Дисертації: "Carcinoma Prostata"

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Brasil, Antonio Augusto Azevedo Vital. "Atrofia prostática em espécimes de prostatectomia radical = há relação topográfica com neoplasia intraepitelial prostática alto grau e adenocarcinoma?" [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308454.

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Анотація:

Orientadores: Athanase Billis, Luciana Rodrigues de Meirelles
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-16T20:47:04Z (GMT). No. of bitstreams: 1 Brasil_AntonioAugustoAzevedoVital_M.pdf: 4698841 bytes, checksum: 5d8edbe0e4ce7ce977504d4197f2f985 (MD5) Previous issue date: 2010
Resumo: A relação entre a atrofia inflamatória com a neoplasia intraepitelial alto grau e o carcinoma, é controversa. Tem sido sugerida uma relação topográfica e que o epitélio proliferativo da atrofia inflamatória possa progredir para neoplasia intraepitelial prostática alto grau (NIPAG) e/ou carcinoma (CA). O propósito do nosso estudo foi analisar em espécimes de prostatectomia radical uma possível relação topográfica entre estas lesões. Um total de 3186 quadrantes pertencentes a 100 prostatectomias radicais completamente representadas, foi analisado. Determinou-se a frequência de quadrantes mostrando: somente atrofia inflamatória (AI), AI+CA, AI+NIPAG, ou AI+NIPAG+CA. A extensão e a distância entre as lesões foram avaliadas através de um método semiquantitativo de contagem de pontos previamente descrito. Também foram analisados focos de atrofia completa ou parcial sem inflamação. Os métodos estatísticos empregados foram os testes de Kruskal-Wallis e Mann-Whitney, e o coeficiente de correlação de Spearman. A média dos quadrantes exibindo somente AI, AI+CA, AI+NIPAG, e AI+NIPAG+CA foi 3.29, 2.51, 0.77, e 0.44; e a amplitude (0-21), (0-11), (0-6), (0-4), respectivamente (p<0.01). A maioria dos focos de AI estavam a uma distância >5mm dos focos de NIPAG e CA. Não houve correlação significativa entre a extensão da AI (p= 0.64, r= 0.05) com a extensão da NIPAG. Houve uma significativa correlação negativa entre a extensão da AI (p=0.01, r=-0.27) com a extensão do CA. Resultados similares foram encontrados considerando focos de atrofia com ou sem inflamação. Focos de atrofia parcial não evidenciaram inflamação crônica inespecífica. Nosso estudo não evidenciou associação topográfica significativa entre AI, NIPAG e/ou CA
Abstract: It is controversial whether there is any relationship of proliferative inflammatory atrophy (PIA) to high-grade prostatic intraepithelial neoplasia (HGPIN) and cancer (CA). It has been suggested a topographic relation and a potential of the proliferative epithelium in PIA to progress to HGPIN and/or CA. The aim of this study was to analyze in radical prostatectomies a possible topographic relation of the lesions. A total of 3186 quadrants from 100 whole-mount consecutive surgical specimens was examined. The frequency of quadrants showing: only PIA, PIA+CA, PIA+HGPIN, or PIA+HGPIN+CA was determined. Extent and distance between the lesions were evaluated by a semiquantitative point-count method previously described. We also studied foci with partial or complete atrophy without inflammation. The statistical methods included the Kruskal-Wallis and the Mann-Whitney tests and the Spearman correlation coefficient. The mean (range) of quadrants showing only PIA, PIA+CA, PIA+HGPIN, and PIA+HGPIN+CA was 3.29 (0-21), 2.51 (0-11), 0.77 (0-6), and 0.44 (0-4), respectively (p<0.01). Most of the foci of PIA were significantly located in a distance >5mm than <5mm from HGPIN or CA. There was no significant correlation between extent of PIA (p=0.64, r=0.05) with extent of HGPIN. There was a significant negative correlation of extent of PIA (p=0.01, r=-0.27) with extent of CA. Similar results were found considering foci either with or without inflammation. Chronic inespecific inflammation was not seen in foci of partial atrophy. A topographic relation of PIA to HGPIN and/or CA was not supported by our study
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas

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2

Silva, Elcio Dias 1951. "Margens cirurgicas na prostatectomia radical : comparação entre cirurgia retropubica e laparoscopica." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312194.

