Trabajo de Investigación Requisito para optar al Título de Cirujano Dentista / Introducción: En la cavidad oral se presentan diversas neoplasias malignas con distintas localizaciones como lengua, reborde alveolar, paladar, piso de boca, mejilla, entre otros. El cáncer oral y orofaríngeo corresponden al 3% de los tumores malignos en hombres y al 2% en mujeres; en Chile estos cánceres tienen una incidencia 1,7% respecto a todos los cánceres. El carcinoma oral de células escamosas (COCE) es el cáncer oral más frecuente (90%), pero también existen otros tipos de tumores orales malignos como sarcomas, linfomas, adenocarcinomas, metástasis, entre otros. El COCE se presenta principalmente en hombres, sobre 45 años, su principal factor de riesgo es el tabaco, su sobrevida a los 5 años no supera el 50%. Estudios en Chile son escasos, por lo que se ha planteado esta tesis para estudiar características sociodemográficas, clínicas y factores de riesgo en pacientes diagnosticados con COCE en la Facultad de Odontología de la Universidad de Chile, y asociar estas características a la sobrevida a 2 años. Material y métodos: Estudio observacional analítico de corte transversal. Se seleccionaron todos los casos diagnosticados con COCE en la Facultad de Odontología de la Universidad de Chile, entre los años 2000-2012, que contaran con información de edad, sexo, RUT y ficha de solicitud de biopsia. Se obtuvo la fecha de defunción y causa de muerte a través del Registro Civil de Chile. Resultados: De un total de 120 pacientes, el 60% correspondió a hombres. La edad media fue de 63,28 años. La localización anatómica de mayor frecuencia fue lengua (27%), y con aspecto clínico de tumoración (44,1%). El 74,1% de los odontólogos tuvo una sospecha de diagnóstico de patología maligna. Los hábitos de consumo de tabaco y alcohol se presentaron principalmente en hombres, pero más de la mitad de esta información no estaba consignada. El 68,3% falleció en el periodo de estudio y de estos, en el 79,2% de los casos la causa de muerte registrada fue cáncer oral. Solo el 48,3% de los pacientes diagnosticados con COCE sobrevivió dos años o más. La sobrevida a 2 años fue mayor en el grupo de pacientes que tenían menos de 55 años, que en el grupo que tenía 55 años y más (p<0,05). Conclusiones: El mayor porcentaje de pacientes diagnosticados con COCE corresponde a hombres y en cuanto a edad sobre 45 años. La sobrevida a dos años fue menor a lo determinado en reportes nacionales previos. Políticas públicas debieran incentivar el diagnóstico precoz de esta patología, a través del autoexamen y por un profesional, en conjunto a prevención primaria de consumo tabaco y alcohol, lo que se espera puede mejorar la sobrevida global a esta patología.

