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Ameloblastoma: perfil biodemográfico comparativo por continente / Ameloblastoma: a continental comparative biodemographic profileHigo, Cristiano Daissuke 22 January 2008 (has links)
O ameloblastoma é uma das neoplasias odontogênicas mais freqüentes universalmente. Seu estudo se reveste de grande importância porque, não obstante benigna, é localmente agressiva, com alto índice de recorrências, sendo o tratamento cirúrgico radical, com margem de segurança, freqüentemente preconizado, e tido, por boa parcela de especialistas, como única alternativa efetiva para seu tratamento. Em decorrência, observam-se, muitas vezes, seqüelas importantes, do ponto de vista funcional e estético, para os pacientes acometidos por essa neoplasia. O objetivo do presente trabalho foi revisar a literatura, traçando um perfil comparativo, por continente, da biodemografia do ameloblastoma, com ênfase na discussão de suas possíveis diferenças e similitudes regionais. As informações coletadas na literatura disponível para consulta indicaram ter sido a segunda neoplasia de origem odontogênica mais prevalente universalmente, ressalvada a consideração sobre os odontomas serem ou não, classificados como neoplasias. Foi mais freqüente no gênero masculino. A localização mais comum do ameloblastoma foi no segmento posterior da mandíbula, sendo essa, uma unanimidade nos trabalhos consultados. Houve diferenças regionais quando se comparou aspecto relativo aos itens estudados (freqüência do ameloblastoma em relação às neoplasias odontogênicas; incidência do ameloblastoma em relação ao gênero). Foi encontrada, na revisão de literatura pesquisada, uma freqüência significativa de informações incompletas com relação aos itens estudados, sendo exceções, os trabalhos referentes aos continentes, europeu e africano / Ameloblastoma is one of the universally most prevalent odontogenic neoplasias. Its correct knowledge has great importance in view of its local aggressiveness potential, although being a benign neoplasia, with a high number of recurrences. The elective treatment for ameloblastoma is the surgical radical resection with safety margins, being in the opinion of many specialists, the only correct method for its management. Notwithstanding of this fact, functional and aesthetical damage has been frequently observed after treatment, among the patients suffering from this neoplasia. The purpose of the present study was to perform a literature review, building a comparative continental profile of ameloblastoma biodemographics, emphasizing the discussion of its possible regional differences and similarities. The information collected from the literature indicated ameloblastoma as the second most frequent odontogenic neoplasia, despite of the consideration on the odontoma classification as a true neoplasia or not. Ameloblastoma was more frequent among male gender and the most common location was in the posterior segment of the jaw, being this data unanimous among the literature. There were regional differences regarding some of the studied variables (freqüency of ameloblastoma related to odontogenic neoplasias and related to gender). Incomplete data was an important occurrence during the literature reviewing, with exception of the papers from European and African continents.