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Анотація:

Orientador: Ubirajara Ferreira
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-06T11:07:31Z (GMT). No. of bitstreams: 1 Silva_ElcioDias_M.pdf: 1742572 bytes, checksum: db8e0fccf7f5b7dd66a71b32ca51cacc (MD5) Previous issue date: 2006
Resumo: Introdução: margem cirúrgica comprometida ou positiva é definida como tumor estendendo-se na superfície de corte do cirurgião. A porcentagem deste evento, resultante de incisão capsular, varia de 1,3 a 71 % (EPSTEIN, 2001). O objetivo deste estudo é comparar o comprometimento das margens cirúrgicas nas prostatectomias radicais realizadas por via retropúbica e laparoscópica, em dois serviços de referência no Brasil. Pacientes e Métodos: foram analisados os exames anátomo-patológjcos de 179 pacientes submetidos a prostatecomia radical por adenocarcinoma de próstata, 89 por via retropúbica e 90 por via laparoscópica. Critérios de inclusão: pacientes com PSA (antígeno específico da próstata) igual ou menor que 15 ng/ml (nanogramas por mililitro) e Gleason igual ou menor que 7 na biópsia prostática, estádio clínico máximo T2. Resultados: houve comprometimento de margem cirúrgica em 41,57 % dos pacientes submetidos à PRR (prostatectomia radical retropúbica), distribuídos da seguinte maneira: 34,21 % nos estádios pT2 (7,69 % no pT2a, zero no pT2b e 40,98 % no pT2c) e 84,61% nos estádios pT3 (77,77 % no pT3a e 100 % no pT3b). Nos pacientes submetidos a PRL (prostatectomia radical laparoscópica) houve margens cirúrgicas positivas em 24,44 % dos pacientes, distribuídos da seguinte maneira: 20,98 % nos estádios pT2 (11,11 % no pT2a, 27,27 % no pT2b e 21,31 % no pT2c) e 55,55 % nos estádios pT3 (zero % no pT3a e 62,50 % no pT3b). Conclusão: nas amostras analisadas, a proporção de margem cirúrgica positiva foi maior nas prostatectomias radicais realizadas pela via retropúbica do que pela laparoscópica (p= 0,023), em dois serviços de referência nas respectivas técnicas, no Brasil. No entanto, o fato das cirurgias retropúbicas serem realizadas por médicos residentes, em instituição de ensino, e as laparoscópicas realizadas por um único cirurgião experiente, e os exames anátomo-patológicos realizados por técnicas e patologistas distintos, não permite a generalização dos resultados. Maior número de pacientes em estudo prospectivo e randomizado seria necessário para uma melhor comparação entre os grupos
Abstract: Introduction: Compromised or positive surgical margin is defined as a tumor extending at the surgeon cutting surface. A percentage from this event, resulted from capsular incision, varies from 1.3 to 71% (EPSTEIN, 2001). The goal of this study is to compare the compromising of surgical margins at the radical prostatectomies performed through both retropubic and laparoscopic way, in two reference medical services in Brazil. Patients and Methods: pathological examinations were analyzed from 179 patients who underwent to radical prostatectomy by prostate adenocarcinoma, 89 patients by retropubic and 90 patients by laparoscopic way. Inclusion criteria: patients with PSA (prostate specific antigen) equal or less than 15 ng/ml (nanograms by miiiliter) and Gleason score equal or less than 7 at the prostate biopsy, maximum clinical T2 stage. Results: There has been compromising of the surgical margin in 41,57% of the patients who underwent to RRP (radical retropubic prostatectomy), distributed in the following way: 34,21% at pT2 stage (7,69% at pT2a, 0% at pT2b and 40,98% at pT2c) and 84,61% at pT3 (77,77% at pT3a and 100% at pT3b) stage. In the patients who had undergone to LRP (Laparoscopic Radical Prostatectomy), there have been positive surgical margins in 24,44% of the patients as following: 20,98% at pT2 stage (11,11% at pT2a. 27,27% at pT2b and 21,31% at pT2c stage) and 55,55% at pT3 stage (0% at pT3a and 62,50% at pT3b) Conclusion: At the analyzed samples, the proportion of positive surgical margin was greater at the radical prostatectomy performed by retropubic route than by laparocospic one (p=0,023), in two reference medical services using the respective techniques in Brazil. However, the fact that the retropubic surgeries were performed by resident doctors, in teaching school-hospital institution, while the laparoscopic ones were performed by a single expert surgeon and that the pathological examinations were performed by both distinct techniques and pathologists, the result generalization is not allowed. A greater number of patients in a randomized and prospective study would be necessary for a better comparison between the groups
Mestrado
Cirurgia
Mestre em Cirurgia

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Worschech, Adriana. "Atrofia parcial em biopsias de agulha de prostata : Util no diagnostico diferencial entre carcinoma e atrofia da prostata?" [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308445.

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Анотація:

Orientador: Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-11-07T16:10:17Z (GMT). No. of bitstreams: 1 Worschech_Adriana_M.pdf: 2136837 bytes, checksum: e169d43b81c649e3dde44c36f7a96278 (MD5) Previous issue date: 2008
Resumo: A atrofia parcial (AP) é uma lesão benigna que mais freqüentemente imita adenocarcinoma, particularmente a variante parcial. AP ocorre com maior freqüência no lobo posterior ou zona periférica e ganhou importância maior com o uso das biópsias por agulha na detecção do carcinoma prostático. A atrofia parcial e a hiperplasia pós-atrófica (atrofia hiperplásica) são as lesões benignas que mais freqüentemente são confundidas com adenocarcinoma. Uma das razões que contribuem para dificultar o diagnóstico da atrofia parcial está relacionada com a ausência de células basais em alguns ácinos. Mais recentemente a aplicação da molécula de AMACR (alfa-metilacil Co-enzima A racemase) como marcador de células neoplásicas através de imunoistoquímica tem auxiliado no diagnóstico diferencial com o adenocarcinoma. Entretanto, sua aplicação na rotina diagnóstica ainda não está estabelecida. A imunoexpressão da AMACR pode causar algumas dúvidas em sua interpretação. Na literatura existem poucos estudos que relatam a expressão da AMACR em atrofia parcial. Avaliamos através da imunoistoquímica a expressão da AMACR e do 34ßE12 (citoqueratina de alto peso molecular) através do coquetel P504S+34ßE12 em material proveniente de 74 biópsias por agulha de próstata correspondendo a 61 pacientes. Foram analisados um total de 1198 ácinos prostáticos (324 ácinos com adenocarcinoma, 213 ácinos normais, 190 ácinos com atrofia parcial, 298 ácinos com hiperplasia pós-atrófica, 139 ácinos com atrofia simples e 34 ácinos com atrofia esclerosante). Nos ácinos com adenocarcinoma a intensidade da marcação da AMACR foi forte em 251/324 (77.5%) e fraca 73/324 (22.5%). Não houveram casos negativos. Nos ácinos normais observou-se marcação para a AMACR forte em 13/213 (6.1%), fraca em 33/213 (15.5%) e negativa em 167/213 (78.4%). A atrofia parcial apresentou marcação para a AMACR fraca em 47/190 (24.7%) e negativa em 143/190 (75.3%). Não houve marcação forte em nenhum dos casos de atrofia parcial. Os ácinos normais mostraram expressão para AMACR negativo, fraco e forte onde os valores foram respectivamente 167/213 (78,4%), 33/213 (15,5%) e 13/213 (6,1%). A atrofia parcial mostrou-se negativa, e fraca para imunoexpressão da AMACR em 143/190 (75,3%) e 47/190 (24,7%) respectivamente. Não foi observada forte positividade em atrofia parcial, no entanto, a fraca positividade observada em cerca de 25% dos ácinos pode causar dificuldade para a interpretação correta no diagnóstico diferencial de câncer e atrofia parcial. A AMACR foi negativa em todos os ácinos da atrofia simples, hiperplásica (ou hiperplasia pós-atrófica) e esclerosante, por conseguinte, sem qualquer ajuda no diagnóstico diferencial de adenocar-cinoma. A distribuição das células basais, observadas na atrofia simples, hiperplásica e esclerosante foram descontínuas e as células do compartimento secretor mostraram imunoexpressão aberrante de 34ßE12 sugerindo um fenótipo intermédio. Analisando-se os estes resultados conclui-se que o diagnóstico diferencial do adenocarcinoma com atrofia parcial deve ser feito com cautela considerando-se que a expressão da AMACR, apesar de fraca em nosso estudo, pode ocorrer em cerca de 25% dos ácinos. Soma-se a este achado o fato de que em 23.2% dos ácinos de atrofia parcial as células basais estão ausentes. Estes dados impõem cautela no difícil diagnóstico diferencial de pequenos focos "suspeitos, mas não diagnósticos de adenocarcinoma da próstata", sendo que, em alguns casos, os critérios puramente morfológicos poderão ser os únicos na identificação da lesão.
Abstract: Prostatic atrophy (PA) is the benign lesion that most frequently mimicks adenocarcinoma particularly the partial variant. PA occurs more frequently in the peripheral zone and gained greater importance with the use of needle biopsies in detecting cancer of the prostate. Partial atrophy and post-atrophic hyperplasia (hyperplastic atrophy) are the benign lesions that most often are confused with adenocarcinoma. One of the reasons that contribute to make the diagnosis of partial atrophy difficult is related to the absence of basal cell in some acini. More recently the application of AMACR (alpha-metilacil Co-enzyme A racemase) as a marker of malignant cells through immunohistochemistry has helped in the differential diagnosis with prostate cancer. However, its application in routine diagnosis is not yet established. The immunoexpression of AMACR may cause some doubt in interpretation. In literature there are few studies that reported the expression of AMACR in partial atrophy. We evaluated by immunohistochemistry the expression of AMACR and 34ßE12 (cytokeratin high-molecular weight) using the cocktail P504S +34ßE12 in 74 needle prostatic biopsies corresponding to 61 patients. We analyzed a total of 1198 prostate acini (324 acini with adenocarcinoma, 213 normal acini, 190 acini with partial atrophy, 298 acini with post-atrophic hyperplasia, 139 acini with simple atrophy and 34 acini with sclerosing atrophy). In adenocarcinoma acini the staining of AMACR was strong in 251/324 (77.5%) and weak in 73/324 (22.5%). There were no negative acini. In normal acini AMACR was strong in 13/213 (6.1%), weak in 33/213 (15.5%) and negative in 167/213 (78.4%). In partial atrophy, acini showed weak AMACR in 47/190 (24.7%) and were negative in 143/190 (75.3%). There was no strong staining in partial atrophy. The immunoexpression of AMACR was negative in all variants of complete atrophy: simple atrophy, hyperplastic atrophy and sclerosing atrophy. Normal acini showed negative, weak, or strong expression in 167/213 (78.4%), 33/213 (15.5%), and 13/213 (6.1%) acini, respectively. Partial atrophy showed negative, and weak expression in 143/190 (75.3%), and 47/190(24.7%) acini, respectively. No strong positivity was seen in partial atrophy, however, the weak positivity seen in approximately 25% of the acini may be a pitfall for the correct interpretation in the differential diagnosis of cancer and partial atrophy. AMACR was negative in all acini of simple, postatrophic hyperplasia and sclerosing atrophy, therefore, with no help in the differential diagnosis of adenocarcinoma. The distribution of basal cells in simple, postatrophic hyperplasia and sclerotic atrophy was discontinuous and the cells of the secretory compartment showed aberrant expression of 34ßE12 suggesting an intermediate phenotype. Analyzing these results it is concluded that the differential diagnosis of prostate cancer with partial atrophy must be done carefully considering that the expression of AMACR, although weak in our study, can occur in about 25% of the acini. Furthermore, in 23.2% acini of partial atrophy the basal cells are absent. In some cases the microscopic identification of partial atrophy will rely only on morphologic criteria.
Mestrado
Ciencias Biomedicas
Mestre em Ciências Médicas