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Made available in DSpace on 2014-06-12T23:04:20Z (GMT). No. of bitstreams: 2 arquivo8858_1.pdf: 8860928 bytes, checksum: 7189139ff23fa781b6d59e692acaa9e2 (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2007 / Com o objetivo de detalhar as características clínico-patológicas dos papilomas centrais e periféricos, diagnosticados em tecido mamário obtido por setorectomia ou biópsia excisional, foi realizado estudo retrospectivo, descritivo, a partir da análise dos laudos de exame anatomopatológico desses materiais, constantes do arquivo do Departamento de Patologia do Hospital de Câncer da Paraíba Fundação Napoleão Laureano, referente ao período de Dezembro de 2000 a Dezembro de 2006. Foram localizados 63 laudos referentes a 54 pacientes do sexo feminino, com idade média de 50,87 ± 11,34 anos, que obedeciam às características de: laudo com diagnóstico de papiloma, independente de qualquer classificação, em ausência de carcinoma invasor, firmado com base em clivagem completa e inclusão total em bloco de parafina, pelo próprio pesquisador, à época do diagnóstico anatomopatológico da lesão; registro de idade, topografia da lesão mamária e resultado de, no mínimo, um exame de imagem anterior à setorectomia, no prontuário da paciente, assim como existência dos blocos de parafina dos respectivos materiais de biópsia excisional. Resultou amostra não probabilística, de conveniência, constituída por 418 lâminas de material de biópsia excisional e de descarga papilar, quando existentes, e 930 cortes histológicos, reavaliados pelo pesquisador e pela Orientadora, por microscopia óptica. Quando necessário, os blocos de parafina foram reprocessado pela técnica de rotina (HE). As variáveis foram: faixa etária da paciente; topografia e lateralidade da lesão, características macroscópicas de descarga papilar, palpabilidade tumoral e aspecto ao exame de imagem, presença de alterações de papila mamária; história familiar de câncer, de biópsia mamária prévia ou de recidiva de papiloma; número de fragmentos de biópsia enviados para exame anatomopatológico, dimensões da peça cirúrgica. Para classificação do padrão citoarquitetural e tipo de lesões em tecido perilesional dos papilomas a categorização foi: padrão papilar clássico, hiperplasia epitelial típica com formação de lúmens secundários (simples, com metaplasia apócrina típica, com padrão apócrino símile, com metaplasia apócrina atípica) e de padrão sólido; hiperplasia epitelial atípica de padrão apócrino símile sólida, hiperplasia epitelial leve com metaplasia apócrina típica, hiperplasia epitelial papilífera com metaplasia apócrina (típica ou atípica), hiperplasia epitelial típica micropapilífera sem eixo conjuntivo, áreas de adenose símile, de hiperplasia mioepitelial e de adenomioepitelioma símile. Houve predomínio de: papiloma em mulheres na faixa etária de 50 a 59 anos (40% centrais e 39,3%, periféricos), em mama direita (60% centrais e 64,3%, periféricos), em região retroareolar (36,5% por papilomas centrais e 25,4% periféricos). Quanto ao motivo da consulta clínica, 18 (28,6%) casos apresentavam tumor palpável (55,6% papilomas centrais e 44,4%, periféricos). Nos casos com tumor não palpável, 23,8% apresentavam apenas descarga papilar (17,12% com papiloma central e 32,1%, periférico). A descarga papilar esteve presente em 38,1% dos casos, 54,2% em papilomas periféricos, na presença de tumor palpável (28,6%). Quanto à presença de descarga papilar espontânea, houve 36,5% casos (43,5% em papilomas centrais e 20,6% em periféricos), predominando aspecto macroscópico sanguinolento (52,2%) (60% em papilomas centrais e 46,2% em periféricos). Dentre os 16 casos com resultado de mamografia registrado em prontuário como BI-RADS® 4 ou 5, o índice de acerto de suspeita de carcinoma igualou-se a 12,5%. À ultra-sonografia mamária, dentre 53 casos, 15,1% tinham achado de ectasia ductal com nódulo sólido intraductal sugestivo de papiloma, confirmado à histopatologia. Considerando