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Ameloblastoma: perfil biodemográfico comparativo por continente / Ameloblastoma: a continental comparative biodemographic profileCristiano Daissuke Higo 22 January 2008 (has links)
O ameloblastoma é uma das neoplasias odontogênicas mais freqüentes universalmente. Seu estudo se reveste de grande importância porque, não obstante benigna, é localmente agressiva, com alto índice de recorrências, sendo o tratamento cirúrgico radical, com margem de segurança, freqüentemente preconizado, e tido, por boa parcela de especialistas, como única alternativa efetiva para seu tratamento. Em decorrência, observam-se, muitas vezes, seqüelas importantes, do ponto de vista funcional e estético, para os pacientes acometidos por essa neoplasia. O objetivo do presente trabalho foi revisar a literatura, traçando um perfil comparativo, por continente, da biodemografia do ameloblastoma, com ênfase na discussão de suas possíveis diferenças e similitudes regionais. As informações coletadas na literatura disponível para consulta indicaram ter sido a segunda neoplasia de origem odontogênica mais prevalente universalmente, ressalvada a consideração sobre os odontomas serem ou não, classificados como neoplasias. Foi mais freqüente no gênero masculino. A localização mais comum do ameloblastoma foi no segmento posterior da mandíbula, sendo essa, uma unanimidade nos trabalhos consultados. Houve diferenças regionais quando se comparou aspecto relativo aos itens estudados (freqüência do ameloblastoma em relação às neoplasias odontogênicas; incidência do ameloblastoma em relação ao gênero). Foi encontrada, na revisão de literatura pesquisada, uma freqüência significativa de informações incompletas com relação aos itens estudados, sendo exceções, os trabalhos referentes aos continentes, europeu e africano / Ameloblastoma is one of the universally most prevalent odontogenic neoplasias. Its correct knowledge has great importance in view of its local aggressiveness potential, although being a benign neoplasia, with a high number of recurrences. The elective treatment for ameloblastoma is the surgical radical resection with safety margins, being in the opinion of many specialists, the only correct method for its management. Notwithstanding of this fact, functional and aesthetical damage has been frequently observed after treatment, among the patients suffering from this neoplasia. The purpose of the present study was to perform a literature review, building a comparative continental profile of ameloblastoma biodemographics, emphasizing the discussion of its possible regional differences and similarities. The information collected from the literature indicated ameloblastoma as the second most frequent odontogenic neoplasia, despite of the consideration on the odontoma classification as a true neoplasia or not. Ameloblastoma was more frequent among male gender and the most common location was in the posterior segment of the jaw, being this data unanimous among the literature. There were regional differences regarding some of the studied variables (freqüency of ameloblastoma related to odontogenic neoplasias and related to gender). Incomplete data was an important occurrence during the literature reviewing, with exception of the papers from European and African continents.
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Clonality and antigen heterogeneity of murine lymphomaFowlis, Deborah Janet January 1988 (has links)
No description available.
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Synthetic and related studies of novel photosensitisorsMaguire, G. January 1988 (has links)
No description available.
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Human papillomaviruses in squamous intraepithelial lesions of the cervixGiannoudis, Athina January 2001 (has links)
No description available.
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Caveolina-1 favorece la activación de rab5 promoviendo la migración y la activación del eje p85α/tiam1/rac-1 en células de cáncer metastásico y en un modelo de metástasis in vivo en ratones c57bl/6Díaz Fuentes, Jorge Esteban January 2015 (has links)
Doctor en Bioquímica / El cáncer constituye una de las principales causas de muerte en Chile y el mundo.
Particularmente, la agresividad de esta enfermedad subyace en la diseminación de las
células tumorales hacia otros tejidos, fenómeno conocido como metástasis. La
metástasis es un proceso multifactorial, siendo la migración celular una de las etapas
más relevantes. Caveolina-1 es una proteína de membrana que en etapas avanzadas
del cáncer aumenta su expresión y promueve la migración celular y metástasis. En este
contexto, Caveolina-1 ha sido asociada a un conjunto de cambios morfológicos
esenciales que permiten la migración e invasión celular, entre estos, la remodelación del
citoesqueleto de actina y el recambio de complejos de adhesión celular. Muchos de
estos eventos dependen del tráfico endosomal, el cual a su vez es finamente regulado
por diversos factores y moléculas, como las GTPasas pequeñas de la familia Rab. Una
de estas proteínas es Rab5, la cual no sólo actúa como regulador maestro de la
endocitosis temprana, sino que además cumple un rol fundamental en la migración
celular. Trabajos recientes han descrito que la interacción entre Rab5 y Caveolina-1
influye en el tráfico endosomal, sin embargo el rol de esta interacción en la migración
celular no había sido investigado.
Entre los reguladores de Rab5, p85α (la subunidad reguladora de PI3K), se caracteriza
por inhibir a Rab5, ya que posee un dominio RabGAP que estimula su actividad
GTPasa. Literatura reciente ha descrito una interacción funcional entre p85α y
Caveolina-1, la cual a su vez depende de la fosforilación de Caveolina-1 en tirosina
(Y14). Lo anterior cobra relevancia, ya que Caveolina-1 ejerce muchos de sus efectos
en migración celular mediante la fosforilación en este residuo.