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Ferreira, Ubirajara 1956. "Valor do toque retal na detecção do carcinoma da prostata." [s.n.], 1988. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309369.

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Анотація:

Orientador : Nelson Rodrigues Netto Junior
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-07-15T00:09:21Z (GMT). No. of bitstreams: 1 Ferreira_Ubirajara_M.pdf: 499048 bytes, checksum: 2798bf061519ed1b76fc43fee13efca4 (MD5) Previous issue date: 1988
Resumo: Com o intuito de quantificar o valor do toque retal no diagnóstico das neoplasias malignas submetemos 125 pacientes portadores de próstata prostáticas, com características palpatórias suspeitas de câncer, com idade variando de 47 a 90 anos, a 137 biópsias transretais da vaglândula prostática (BTR). Analisamos ainda, os índices de positividade para câncer à BTR de acordo com as faixas etárias, com a queixa principal e com os estadiamentos clínicos ao toque retal. Concluímos que: 1) O valor preditivo positivo do toque retal suspeito de câncer foi de 39,2%; 2). O índice de positividade nos paciente com próstata muito suspeita (Estádio C, 53,5%) foi significantemente maior do que nos pacientes com próstata pouco suspeita (Estádio B, 27,5%) 3) A incidência de câncer prostático foi maior nos indivíduos com idade acima de 80 anos e nos que não apresentavam prostatismo como queixa principal.
Mestrado
Mestre em Ciências Médicas

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5

SORRENTINO, Domenico. "L’espressione del PCA3 in pazienti a rischio di carcinoma della prostata: uno studio prospettico." Doctoral thesis, Università degli Studi di Palermo, 2014. http://hdl.handle.net/10447/91194.

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6

Souza, Carlos Alberto Fontes de. "Carcinoma histologico da prostata em autopsias : frequencia, origem, extensão, graduação e nomenclatura." [s.n.], 2003. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308449.

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Анотація:

Orientador: Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-03T16:53:25Z (GMT). No. of bitstreams: 1 Souza_CarlosAlbertoFontesde_M.pdf: 8934988 bytes, checksum: 7aa3de870e5f17a1b307904b48410892 (MD5) Previous issue date: 2003
Resumo: Objetivos: Estudar a Freqüência do carcinoma incidentalmente encontrado em autópsias, procurar alguma evidência morfológica para um possível melhor comportamento quando a neoplasia se origina na zona de transição, analisar a graduação histológica e discutir a terminologia empregada para se referir a esta neoplasia. Material e Métodos: As próstatas de autópsias de 150 homens com mais de 40 anos de idade foram dissecadas em zonas de transição e periférica através de um corte passando por um plano indicado pelo trajeto do ducto ejaculador e procederam-se cortes frontais seriados em intervalos de 0,3 a 0,5cm. No exame microscópico dos cortes observou-se presença ou não de adenocarcinoma, extensão da neoplasia avaliando-se o número de fragmentos que a apresentavam e a graduação histológica utilizando-se o sistema Gleason. Os dados foram analisados estatisticamente pelo teste do X2 para diferenças entre proporções ao nível de significância de 0,05...Observação: O resumo, na íntegra, poderá ser visualizado no texto completo da tese digital
Abstract: Objectives: To study the frequency of incidentally found carcinoma of the prostate in autopsies, to find any morphological evidence for a possible better behavior when neoplasia originates in the transition zone, to analyze the histologic grading, and to discuss the terminology used when referring to this neoplasia. Material and methods: The prostates from 150 autopsied men were dissected in transition and peripheral zones through a section passing a plane indicated by the course of the ejaculatory duct, and a step section method was used to cut the prostate in coronal planes in intervals of 0,3-0,5cm. The microscopic examination included presence or absence of carcinoma, extension evaluated according to the percentage of sections showing the neoplasia and histologic grading according to the Gleason system. The data were statistically analyzed thrugh the chi-square test to determine the differences in proportion at a significance level of O,05 ...Note: The complete abstract is available with the full electronic digital thesis or dissertations
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas

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7

Hopp, Renato Nicolás 1984. "Correlação entre a proporção 2D:4D, carcinoma espinocelular oral e adenocarcinoma de prostata." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289241.

