranged from 7 to 77years old, with a mean of 41.4years. The average age of patients with carcinomas and sarcomas were 48.53 and 19years old, respectively. As malignant odontogenic tumors are very rare, this series helps to better clarify their relative frequency, predominant subtypes, and clinical characteristics in Latin America20438038

Immunohistochemical Expression Of P16, P21, P27 And Cyclin D1 In Oral Nevi And Melanoma

The acquisition of abnormalities at G1/S is considered a crucial step in the genesis and progression of melanoma. The expression of cell cycle regulators has also been used in various neoplasms as an adjunct to diagnosis. The aim of this study was to compare the expression of p16, p21, p27 and cyclin D1 in oral nevi and melanomas. Expression of these cell cycle regulatory proteins was evaluated by immunohistochemistry in 51 oral melanocytic lesions, including 38 intramucosal nevi and 13 primary oral melanomas. p16 and p27 were highly expressed in intramucosal nevi, whereas p21 and cyclin D1 expression was higher in oral melanomas. The results indicate that p21 and cyclin D1 may be involved in the development of oral melanomas, and eventually they may be useful in the differential diagnoses of oral benign and malignant melanocytic lesions. © 2012 Springer Science+Business Media, LLC.63297304Tanaka, N., Odajima, T., Mimura, M., Expression of Rb, pRb2/p130, p53, and p16 proteins in malignant melanoma of oral mucosa (2001) Oral Oncol, 37, pp. 308-314Meier, F., Satyamoorthy, K., Nesbit, M., Molecular events in melanoma development and progression (1998) Front Biosci, 15, pp. 1005-1010Tchernev, G., Orfanos, C.E., Downregulation of cell cycle modulators p21, p27, p53, Rb and proapoptotic Bcl-2-related proteins Bax and Bak in cutaneous melanoma is associated with worse patient prognosis: preliminary findings (2007) J Cutan Pathol, 34, pp. 247-256Michalides, R.J., Cell cycle regulators: mechanisms and their role in aetiology, prognosis, and treatment of cancer (1999) J Clin Pathol, 52, pp. 555-568Li, W., Sanki, A., Karim, R.Z., The role of cell cycle regulatory proteins in the pathogenesis of melanoma (2006) Pathology, 38, pp. 287-301Stefanaki, C., Stefanaki, K., Antoniou, C., Cell cycle and apoptosis regulators in Spitz nevi: comparison with melanomas and common nevi (2007) J Am Acad Dermatol, 56, pp. 815-824Stefanaki, C., Stefanaki, K., Antoniou, C., G1 cell cycle regulators in congenital melanocytic nevi. Comparison with acquired nevi and melanomas (2008) J Cutan Pathol, 35, pp. 799-808Poyraz, A., Akyürek, N., Gönül, I.I., Erdem, O., P21 and Bax expression in cutaneous malignant melanomas: correlation with histologic prognostic parameters (2004) J Exp Clin Cancer Res, 23, pp. 625-631Ivan, D., Diwan, A.H., Esteva, F.J., Prieto, V.G., Expression of cell cycle inhibitor p27Kip1 and its inactivator Jab1 in melanocytic lesions (2004) Mod Pathol, 17, pp. 811-818Bachmann, I.M., Straume, O., Akslen, L.A., Altered expression of cell cycle regulators Cyclin D1, p14, p16, CDK4 and Rb in nodular melanomas (2004) Int J Oncol, 25, pp. 1559-1565Prasad, M.L., Patel, S.G., Huvos, A.G., Shah, J.P., Busam, K.J., Primary mucosal melanoma of the head and neck: a proposal for microstaging localized, stage I (lymph node-negative) tumors (2004) Cancer, 100, pp. 