Por otro lado, trabajos recientes indican que Rab5 activa a Rac-1, a través del
reclutamiento de la GEF Tiam1, fomentando la formación de lamellipodios y la
polimerización de actina en sitios específicos de membrana. Además, trabajos de
nuestro laboratorio demostraron que Caverolina-1 promueve la activación de Rac-1
en células metastásicas. Todos estos eventos llevan a que la célula adquiera
cambios morfológicos que le permiten migrar. Por lo tanto, es importante investigar el
papel potencial que desempeñaría Caveolina-1 en la regulación de este circuito, así
como su relevancia en la migración celular.
En esta tesis, se investigó los mecanismos asociados al efecto promotor de
migración y metástasis de Caveolina-1, identificando un nuevo eje de
señalización “p85α/Rab5/Tiam1/Rac-1”. A su vez, se evaluó la relevancia de
este eje en un modelo preclínico, evaluando la metástasis in vivo en ratones
C57BL/6.
Los resultados obtenidos durante el desarrollo de esta tesis indican que Caveolina-1
promueve la migración, invasión y la activación de Rab5 en tres líneas celulares
metastásicas: HT-29(US) de cáncer de colon, B16-F10 de melanoma murino y MDAMB-
231 de cáncer de mama. En relación a esto último, la expresión de Caveolina-1
promueve un aumento en el tamaño de los endosomas tempranos, pero no debido a
la estabilización de Rab5 en éstos, sino que debido al secuestro de p85α en un
complejo proteico. Interesantemente, el efecto de p85α en la inhibición de Rab5 es
asociado a su actividad GAP, y no involucra la activación de PI3K.
Mediante ensayos de silenciamiento y reconstitución, se observó que la expresión y
actividad de Rab5 son fundamentales para que Caveolina-1 promueva migración e
invasión celular, así como también la activación de Rac-1. La activación de Rac-1 por
Caveolina-1 y Rab5 requiere de Tiam1, la cual es reclutada a endosomas tempranos
de manera dependiente de Caveolina-1. Finalmente, se demostró que Caveolina-1
requiere de Rab5, p85α y Rac-1 para promover invasión in vitro y metástasis in vivo
en ratones C57BL/6.
De esta manera, este trabajo de tesis aporta nueva evidencia acerca de los
mecanismos moleculares involucrados en la migración y metástasis inducida por
Caveolina-1, proponiendo un nuevo eje de señalización p85α/Rab5/Tiam1/Rac-1, el
cual involucra proteínas comúnmente alteradas en cáncer, y por lo tanto,
contribuyendo con la identificación de nuevos blancos potenciales terapéuticos / Cancer is a leading cause of disease in Chile and worldwide. During the development
and progression of this disease, normal cells convert to the cancerous state by acquiring
specific characteristics. Of these metastasis is widely considered particularly important
because it is this trait of cancer cells that is responsible for the large majority of deaths in
cancer patients. Caveolin-1 is a membrane protein with vastly differing roles in cancer
that range from functioning as a tumor suppressor to promoting tumor cell migration
invasion and metastasis. Concomittant with this unfavorable role in tumor progression,
expression of this protein frequently increases in advanced stages of cancer and is
viewed there as a marker for poor patient prognosis and survival. In this cellular context,
it is important to gain better insight to how Caveolin-1 promotes the acqusition of a more
invasive cellular phenotype.