padrões arquiteturais predominantes os que ocupavam mais de 50% da lesão papilomatosa como um todo, predominou o padrão clássico, (52% centrais e 48% periféricos), seguindo-se hiperplasia mioepitelial (28,6% centrais e 20% periféricos). Nos papilomas com carcinoma (12,7%), 33,3% eram centrais, 66,7%, periféricos (destes, 25% perilesionais). Em um caso, havia hiperplasia típica com formação de lumens secundários. Dentre os casos de carcinoma intraductal associado a papiloma, predominaram os padrões papilífero cribriforme apócrino (34%) e papilífero apócrino (26%). Houve dois casos com carcinoma intraductal de padrões micropapilífero e cribriforme apócrino e carcinoma intraductal de padrão cribriforme apócrino símile, em área perilesional. Os resultados da presente pesquisa permitiram evidenciar as dificuldades envolvidas no diagnóstico dos papilomas e reforçaram a idéia da necessidade de excisão dessa lesão, evitando assim as recidivas e a evolução para malignização

El texto completo de este trabajo no está disponible en el Repositorio Académico UPC por restricciones de la casa editorial donde ha sido publicado. / A 24-year-old pregnant woman arrived at the emergency service at 34 weeks of gestational age with intermittent right upper abdominal pain. An abdominal ultrasound was performed showing signs of hepatopathy with multiple neo-formative nodules with mild ascites and fetal biometry confirmed at 34 weeks gestation. During her hospitalization, an emergency caesarean was induced with favorable result in the survival of the mother and the baby. / Revisión por pares

Sarcomatoid, or spindle cell squamous cell carcinoma (SCSC), is relatively uncommon, but may be encountered. It poses a challenge in differential diagnosis that includes other spindle cell neoplasms. We present a case where the lesion existed for 20 years and raised the potential of chronicity as a factor in inducing spindle cell morphology. Detailed immunohistochemical features are demonstrated, and discussion of the differential diagnosis is offered. The patient was an 89-year-old African-American female with an exophytic and polypoid mass of the right upper arm measuring 5.5 × 5.5 × 3.0 cm. The mass had been present for the last 20 years, and was gradually and very slowly increasing in size. After refusing surgery several times, she finally agreed to have an excision. The tumor proved to be SCSC.

Distinction of primary skin adnexal carcinomas from cutaneous metastasis of adenocarcinomas is challenging. In this study, we evaluated podoplanin immunoreactivity in a series of primary skin adnexal tumors and adenocarcinomas metastatic to skin using a D2-40 antibody. The initial test series were composed of a total of 93 cases including 32 primary skin adnexal carcinomas, 46 benign primary adnexal tumors, and 15 cutaneous metastatic adenocarcinomas. We found that variable D2-40 reactivity was seen in all of the primary cutaneous carcinomas including sebaceous carcinomas (10/10), squamous cell carcinomas (10/10), porocarcinomas (4/4), trichilemmal carcinomas (4/4), skin adnexal carcinomas not otherwise specified (4/4), and in the majority of benign skin adnexal tumors. In contrast, no podoplanin immunoreactivity was seen in any of the 15 (0/15) cutaneous metastases. To confirm the initial findings and to further explore the utility of podoplanin reactivity in the distinction of these tumors, we also examined a test set of 35 unknown cases, including 21 adenocarcinomas metastatic to skin and 14 primary adnexal tumors, in a blinded fashion. In this test set of cases, podoplanin was negative in 22 cases and positive in 13 cases. Of the 22 podoplanin negative cases, 20 were proven to be metastatic adenocarcinoma. Of the 13 D2-40 positive cases, 12 were proven to be primary adnexal tumors. Our results suggest that podoplanin can be a useful tool to distinguish primary skin adnexal carcinomas form adenocarcinomas metastatic to skin with high sensitivity (94.5%) and specificity (97.2%).