1657-1664Sauroja, I., Smeds, J., Vlaykova, T., Analysis of G(1)/S checkpoint regulators in metastatic melanoma (2000) Genes Chromosomes Cancer, 28, pp. 404-414Alonso, S.R., Ortiz, P., Pollán, M., Progression in cutaneous malignant melanoma is associated with distinct expression profiles: a tissue microarray-based study (2004) Am J Pathol, 164, pp. 193-203Baldovini, C., Tosi, A.L., Di Oto, E., Genetic markers of oral malignant melanoma analysed by fluorescence in situ hybridisation (FISH) (2011) Virchows Arch, 459, pp. 167-173Ghiorzo, P., Mantelli, M., Gargiulo, S., Inverse correlation between p16INK4A expression and NF-kappaB activation in melanoma progression (2004) Hum Pathol, 35, pp. 1029-1037Keller-Melchior, R., Schmidt, R., Piepkorn, M., Expression of the tumor suppressor gene product p16INK4 in benign and malignant melanocytic lesions (1998) J Invest Dermatol, 110, pp. 932-938Straume, O., Akslen, L.A., Alterations and prognostic significance of p16 and p53 protein expression in subgroups of cutaneous melanoma (1997) Int J Cancer, 74, pp. 535-539Straume, O., Sviland, L., Akslen, L.A., Loss of nuclear p16 protein expression correlates with increased tumor cell proliferation (Ki-67) and poor prognosis in patients with vertical growth phase melanoma (2000) Clin Cancer Res, 6, pp. 1845-1853Li, Q., Murphy, M., Ross, J., Sheehan, C., Carlson, J.A., Skp2 and p27kip1 expression in melanocytic nevi and melanoma: an inverse relationship (2004) J Cutan Pathol, 31, pp. 633-642Flørenes, V.A., Maelandsmo, G.M., Kerbel, R.S., Slingerland, J.M., Nesland, J.M., Holm, R., Protein expression of the cell-cycle inhibitor p27Kip1 in malignant melanoma: inverse correlation with disease-free survival (1998) Am J Pathol, 153, pp. 305-312Karjalainen, J.M., Eskelinen, M.J., Kellokoski, J.K., Reinikainen, M., Alhava, E.M., Kosma, V.M., p21(WAF1/CIP1) expression in stage I cutaneous malignant melanoma: its relationship with p53, cell proliferation and survival (1999) Br J Cancer, 79, pp. 895-902Maelandsmo, G.M., Holm, R., Fodstad, O., Kerbel, R.S., Flørenes, V.A., Cyclin kinase inhibitor p21WAF1/CIP1 in malignant melanoma: reduced expression in metastatic lesions (1996) Am J Pathol, 149, pp. 1813-1822Nagasaka, T., Lai, R., Medeiros, L.J., Cyclin D1 overexpression in Spitz nevi: an immunohistochemical study (1999) Am J Dermatopathol, 21, pp. 115-120Sauter, E.R., Yeo, U.C., von Stemm, A., Cyclin D1 is a candidate oncogene in cutaneous melanoma (2002) Cancer Res, 62, pp. 3200-3206Flørenes, V.A., Faye, R.S., Maelandsmo, G.M., Nesland, J.M., Holm, R., Levels of cyclin D1 and D3 in malignant melanoma: deregulated cyclin D3 expression is associated with poor clinical outcome in superficial melanoma (2000) Clin Cancer Res, 6, pp. 3614-3620Pardo, M., Piñeiro, A., de la Fuente, M., Abnormal cell cycle regulation in primary human uveal melanoma cultures (2004) J Cell Biochem, 93, pp. 708-720Hicks, M.J., Flaitz, C.M., Oral mucosal melanoma: epidemiology and pathobiology (2000) Oral Oncol, 36, pp. 152-169Buery, R.R., Siar, C.H., Katase, N., NRAS and BRAF mutation frequency in primary oral mucosal melanoma (2011) Oncol Rep, 26, pp. 783-787Saldanha, G., Potter, L., Daforno, P., Pringle, J.H., Cutaneous melanoma subtypes show different BRAF and NRAS mutation frequencies (2006) Clin Cancer Res, 12, pp. 4499-450