In these migration-related events, endosomal trafficking reportedly plays a fundamental
role and Caveolin-1 is known to promote recycling of membrane components and the
activation of GTPases at the leading edge. A key membrane-associated protein involved
in such processes is Rab5, a small Rho GTPase that acts as a master regulator of early
endocytosis. Recently, evidence has been provided suggesting that p85α, the regulatory
subunit of PI3K, is a Rab5 GAP that controls Rab5 inactivation. Structurally, p85α has
two SH2 domains, involved in binding to tyrosine-phosphorylated proteins, often
including receptors and adaptor proteins. Caveolin-1, on the other hand, is known to
promote the migratory and invasive capacity of tumor cells via phosphorylation on
tyrosine-14. Furthermore, Rab5 activates Rac-1 and promotes lamellipodia formation,
through recruitment of the GEF Tiam1. Together, these events lead to changes that
permit cell migration. However, the precise mechanisms by which Caveolin-1
participates in the regulation of such processes and specifically whether Caveolin-1
enhanced migration and invasion in vitro involves a novel p85α / Rab5 / Tiam1 / Rac-1
signaling axis remained to be determined. Also, a model of B16F10 murine melanoma
metastasis in syngeneic C57BL / 6 mice was employed to evaluate the relevance of
Rab5, p85α and Rac-1 in promoting Caveolin-1-enhanced lung metastasis in vivo.
The results obtained during this thesis demonstrate that Caveolin-1 promoted migration,
invasion and activation of Rab5 in the metastatic cell lines HT-29 (US), B16-F10 and MDA-MB-231. Moreover, the expression of Caveolin-1 was shown to increase the
average size of early endosomes in B16F10 cells, consistent with a role in the activation
of Rab5. To study molecular mechanisms that explain these results, the expression of
p85α was shown to decrease Rab5 activation induced by Caveolin-1. Using inhibitors,
the activation of Rab5 by Caveolin-1 was shown to be independent of PI3K activity.
Moreover, expression of Rab5 was required for Caveolin-1 to promote cell migration and
invasion. Importantly, the activation of the small GTPase Rac-1 induced by Caveolin-1
required the presence of Rab5 to promote migration. Furthermore, evidence is provided
showing that recruitment of the Rac1 GEF Tiam1 to early endosomes was enhanced in
the Caveolin-1 positive cells. Finally, using short-hairpin knock-down technology Rab5,
p85α and Rac-1 were shown to be required for Caveolin-1 to promote migration and
invasion in vitro, as well as metastasis in vivo in C57BL / 6 mice.
In conclusion, the results of this thesis shed light on the molecular mechanisms involved
in Caveolin-1-enhanced migration, invasion and metastasis and propose the existence
of a novel p85α / Rab5 / Tiam1 / Rac-1 signaling axis downstream of Caveolin-1 that
contributes to deregulation in cáncer and potentially represents an interesting target for
treatments in cancer patients / Conicyt; Fondecyt; Anillo ACT 1111
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E-cadherina potencia a caveolina-1 como supresor de tumores y reduce su efecto promotor de metástasisLobos González, Lorena January 2011 (has links)
Tesis presentada a la Universidad de Chile
para optar al grado de Doctor en Bioquímica / Caveolina-1 es una proteína de membrana esencial en la formación de caveolas, participa en el transporte de colesterol, actúa como proteína de andamiaje en señalización y ha sido descrita como un supresor de tumores. Por otro lado, la presencia de Caveolina-1 juega un rol esencial en la polarización celular durante el proceso migratorio, ya que controla la localización de moléculas de señalización y regula la activación de proteínas que participan en migración. Sin embargo, no sólo la presencia de Caveolina-1 es esencial para la migración celular, sino también la fosforilación de Caveolina-1 en Tirosina 14. Considerando que la migración celular es esencial para la metástasis, Caveolina-1 ha sido descrita también como un promotor de metástasis. Este comportamiento dual ha causado controversia y ha dado origen a un gran número de investigaciones en desarrollo actúalmente en la comunidad científica.
El principal objetivo de esta tesis fue establecer, en un modelo in vivo inmunocompetente, si Caveolina-1 tiene o no este rol dual en cáncer usando como modelo células de melanoma. Estudiamos en ratones C57-BL/6 el comportamiento de las líneas tumorales B16-F0 y B16-F10, ambas líneas singénicas con la cepa C57-BL/6, y por lo tanto no existe rechazo inmunológico. Estas células al ser subcutáneamente en estos ratones tienen la capacidad de formar tumores sólidos y a la vez, si se inyectan por la vía intravenosa, generan focos de metástasis en el pulmón de los ratones. Por lo tanto, con este sistema estudiamos el rol dual de Caveolina-1 en un mismo modelo in vivo. Una vez inoculados los animales en el lomo (vía subcutánea) o por la vena lateral de la cola (vía intravenosa), con las células seguimos la formación de tumores y cuantificamos la metástasis a nivel pulmonar, respectivamente.