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Orientador: Jacks Jorge Junior
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
Made available in DSpace on 2018-08-15T05:55:23Z (GMT). No. of bitstreams: 1 Hopp_RenatoNicolas_M.pdf: 862592 bytes, checksum: 59ebe0fd5b004e6abb8300211e9a8e2c (MD5) Previous issue date: 2010
Resumo: A relação entre o dedo indicador e o dedo anelar também chamada 2D:4D tem sido utilizada por pesquisadores como possível marcador de comportamento humano, de características psicológicas e até mesmo de doenças influenciadas pelo gênero. A diferença entre o segundo e o quarto dedo das mãos é estabelecida ainda no útero, parece não ser afetada pela puberdade e reflete um fator importante - a exposição intra-uterina a hormônios sexuais, estrógeno, progesterona e testosterona. A ligação entre a formação dos dedos e a exposição à testosterona ou ao estrógeno parece estar associada à ação dos genes da família Homeobox ou Hox que são essenciais para a diferenciação tanto dos dedos quanto do sistema urogenital. Também é postulado que o comprimento dos dedos das mãos pode estar ligado a seqüências de nucleotídeos do gene receptor de andrógenos. Este estudo objetivou avaliar a possível associação entre a relação 2D:4D e a prevalência do carcinoma espinocelular oral e do adenocarcinoma de próstata, bem como estabelecer um padrão de normalidade para esta relação em uma população da cidade de Piracicaba - SP. Ao todo, 265 indivíduos entre 18 e 80 anos tiveram a palma da mão direita fotografada por câmera digital acoplada a um dispositivo padronizador desenvolvido para este estudo, além de responder a perguntas sobre hábitos como etilismo e tabagismo, freqüência de exames para a prevenção de câncer e incidência de distúrbios hormonais. Todas as fotos foram feitas por um único examinador. Os indivíduos foram divididos em cinco grupos, carcinoma espinocelular (CEC, n=50), lesão pré-maligna (PM, n=50), sem lesão (NOR, n=50), hiperplasia prostática benigna (HPB, n=49) e câncer de próstata (PRO, n=27), subdivididos por gênero. Os dados foram analisados estatisticamente utilizando teste t de Student e ANOVA no software Microsoft Excel®. Neste estudo, homens apresentaram 2D:4D significativamente mais baixo do que mulheres (p=0,03). Foi encontrada correlação significativamente negativa entre 2D:4D e o aparecimento do carcinoma espinocelular oral em mulheres quando comparado a pacientes sem lesão e correlação positiva quando comparados a lesões pré-malignas (p=0,04 e p=0,02 respectivamente). Homens sem lesão oral tiveram 2D:4D mais alto em comparação com homens com lesões pré- malignas e mais baixo em comparação com homens que tinham lesões orais malignas, no entanto este dado não foi significativo. Homens com 2D:4D baixo apresentaram maior prevalência de câncer de próstata quando comparados com portadores de hiperplasia prostática benigna e a pacientes sem lesão, porém este dado não foi significativo. O método digital de análise da proporção 2D:4D apresentou facilidade de uso, reprodutibilidade significativa e baixo custo. Ainda são precoces as correlações que podem ser estabelecidas entre o 2D:4D e as lesões orais e prostáticas malignas e pré-malignas. Esta proporção poderia contribuir, em acréscimo, à pesquisa dos fatores de risco classicamente descritos e como fator adicional na orientação de pacientes sob risco de desenvolver tais lesões. No entanto, estudos adicionais são necessários para confirmar a validade desta correlação.
Abstract: The ratio between the index and ring finger, also called 2D:4D, has been attributed by researchers as a possible marker for a plethora of conditions involving human behavior, psychological traits and gender-linked diseases. The difference between these fingers is established in utero, seems not to be affected by puberty and reflects an important factor - intra-uterine exposure to sex hormones estrogen, testosterone and progesterone. The link between finger development and exposure to testosterone or estrogen seems to be connected in the action of the Homeobox gene family, which is crucial for the development of both fingers and urogenital system. It is also postulated that finger length may be connected to nucleotide sequences of the androgen receptor gene. This study aimed to evaluate the possible association between 2D:4D and the incidence of squamous cell carcinoma and prostate cancer, as well as to establish a normal pattern for this ratio in a population of Piracicaba - SP. A sum of 265 subjects between 18 and 80 years of age had photographs of their right hands taken by a digital camera using a standardizing device. They also responded to a questionnaire regarding habits as tobacco and alcohol consumption, frequency of preventive cancer examination, and incidence of hormonal disturbances. All photographs were taken by a single examiner. Individuals were assigned to five groups, squamous cell carcinoma (SCC, n=50), pre-malignant lesions (PML, n=50), no lesion (NOL, n=50), benign prostatic hyperplasia (BPH, n=49) and prostate cancer (PCA, n=27), subdivided by gender. Statistical analysis was performed by means of Student's t test and ANOVA on Microsoft Excel®. Finger length ratio was significantly lower for males (p=0,03). We found a significantly negative correlation between 2D:4D and the prevalence of squamous cell carcinoma and a significantly positive correlation between 2D:4D and pre-malignant lesions in women (p=0.04 and p=0.02 respectively). Male patients with prostate cancer presented higher prevalence of prostate cancer when compared to patients with benign prostatic hyperplasia and patients without prostatic lesions, but this was not significant. Finger length ratio and its relation to oral and prostatic lesions is still in early development. Research may contribute in the future as an additional factor regarding the influence of classically known etiological factors and as an educational factor for patients under risk of developing such diseases. Additional research is still necessary to confirm the validity of this correlation.
Mestrado
Patologia
Mestre em Estomatopatologia