Expression of fatty acid synthase (FASN) in oral nevi and melanoma

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)OBJECTIVE: The aim of this study was to determine the expression of fatty acid synthase (FASN) in oral nevi and melanomas, comparing the results with correspondent cutaneous lesions. MATERIALS AND METHODS: Expression of FASN was evaluated by immunohistochemistry in 51 oral melanocytic lesions, including 38 intramucosal nevi and 13 primary oral melanomas, in 10 cutaneous nevi and in 14 melanomas. RESULTS: Fatty acid synthase was strongly expressed only in melanomas, either of the oral mucosa or cutaneous. On the other hand, most oral and cutaneous nevi were negative, with a few oral cases showing focal and weak expression. CONCLUSION: Fatty acid synthase is expressed in malignant melanocytes, and it can be a helpful marker to distinguish oral melanomas from oral melanocytic nevi. Oral Diseases (2011) 17, 808-812178808812Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Immunohistochemical expression of Skp2 protein in oral nevi and melanoma

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Objective: The aim of this study was to analyze the immunohistochemical expression of Skp2 protein in 38 oral nevi and 11 primary oral melanomas. Study Design: Expression of this ubiquitin protein was evaluated by immunohistochemistry in 49 oral melanocytic lesions, including 38 intramucosal nevi and 11 primary oral melanomas. The labeling index (LI) was assessed considering the percentage of cells expressing nuclear positivity out of the total number of cells, counting 1000 cells per slide. Results: Skp2 protein was rarely expressed in intramucosal nevi, in contrast to oral melanomas, which showed high levels of this protein. Conclusion: These results indicate that Skp2 protein may play a role in the development and progression of oral melanomas, and it also could be useful as an immunohistochemical marker for differential diagnosis of oral benign and malignant melanocytic lesions.183E388E391Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)CAPES [CAPES/PDSE 8661-11-1

Expression of minichromosome maintenance 2, Ki-67, and geminin in oral nevi and melanoma

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Evaluation of cell cycle using antibodies against nuclear proteins involved in regulating DNA replication has gained special interest in the effort to predict biologic behavior of benign and malignant tumors. The aim of this study was to analyze the expression of minichromosome maintenance 2, Ki-67, and geminin in oral nevi and melanomas. Expression of these cell proliferation markers was evaluated by immunohistochemistry in 49 oral melanocytic lesions, including 38 intramucosal nevi and 11 primary oral melanomas. The labeling index of each proliferation marker was assessed considering the percentage of cells expressing nuclear positivity out of the total number of cells, counting 1000 cells per slide. Minichromosome maintenance 2, Ki-67, and geminin were rarely expressed in intramucosal nevi, in contrast to oral melanomas, which showed high levels of these cell proliferation markers, particularly minichromosome maintenance 2, indicating it is a more sensitive marker in primary oral melanomas than Ki-67 and geminin. These results indicate that these markers may be involved in the pathogenesis of oral melanomas and could be eventually useful as an additional diagnostic tool for differential diagnosis of oral benign and malignant melanocytic lesions. (C) 2013 Elsevier Inc. All rights reserved.1713236Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)CAPES [CAPES 8661-11-1

International collaborative study on ghost cell odontogenic tumours: calcifying cystic odontogenic tumour, dentinogenic ghost cell tumour and ghost cell odontogenic carcinoma

BACKGROUND: Calcifying odontogenic cyst was described first by Gorlin et al. in 1962; since then several hundreds of cases had been reported. In 1981, Praetorius et al. proposed a widely used classification. Afterwards, several authors proposed different classifications and discussed its neoplastic potential. The 2005 WHO Classification of Odontogenic Tumours re-named this entity as calcifying cystic odontogenic tumour (CCOT) and defined the clinico-pathological features of the ghost cell odontogenic tumours, the CCOT, the dentinogenic ghost cell tumour (DGCT) and the ghost cell odontogenic carcinoma (GCOC). METHODS: The aim of this paper was to review the clinical-pathological features of 122 CCOT, DGCT and GCOC cases retrieved from the files of the oral pathology laboratories from 14 institutions in Mexico, South Africa, Denmark, the USA, Brazil, Guatemala and Peru. It attempts to clarify and to group the clinico-pathological features of the analysed cases and to propose an objective, comprehensive and useful classification under the 2005 WHO classification guidelines. RESULTS: CCOT cases were divided into four sub-types: (i) simple cystic; (ii) odontoma associated; (iii) ameloblastomatous proliferating; and (iv) CCOT associated with benign odontogenic tumours other than odontomas. DGCT was separated into a central aggressive DGCT and a peripheral non-aggressive counterpart. For GCOC, three variants were identified. The first reported cases of a recurrent peripheral CCOT and a multiple synchronous, CCOT are included. CONCLUSIONS: Our results suggest that ghost cell odontogenic tumours comprise a heterogeneous group of neoplasms which need further studies to define more precisely their biological behaviour.37530230