Los ensayos realizados in vivo en las células B16-F0 mostraron que Caveolina-1 era capaz de suprimir la formación de tumores, retardando al doble el tiempo de aparición de éstos. Al silenciar los niveles de expresión de Caveolina-1 en las B16-F0 Caveolina-1 mostró promover metástasis no sólo a nivel de pulmón, a la vez mostró nódulos metastasicos en ganglios, riñón, bazo e hígado.
Los ensayos en los ratones C57BL/6 con las células B16-F10 con y sin expresión de Caveolina-1 mostraron una reducción del 60 % en el tamaño de los tumores formado por las células que expresaron Caveolina-1 comparado con las que no la expresaron. En los ensayos de metástasis, las células que expresaron Caveolina-1 causaron al menos dos veces más metástasis pulmonar. Estos resultados mostraron por primera vez en un modelo in vivo que Caveolina-1 es capaz de actúar tanto como supresor tumoral y como promotor de metástasis.
Usando el mismo modelo de estudio, para analizar el rol dual de Caveolina-1 continuamos con un análisis mutacional, específicamente usando una población celular que expresó Caveolina-1 no fosforilable en la posición de la Tirosina-14 (B16-F10(cav-1/Y14F) y se realizaron los ensayos de supresión de tumor y metástasis. Los resultados revelaron que Tirosina-14 era esencial para otorgarla a Caveolina-1 la capacidad de actúar como una molécula promotora de metástasis, pero al mismo tiempo este residuo no era esencial para el rol supresor de tumores.
Por otra parte, evaluamos in vivo la capacidad de E-cadherina de modular los dos roles descritos para Caveolina-1 en las células B16-F10. En estas, la presencia de E-cadherina cumple una función sinérgica sobre Caveolina-1 en su rol supresor de tumores, llegando incluso a inhibir completamente la formación de tumor dependiendo de la expresión de E-cadherina de manera directamente proporcional. Al mismo tiempo E-cadherina mostró frenar el efecto promotor de metástasis dado por Caveolina-1, es decir, ambas proteínas juntas en las células B16-F10 evitan la formación de tumores metastasicos en el pulmón o en cualquier otra parte del cuerpo del animal. / Caveolin-1 is a membrane protein essential for the formation of caveolae, is involved in cholesterol transport, acts as a signaling scaffold protein and has been described as a tumor suppressor. On the other hand, the presence of caveolin-1 plays an essential role in cell polarization during the migration process as it controls the localization of signaling molecules and regulates the activation of proteins involved in migration. However, not only the presence of caveolin-1 is essential for cell migration, but also the phosphorylation of caveolin-1 on Tyrosine 14. Whereas cell migration is essential for metastasis, caveolin-1 has also been described as a promoter of metastasis. This dual behavior has caused controversy and led to a large number of investigations currently under development in the scientific community.
The main objective of my research is to establish, in an immunocompetent in vivo model, caveolin-1 whether or not this dual role in cancer melanoma. We study a model where we use mice C57-BL / 6 and tumor lines F0 B16, B16 and F10, both lines syngeneic with the strain C57-BL / 6, ie, no immune rejection. These cells to be inoculated subcutaneously in mice have the ability to form solid tumors and also, if injected intravenously, generate foci of metastases in the lungs of mice. Therefore, with this system we can study the dual role of caveolin 1 in the same model in vivo. Once inoculated animals in a case in the back of the animal (subcutaneously) and the lateral tail vein (intravenously), the cells follow the formation of tumors and quantified the lung metastases, respectively.