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O câncer de cavidade oral é uma das neoplasias mais comuns no Brasil e no mundo, porém seu prognóstico ainda é incerto principalmente devido ao diagnóstico tardio e presença de metástases. A análise de fatores relacionados ao prognóstico dessa doença é de suma importância e, o receptor de quimiocina denominado CXCR4, está sendo relacionado a um pior prognóstico devido a maior capacidade de invasão das células que o expressam, em diversas neoplasias. Apesar dessa relação estar demonstrada em vários tipos de cânceres, com relação ao de cavidade oral pouco se sabe até o momento. Assim, objetivo desse trabalho foi analisar a expressão imuno-histoquímica do receptor de quimiocina CXCR4 em carcinomas epidermóides de cavidade oral, e relacioná-la com variáveis clínicas e histológicas. Foram obtidos 94 blocos de carcinomas epidermóides oriundos de instituições parceiras para obtenção de cortes histológicos convencionais, corados com hematoxilina e eosina (HE), e cortes de TMA (tissue microarray). Foi realizado imuno-histoquímica para anticorpo anti-CXCR4 (ab124824, ABCAM, EUA) e análise da marcação em lâminas de TMA utilizando o software Image J (versão 1.49u). A intensidade de marcação imuno-histoquímica foi correlacionada com dados clínicos (TNM, tabagismo, etilismo e sobrevida) e histopatológicos (diferenciação histológica, infiltrado inflamatório e infiltração vascular, linfática e perineural) dos pacientes. Dos casos analisados 74,4% exibiram uma marcação fortemente positiva para o CXCR4, enquanto que o epitélio não tumoral mostrou uma marcação negativa ou fracamente positiva (71,1%; p=0,011). Tumores classificados como \"bem diferenciados\" apresentaram marcação fortemente positiva para a proteína estudada (53,3%; p=0,049). Não houve associação entre a marcação imuno-histoquímica do CXCR4 com sobrevida global em 5 anos (?2= 0.3, p=0.565). Os resultados sugerem que a alta expressão dessa proteína não influencia no prognóstico e na sobrevida desses pacientes. / Oral cancer is one of the most common neoplasia in Brazil and the world. Mainly due to a late diagnosis and presence of metastases its prognosis is still uncertain. Finding biological markers related to the prognosis of this disease is of paramount importance. The chemokine receptor CXCR4 is being related to a worse prognosis in several neoplasms because cells expressing it acquire a greater capacity of invasion. Although this relationship is demonstrated in several types of cancers, in the oral cavity it is uncertain. The aim of this study was to analyze by immunohistochemistry the CXCR4 chemokine receptor expression in oral squamous cell carcinomas, and related to clinical and histological variables. Conventional histological sections stained with hematoxylin and eosin (HE) were acquired from 94 blocks of oral squamous cell carcinoma for histological analysis. TMA (tissue microarray) was assembled from these blocks for anti-CXCR4 immunohistochemistry (ab124824, ABCAM, USA). Staining analysis was performed using Image J software (version 1.49u). The immunohistochemical signal intensity was correlated with clinical (TNM, smoking, alcoholism and survival) and histopathological parameters (histological differentiation, inflammatory infiltration, vascular, lymphatic and perineural infiltration). From the cases studied 74.4% showed a strong positivity for CXCR4, and the non-tumoral epithelium was negative or weakly positive (71.1%; p = 0.011). Tumors histologically well differentiated were strongly positive for the protein studied (53.3%; p = 0.049). There was no association between CXCR4 signal and global survival in 5 years (?2= 0.3, p=0.565). These results suggest that a high expression of CXCR4 it is not related to prognosis and survival of patients of patients with oral squamous cell carcinoma.