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Gurgel, da Trindade Meira Henriques Luciana. "Avaliação imunohistoquímica com marcador de citoqueratina de alto peso molecular (34BE12) na caracterização de benignidade em lesões da próstata." Universidade Federal de Pernambuco, 2003. https://repositorio.ufpe.br/handle/123456789/8932.

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Os carcinomas da próstata são as neoplasias malignas de maior prevalância no sexo masculino. Na última década os progressos na tecnologia de imagem, através da punção-biópsia sob controle ultra-sonográfico e a utilização dos exames bioquímicos para detecção do antígeno prostático específico, tornaram possível o diagnóstico de lesões iniciais, muitas em pacientes mais jovens. Como conseqüência, para o patologista vieram as dificuldades de interpretação de lesões muito pequenas ou histologicamente mal definidas, como a diferenciação entre hiperplasia adenomatosa atípica e adenocarcinoma bem diferenciado. Termos como proliferação de pequenas glândulas de significado incerto passaram a ser utilizados para as lesões duvidosas, requerendo progredir na investigação. A literatura tem demonstrado que a imunomarcação pelo anticorpo monoclonal anti-citoqueratina de alto peso molecular (34βE12) é útil na confirmação de benignidade pela demonstração da camada de células basais. Em nosso meio esse marcador tem sido pouco utilizado. O estudo em tela visa analisar os primeiros resultados do método no Departamento de Patologia do Hospital de Câncer de Pernambuco. A partir dos arquivos deste serviço, foram selecionados 20 casos de um total de 172 registrados entre junho de 1997 e março de 2002. Esses casos constituiram dois grupos, o primeiro formado por dez casos com diagnóstico de hiperplasia nodular benigna da próstata e o segundo por dez casos de adenocarcinoma prostático. Cada grupo incluiu 20 espécimes, dez obtidos por punção-biópsia e dez por ressecção cirúrgica, constituindo 40 amostras para revisão histológica e realização do exame imunohistoquímico. A imunomarcação demonstrou a camada de células basais em todas as lesòes benignas tanto no material de punção-biópsia (10/10), como nas peças cirúrgicas (10/10) revelando 100% de positividade. Nos casos de adenocarcinoma, não houve demonstração da camada de células basais, tanto no material de punção-biópsia (10/10) quanto no de prostatectomia (10/10), resultando em 100% de negatividade. Os resultados confirmam os dados da literatura quanto à acurácia do método na confirmação da existência da camada de células basais, sendo recomendável no esclarecimento de lesões duvidosas para exclusão de malignidade

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Braglia, Luca <1993&gt. "Identificazione di un nuovo meccanismo microRNA-dipendente di resistenza all'inibizione della via di segnale PI3K/AKT nel carcinoma della prostata." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amsdottorato.unibo.it/10259/1/Braglia_Luca_Tesi.pdf.