The tests performed in vivo in B16-F0 cells show that caveolin-1 is able to suppress tumor formation, slowing to twice the time of appearance of these. Metastases in trials of these same cells, caveolin-1 showed promote metastases not only in both lung metastatic lymph nodes showed kidney, spleen and liver. By silencing the expression levels of caveolin-1 in B16-F0 results showed that both roles of caveolin-1 is lost.
Trials in C57BL / 6 mice with B16 F10 cells with and without expression of caveolin-1 show that there is a 60% reduction in the size of tumors formed by cells expressing caveolin-1 compared with those without expressed. In trials of metastasis, the cells expressing caveolin-1 cause at least twice as lung metastases. These results show for the first time in an in vivo model that caveolin 1 is able to act as both tumor suppressor and a promoter of metastasis. Using the same model to study, to analyze the dual role of caveolin-1 continue with mutational analysis, specifically using a cell population that expresses caveolin-1 is not phosphorylated at the position of tyrosine-14 (B16 F10 (cav 1/Y14F) tests were performed in tumor suppression and metastasis. The results show that tyrosine-14 is essential for caveolin-1 to grant it the ability to act as a metastasis-promoting molecule, but at the same time, this residue is not essential for the role tumor suppressor.
Moreover, we evaluate in vivo the ability of E-cadherin to modulate the two roles described for caveolin-1 in B16-F10 cells. In these, the presence of E-cadherin plays a synergistic role of caveolin-1 in tumor suppressor role, even to completely inhibit tumor formation depending on the expression of E-cadherin in direct proportion. While E-cadherin stops the metastasis-promoting effect given by caveolin-1, ie both proteins together in B16 F10 cells prevent the formation of metastatic tumors in the lung or elsewhere in the body of the animal. / Conicyt; FONDECYT-FONDAP
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Development of liposomal formulations for photodynamic therapy of cancerRodrigues, Manuela Jorge Estevinho January 2011 (has links)
Tese de mestrado integrado. Bioengenharia. Universidade do Porto. Faculdade de Engenharia. 2011
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Evaluation of HFT's In Vitro and effects on the cells viabilityGarcia, Mónica Pereira January 2009 (has links)
Tese de mestrado. Engenharia Biomédica. Faculdade de Engenharia. Universidade do Porto. 2009
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Imunoexpressão da Caderina-E nas cervicites, nas lesões intraepiteliais escamosas e no carcinoma invasor do colo uterino / E-Cadherin immunoexpression in cervicitis, squamous intraepithelial lesions and invasive carcinoma of the uterine cervixCavalcante, José Roosivelt January 2013 (has links)
CAVALCANTE, José Roosivelt. Imunoexpressão da caderina-E nas cervicites, nas lesões intraepiteliais escamosas e no carcinoma invasor do colo uterino. 2013. 77 f. Dissertação (Mestrado em Patologia) - Universidade Federal do Ceará. Faculdade de Medicina, Fortaleza, 2013. / Submitted by denise santos (denise.santos@ufc.br) on 2013-11-13T16:09:56Z
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Previous issue date: 2013 / Cervical cancer is one of the most important public health problems around the world. About 17.540 new cases are expected, in Brazil, for 2013. Actually, it’s believed that the majority of cervical cancers begin with non invasive dysplastic lesions, the cervical intraepithelial neoplasias. The acquisition of invasive properties, in epithelial malignancies, is associated to the disruption of intercellular adhesions. The adhesion molecules play a pivotal role in these intercellular bindings and E-cadherin is considered one of the most important among them. In normal epithelial tissues its presence in cell membrane is recognized and it was shown that a down regulation of these proteins in the majority of solid tumors may contribute to facilitate the invasive process. The aim, of this research, was to investigate the E-cadherin immunoexpression in cervicitis, in SILs and in