Li Ching-wan. / Thesis submitted in: November 2001. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 104-130). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACTS (ENGLISH/CHINESE) --- p.iii / LIST OF FIGURES --- p.xi / LIST OF TABLES --- p.xiii / LIST OF ABBREVIATIONS --- p.xiv / Chapter CHAPTER1 --- INTRODUCTION / Chapter 1.1. --- Liver Cancer --- p.1 / Chapter 1.2. --- Hepatocellular Carcinoma --- p.1 / Chapter 1.2.1. --- Types of Liver Cancer --- p.1 / Chapter 1.2.2. --- Epidemiology --- p.4 / Chapter 1.2.2.1. --- Geographical Distribution --- p.4 / Chapter 1.2.2.2. --- Age and Gender Distribution --- p.8 / Chapter 1.2.3. --- Etiologic Factors --- p.9 / Chapter 1.2.3.1. --- Chronic Infection with Hepatitis B (HBV) and C (HCV) Viruses --- p.9 / Chapter 1.2.3.2. --- Aflatoxin B1 --- p.11 / Chapter 1.2.3.3. --- Alcohol --- p.12 / Chapter 1.2.3.4. --- Summary --- p.12 / Chapter 1.3. --- HCC in Hong Kong --- p.14 / Chapter 1.4. --- Role of Viral Hepatitis B in HCC --- p.17 / Chapter 1.4.1. --- HBV Genome --- p.17 / Chapter 1.4.2. --- Consequences of HBV DNA Integration --- p.17 / Chapter 1.4.2.1. --- HBV Integration --- p.17 / Chapter 1.4.2.2. --- Transactivation of Cellular Genes by HBV DNA --- p.19 / Chapter 1.4.2.3. --- Chromosomal DNA Instability --- p.20 / Chapter 1.5. --- Genetic Alterations in HCC --- p.21 / Chapter 1.5.1. --- Tumor Suppressor Gene --- p.21 / Chapter 1.5.2. --- Proto-oncogene --- p.23 / Chapter 1.5.3. --- Genetic Studies in HCC --- p.23 / Chapter 1.5.3.1. --- Loss of Heterozygosity (LOH) --- p.25 / Chapter 1.5.3.2. --- Comparative Genomic Hybridization (CGH) --- p.26 / Chapter 1.5.3.3. --- Array CGH --- p.26 / Chapter 1.5.4. --- Large-Scale Genetic Analysis in HCC --- p.27 / Chapter CHAPTER2 --- RATIONALE IN THIS STUDY --- p.35 / Chapter CHAPTER3 --- MATERIALS AND METHODS / Chapter 3.1. --- Patients and Materials --- p.38 / Chapter 3.1.1. --- DNA Extraction --- p.40 / Chapter 3.2. --- Loss of Heterozygosity Analysis on Chromosome 4q --- p.40 / Chapter 3.2.1. --- Microsatellite Markers --- p.41 / Chapter 3.2.2. --- Amplification of Target Sequences by PCR --- p.42 / Chapter 3.2.2.1. --- 5-end Labeling Primers --- p.42 / Chapter 3.2.2.2. --- Amplification of Target Sequences --- p.42 / Chapter 3.2.3. --- Denaturing Polyacrylamide Gel --- p.44 / Chapter 3.2.3.1. --- Electrophoresis --- p.44 / Chapter 3.2.4. --- Detection of Loss of Heterozygosity (LOH) --- p.45 / Chapter 3.2.5. --- Duplex PCR Analysis of Homozygous Deletion --- p.45 / Chapter 3.3. --- Amplification Analysis by Array-CGH --- p.46 / Chapter 3.3.1. --- Nick-Translation --- p.49 / Chapter 3.3.2. --- Hybridization --- p.49 / Chapter 3.3.3. --- Imaging and Data Analysis --- p.50 / Chapter 3.3.4. --- Determination of Normal Range for All Cases --- p.51 / Chapter 3.3.5. --- Assessment of Data Quality --- p.51 / Chapter 3.4. --- Statistical Analysis --- p.52 / Chapter CHAPTER4 --- RESULTS / Chapter 4.1. --- Loss of Heterozygosity Analysis on Chromosome 4q --- p.53 / Chapter 4.1.1. --- Region I of Smallest