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Benché le alterazioni della via PI3K/AKT siano molto sudiate a causa del loro ruolo nella tumorigenesi, e rappresentino pertanto un importante bersaglio terapeutico, i risultati di numerosi studi clinici con inibitori di PI3K o AKT sono finora deludenti, in parte a causa dell’insorgenza di resistenza provocata dall'interruzione dei circuiti di feedback negativo. In questo studio, abbiamo scoperto che l’inattivazione farmacologica di AKT in cellule di carcinoma prostatico PC3 porta alla down-regolazione di un microRNA con funzione di oncosoppressore, il miR-145-5p, e ad un drammatico aumento di espressione di uno dei suoi geni target, cioè N/KRas. E’ interessante sottolineare che questo microRNA è considerato un marker di progressione metastatica nel carcinoma prostatico, il cui livello di espressione aiuta a discriminare tra pazienti con iperplasia prostatica benigna e cancro alla prostata. Inoltre, la bassa espressione di miR-145 aumenta il rischio di progressione della malattia da localizzata a metastatica. La conferma che l’aumento di Ras, osservato sia in termini di mRNA che di proteina, è dipendente dalla caduta del miR-145-5p, è stata poi ottenuta tramite un modello di PC3 ingegnerizzate per ottenere il silenziamento inducibile del miR-145-5p. Tramite un array di fosfoproteine siamo poi stati in grado di verificare che l’aumento di Ras provoca la riattivazione della cascata di PI3K/AKT e di ERK. Dal punto di vista meccanicistico, quindi, lo studio ha portato all’identificazione di un nuovo meccanismo di resistenza adattativa, in cui l’inattivazione di AKT provoca una caduta del miR-145-5p che, a sua volta, aumenta l’espressione di Ras e riattiva il signaling di PI3K, rendendo inefficace il trattamento farmacologico. Questi risultati sono particolarmente rilevanti alla luce di recenti studi (NCT04493853; NCT03072238; NCT02525068) e di trial clinici in corso (NCT04737109; NCT03673787), basati sulla somministrazione combinata di inibitori della sintesi degli androgeni con gli inibitori di AKT capitasertib o ipatasertib.
Although aberrantly active PI3K / AKT pathway is regarded as a main therapeutic target due to its role in tumorigenesis. It therefore not surprising that a number of inhibitory drugs have been trialled for both solid and hematological malignancies. however, the results of clinical studies with such PI3K or AKT inhibitors have been so far disappointing, also because of resistance caused by interruption of negative feedback circuits. In this study, we found that pharmacological inactivation of AKT in PC3 prostate cancer cells leads to down-regulation of a tumor suppressor microRNA, miR-145-5p and to a dramatic increase in the expression of one of its target genes, namely N / KRas. Interestingly, levels of miR-145 help discriminate between benign prostatic hyperplasia and prostate cancer patients, while miR-145 loss increases risk for localized to metastatic disease progression. Low expression of miR-145 is part of a miRNA signature to predict poor survival of PC patients. Confirmation that the observed drop of miR-145-5p triggers an increase of Ras, detected both in terms of mRNA and protein, was obtained using PC3 cells engineered by us to transiently silence the 145-5p guide strand of miR-145 following exposure to doxycycline. Furthermore, through a phosphoprotein array we were then able to validate that such burst of Ras expression elicits reactivation of both the PI3K / AKT and ERK cascades. From a mechanistic point of view, therefore, this study led to the identification of a new adaptive resistance mechanism, in which the inactivation of AKT causes a down-regulation of miR-145-5p, which, in turn, increases Ras expression and reactivates PI3K signaling, lessening drug treatment efficacy. These results are particularly relevant in light of recently published (NCT04493853; NCT03072238; NCT02525068) as well as ongoing (NCT04737109; NCT03673787) clinical trials, based on the combination of androgen deprivation therapy with the AKT inhibitors capitasertib or ipatasertib.

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D'AMICO, FRANCA. "Studio dell'espressione dei geni del metabolismo degli androgeni e caratterizzazione del profilo citogenetico per la ricerca di biomarcatori genomici in linee primarie di carcinoma della prostata." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/680.