the invasive carcinomas of the uterine cervix. Samples specimens consisted of 83 cases of uterine cervical biopsies and conizations retrieved from the Department of Pathology and Forensic Medicine files of the Federal University of Ceará (Brazil) in 2007 and 2010, distributed, by diagnostic, as follows: Cervicitis = 8 cases; Low Squamous Intraepithelial Lesion (LSIL) = 24 cases; High Squamous Intraepithelial Lesion (HSIL) = 28 cases; and Invasive Carcinoma = 23 cases. Immunohistochemistry (IHC) was performed with the anti-E-cadherin monoclonal antibody and it was considered positive the membranar expression, and, negative, the absence of membranar expression. The Fisher’s exact test was the choice for the contingency tables calculations. The immunostaining results were: Cervicitis = (12%) negative and 7/8 (88%) positive cases to E-cadherin; LSILs = 7/24 (29%) negative cases and 17/24 (71%) positive; HSILs = 7/28 (25%) negative and 21/28 (75%) positive; Invasive Carcinoma = 19/23 (83%) negative and 4/23 (17%) positive. The negative expression was much more frequent in SILs (27%) when compared to cervicitis (12%), although no significant difference (p = 0,6657). In SILs, a bigger E-cadherin loss was noted in undifferentiated cells at the basal third of epithelial thickness. Finally it was shown that the absence of E-cadherin membranar expression was much more frequent in the uterine cervix invasive carcinoma when compared to LSILs and HSILs. These data showed the E-cadherin importance in cervical carcinogenesis, nonetheless, several aspects remain without explication and new researches are to be performed. / O câncer do colo do útero é um dos mais preocupantes problemas de saúde pública do planeta. São esperados para 2013, no Brasil, 17.540 casos novos. Acredita-se atualmente que a maior parte dos cânceres cervicais se desenvolve a partir das neoplasias intraepiteliais cervicais. A aquisição de propriedades invasivas dos tumores malignos está associada ao desequilíbrio nas adesões intercelulares. As moléculas de adesão têm papel fundamental nestas uniões e a caderina-E é uma das mais importantes. Está comprovada a sua presença na membrana celular de tecidos epiteliais normais e foi demonstrado que esta proteína tem sua expressão diminuída na maioria dos tumores sólidos, o que favorece o processo de invasão. O objetivo, neste estudo, foi investigar a imunoexpressão da caderina-E nas Cervicites, nas Lesões Intraepiteliais Escamosas (LIE) e no Carcinoma Invasivo do colo uterino. A amostra consistiu de 83 casos de biópsias e cones de colo do útero obtidos dos arquivos do Departamento de Patologia e Medicina Legal da Universidade Federal do Ceará, em 2007 e 2010, com os seguintes diagnósticos: Cervicite = 8 casos; Lesão Intraepitelial Escamosa de Baixo Grau (LIEBG) = 24 casos; Lesão Intraepitelial Escamosa de Alto Grau (LIEAG) = 28 casos; Carcinoma Invasor = 23 casos. A imunohistoquímica (IHQ) foi efetuada com o anticorpo monoclonal anti-caderina-E, tendo sido considerada positiva a presença de expressão membranar, e negativa, a ausência de expressão. O teste exato de Fisher foi utilizado para os cálculos das tabelas de contingencias. Os resultados da imunomarcação foram: Cervicites = 1/8 (12%) negativos e 7/8 (88%) casos positivos para caderina-E; LIEBG = 7/24 (29%) casos negativos e 17/24 (71%) positivos; LIEAG = 7/28 (25%) negativos e 21/28 (75%) positivos; Carcinoma Invasor = 19/23 (83%) negativos e 4/23 (17%) positivos. A expressão negativa foi muito mais frequente nas LIEs (27%), comparadas com as Cervicites (12%) apesar de diferença não significante (p = 0,6657). Nas LIEs, uma maior perda da caderina-E foi notada nas células menos diferenciadas do 1/3 basal da espessura epitelial. Finalmente, observou-se que a ausência de expressão membranar da caderina-E foi muito mais frequente no carcinoma epidermóide invasor do que nas lesões intraepiteliais escamosas do colo do útero. Estes dados mostraram a importância da caderina-E na carcinogênese do colo uterino, no entanto, muitos aspectos permanecem sem explicação e novos estudos são necessários.
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