Apixaban versus warfarin in patients with atrial fibrillation

BACKGROUND: Vitamin K antagonists are highly effective in preventing stroke in patients with atrial fibrillation but have several limitations. Apixaban is a novel oral direct factor Xa inhibitor that has been shown to reduce the risk of stroke in a similar population in comparison with aspirin. METHODS: In this randomized, double-blind trial, we compared apixaban (at a dose of 5 mg twice daily) with warfarin (target international normalized ratio, 2.0 to 3.0) in 18,201 patients with atrial fibrillation and at least one additional risk factor for stroke. The primary outcome was ischemic or hemorrhagic stroke or systemic embolism. The trial was designed to test for noninferiority, with key secondary objectives of testing for superiority with respect to the primary outcome and to the rates of major bleeding and death from any cause. RESULTS: The median duration of follow-up was 1.8 years. The rate of the primary outcome was 1.27% per year in the apixaban group, as compared with 1.60% per year in the warfarin group (hazard ratio with apixaban, 0.79; 95% confidence interval [CI], 0.66 to 0.95; P<0.001 for noninferiority; P = 0.01 for superiority). The rate of major bleeding was 2.13% per year in the apixaban group, as compared with 3.09% per year in the warfarin group (hazard ratio, 0.69; 95% CI, 0.60 to 0.80; P<0.001), and the rates of death from any cause were 3.52% and 3.94%, respectively (hazard ratio, 0.89; 95% CI, 0.80 to 0.99; P = 0.047). The rate of hemorrhagic stroke was 0.24% per year in the apixaban group, as compared with 0.47% per year in the warfarin group (hazard ratio, 0.51; 95% CI, 0.35 to 0.75; P<0.001), and the rate of ischemic or uncertain type of stroke was 0.97% per year in the apixaban group and 1.05% per year in the warfarin group (hazard ratio, 0.92; 95% CI, 0.74 to 1.13; P = 0.42). CONCLUSIONS: In patients with atrial fibrillation, apixaban was superior to warfarin in preventing stroke or systemic embolism, caused less bleeding, and resulted in lower mortality. Copyright © 2011 Massachusetts Medical Society. All rights reserved

Apixaban compared with warfarin in patients with atrial fibrillation and previous stroke or transient ischaemic attack: A subgroup analysis of the ARISTOTLE trial

Background: In the ARISTOTLE trial, the rate of stroke or systemic embolism was reduced by apixaban compared with warfarin in patients with atrial fibrillation (AF). Patients with AF and previous stroke or transient ischaemic attack (TIA) have a high risk of stroke. We therefore aimed to assess the efficacy and safety of apixaban compared with warfarin in prespecified subgroups of patients with and without previous stroke or TIA. Methods: Between Dec 19, 2006, and April 2, 2010, patients were enrolled in the ARISTOTLE trial at 1034 clinical sites in 39 countries. 18 201 patients with AF or atrial flutter were randomly assigned to receive apixaban 5 mg twice daily or warfarin (target international normalised ratio 2·0-3·0). The median duration of follow-up was 1·8 years (IQR 1·4-2·3). The primary efficacy outcome was stroke or systemic embolism, analysed by intention to treat. The primary safety outcome was major bleeding in the on-treatment population. All participants, investigators, and sponsors were masked to treatment assignments. In this subgroup analysis, we estimated event rates and used Cox models to compare outcomes in patients with and without previous stroke or TIA. The ARISTOTLE trial is registered with ClinicalTrials.gov, number NTC00412984. Findings: Of the trial population, 3436 (19%) had a previous stroke or TIA. In the subgroup of patients with previous stroke or TIA, the rate of stroke or systemic embolism was 2·46 per 100 patient-years of follow-up in the apixaban group and 3·24 in the warfarin group (hazard ratio [HR] 0·76, 95% CI 0·56 to 1·03); in the subgroup of patients without previous stroke or TIA, the rate of stroke or systemic embolism was 1·01 per 100 patient-years of follow-up with apixaban and 1·23 with warfarin (HR 0·82, 95% CI 0·65 to 1·03; p for interaction=0·71). The absolute reduction in the rate of stroke and systemic embolism with apixaban versus warfarin was 0·77 per 100 patient-years of follow-up (95% CI -0·08 to 1·63) in patients with and 0·22 (-0·03 to 0·47) in those without previous stroke or TIA. The difference in major bleeding with apixaban compared with warfarin was 1·07 per 100 patient-years (95% CI 0·09-2·04) in patients with and 0·93 (0·54-1·32) in those without previous stroke or TIA. Interpretation: The effects of apixaban versus warfarin were consistent in patients with AF with and without previous stroke or TIA. Owing to the higher risk of these outcomes in patients with previous stroke or TIA, the absolute benefits of apixaban might be greater in this population. Funding: Bristol-Myers Squibb and Pfizer. © 2012 Elsevier Ltd