Common Deletion Region --- p.54 / Chapter 4.1.2. --- Region II of Smallest Common Deletion Region --- p.54 / Chapter 4.2. --- Amplification Analysis by Array-CGH --- p.62 / Chapter CHAPTER5 --- DISCUSSION / Chapter 5.1. --- LOH Analysis on Chromosome 4q --- p.73 / Chapter 5.1.1. --- LOH of Chromosome 4q in Various Cancers --- p.74 / Chapter 5.1.1.1. --- Hepatocellular Carcinomas --- p.74 / Chapter 5.1.1.2. --- Other Neoplasia --- p.76 / Chapter 5.1.2. --- Functional Studies on Chromosome 4 --- p.76 / Chapter 5.1.3. --- Putative Tumor Suppressors on Chromosome 4q --- p.80 / Chapter 5.1.3.1. --- Region I (4q27-q28.1) --- p.80 / Chapter 5.1.3.1.1. --- MAD2L1 (4q27) --- p.80 / Chapter 5.1.3.2. --- Region II (4q35.2) --- p.81 / Chapter 5.1.3.2.1. --- INGlL(4q35.1) --- p.81 / Chapter 5.1.3.2.2. --- FAT (4q34-q35) --- p.81 / Chapter 5.1.3.2.3. --- Caspase 3 (4q35) --- p.82 / Chapter 5.1.4. --- Limitation of this Study --- p.83 / Chapter 5.1.4.1. --- Markers --- p.83 / Chapter 5.1.4.1.1. --- Limitation of the Markers --- p.83 / Chapter 5.1.4.1.2. --- Location of the Microsatellite Markers --- p.83 / Chapter 5.1.4.2. --- Tissue Samples --- p.84 / Chapter 5.1.4.2.1. --- Normal Reference --- p.84 / Chapter 5.1.4.2.2. --- Pathologic Characterization --- p.85 / Chapter 5.1.5. --- Future Studies --- p.85 / Chapter 5.1.5.1. --- Improvement of the Experiment --- p.85 / Chapter 5.1.5.2. --- Extension of the Present Study --- p.86 / Chapter 5.2. --- Amplification Analysis by Array-CGH --- p.88 / Chapter 5.2.1. --- Amplicons Showing Amplification in HCC --- p.89 / Chapter 5.2.1.1. --- Locus of 17q23 --- p.89 / Chapter 5.2.1.1.1. --- D17S1670 --- p.89 / Chapter 5.2.1.1.2. --- RPS6KB1 --- p.91 / Chapter 5.2.1.2. --- Locus of 1q25-q31 --- p.92 / Chapter 5.2.1.2.1. --- LAMC2 --- p.92 / Chapter 5.2.1.3. --- Locus of 3q26.3 --- p.93 / Chapter 5.2.1.3.1. --- PIK3CA --- p.93 / Chapter 5.2.1.4. --- Locus of 8p22 --- p.94 / Chapter 5.2.1.4.1. --- CTSB --- p.94 / Chapter 5.2.1.5. --- Locus of 6q22 --- p.95 / Chapter 5.2.1.5.1. --- MYB --- p.95 / Chapter 5.2.1.6. --- Locus of 20ql3 --- p.96 / Chapter 5.2.1.6.1. --- CSE1L --- p.96 / Chapter 5.2.1.7. --- Locus of Ip36.2-p35.1 --- p.97 / Chapter 5.2.1.7.1. --- FGR --- p.97 / Chapter 5.2.1.8. --- Locus of 7q21.1 --- p.98 / Chapter 5.2.1.8.1. --- PGY1 --- p.98 / Chapter 5.2.2. --- Amplicons Showing Deletion in HCC --- p.99 / Chapter 5.2.2.1. --- Loss at 11ql3 and 14q32.3 --- p.99 / Chapter 5.2.3. --- Limitation of the Study --- p.100 / Chapter 5.2.3.1. --- Samples and Materials --- p.100 / Chapter 5.2.4. --- Further Study --- p.101 / Chapter 5.2.4.1. --- Confirmation of the Result in Various Levels --- p.101 / Chapter 5.2.4.2. --- Assessment of the Significant Losses on Chromosomes 11ql3 and 14ql3 --- p.101 / Chapter 5.2.5. --- Application of Microarray in Genetic Studies --- p.102 / Chapter 5.2.5.1. --- Deletion Analysis --- p.102 / Chapter 5.2.5.2 --- Tissue Microarray --- p.103 / Chapter 5.2.5.3. --- cDNA Microarray --- p.103 / Chapter chapter6 --- references --- p.104