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Obiettivi principali di questa tesi di dottorato sono lo studio dell’espressione genica e del profilo citogenetico, basato sulla tecnologia dei microarrays, per l’identificazione di potenziali biomarcatori genomici quali geni candidati per la comprensione della patogenesi molecolare del tumore della prostata, in linee primarie ottenute da campioni di carcinoma prostatico dopo rimozione chirurgica e lo studio degli eventuali geni differenzialmente espressi nelle colture primarie in linfociti estratti da sangue periferico di pazienti affetti da carcinoma prostatico e non trattati farmacologicamente, allo scopo di verificare se l’espressione differenziale è riscontrata anche nel sangue. E’ stato costruito un array a bassa densità costituito da 205 geni (“androchip”) selezionati sulla base del loro provato o potenziale ruolo nella cancerogenesi del carcinoma prostatico relazionati al pathway degli androgeni. E’ stata osservata un’alterata espressione dei geni coinvolti nella progressione verso l’androgeno indipendenza (BCL2, CALR e VIM) e nel contempo una diminuzione del gene PKC-beta, marcatore delle fasi iniziali della progressione del tumore. Inoltre è stato riscontrato un elevato aumento dell’espressione del gene NQO1. Questo gene è in grado di trasformare un farmaco anti tumorale, il β-lapacone, nella sua forma attiva e pertanto potrebbe essere un gene chiave nelle scelte terapeutiche da parte dei clinici. D’altro canto, dopo gli esperimenti di a-CGH non si è riscontrata alcuna anomalia a carico del corredo genomico delle linee primarie analizzate ad eccezione della perdita del cromosoma Y riscontrata in una linea primaria su dieci analizzate, prima con la piattaforma a BAC e confermata con la piattaforma Agilent a oligonucleotidi. Per quanto riguarda lo studio dei biomarcatori nel sangue di pazienti affetti da carcinoma prostatico, sono stati analizzati i geni NQO1, PKC-beta, BCL2 e ERBB2. Nel complesso i nostri dati hanno mostrato una effettiva variazione dell’espressione dei quattro geni esaminati. in particolare abbiamo riscontrato, in alcuni pazienti, una diminuzione dell’espressione di PCK-beta, gene ipo-espresso nelle primissime fasi della malattia e un aumento di espressione del gene ERBB2, gene correlato ad androgeno indipendenza e metastasi. In conclusione, questo lavoro ha portato all’individuazione di marcatori di prognosi sfavorevole in linee primarie ottenute da pazienti con carcinoma prostatico e all’identificazione e alla conferma del potenziale ruolo del gene ERBB2 come marcatore di prognosi nel sangue.
The aims of this study where to investigate expression profiles of genes related to androgen signaling and to screen genomic alterations in primary epithelial cultures derived from tissue explanted from patients undergoing radical prostatectomy to better understanding the rule of androgen pathway and of genomic copy number changes in the development and progression of prostate cancer. Moreover, we investigated expression profiles of selected genes (NQO1, PKC-beta, BCL2 e ERBB2) in circulating blood cells of prostate cancer patients to discover new biomarkers for diagnostic purposes. To carry out these aims we developed a low density home made oligonucleotide-array composed of 205 genes selected on the basis of their proved or potential role in prostate cancerogenesis related to androgen signalling (“AndroChip”), and we carried out array-based comparative genomic hibridization (aCGH) on primary epithelial cultures derived from tissue explanted from patients undergoing radical prostatectomy. After microarray experiments, considering only genes resulted significant in all primary cancer cell lines and whose differential expression had a threeshold>±1,5, we identified a total of 15 genes. In summary, we observed differential expression of genes (BCL2, CALR e VIM) able to confer androgen- independent growth and down regulation of PKC-beta gene that may be down-regulated at an early stage in the pathogenesis of prostate cancer. Moreover, we found over expression of NQO1 gene. High levels of NQO1 gene expression have been observed in many cancers as compared to normal tissues of the same origin. NQO1 bioactivates an anti-cancer agent, Beta-lapachone and so this gene could be exploitable target for the treatment of cancer cells that overexpress this enzyme. After aCGH experiment, we did not reveal genomic imbalances in 9 of the 10 samples examined. In one semple we detected the loss of the Y chromosome. These results demonstrate that no specific genomic biomarkers are detectable for early stage prostatic cancer. Moreover, we studied NQO1, PKC-beta, BCL2 e ERBB2 expression by RT-PCR real-time in peripheral blood mononuclear cell fraction samples of 7 patients with prostate cancer. All thogether, our results showed an differential expression profiles of examinated genes. In particular, we found down regulation of PCK-beta and up regulation of ERBB2. In conclusion, this study allowed to identify prognosis biomarkers in primary cell lines and confirmed that ERBB2 gene can be use as prognosis marker in blood.

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Friedrich, Beate. "Cathepsine B, H, L und ihre Inhibitoren im Gewebe und in Zellkulturen der Prostata." Doctoral thesis, [S.l.] : [s.n.], 1999. http://deposit.ddb.de/cgi-bin/dokserv?idn=957675186.

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Agostini, Michelle. "Estudo da expressão da enzima desubiquitinante USP2a e de sua interação com a proteina clatrina em celulas derivadas de carcinomas espinocelulares bucais e de prostata humanos." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/290694.

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Orientador: Edgard Graner
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: O sistema ubiquitina-proteossomo degrada proteínas marcadas com etiquetas de Ub. A ubiquitinação é um processo reversível e moléculas de Ub podem ser desconjugadas pelas enzimas desubiquitinantes (DUBs), que evitam a degradação e aumentam a meia vida de seus substratos. A DUB USP2a foi identificada na próstata humana, é regulada por andrógenos e tem sua expressão aumentada em adenocarcinomas. USP2a protege a enzima ácido graxo sintase (FAS) da degradação, a qual é superexpressa em vários tipos de tumores, inclusive nos carcinomas espinocelulares (CECs) bucais. O objetivo deste trabalho foi estudar a expressão desta DUB e seu papel biológico em células derivadas de CECs bucais humanos. Foram detectados RNAs mensageiros para USP2a nas quatro linhagens celulares estudadas, principalmente nas linhagens SCC-4 e -15. Os níveis protéicos de USP2a foram semelhantes nas quatro linhagens, sendo ligeiramente maiores na SCC-9 e -25. Portanto, não foi encontrada uma correlação entre a quantidade de RNAs mensageiros e dos produtos protéicos de USP2a. Através de experimentos de imunofluorescência, demonstramos USP2a no citoplasma das células SCC-9, havendo uma concentração na região perinuclear em algumas células. A expressão forçada de USP2a nas células SCC- 9 não conferiu vantagem proliferativa, no entanto, a superexpressão de um duplomutante parece ter diminuído a proliferação. Ao contrário do que ocorre nas células LNCaP, a inibição da expressão de USP2a através de RNAi nas células SCC-9 causou discreta indução de apoptose. O tratamento das células SCC-9 com diferentes concentrações do fator de crescimento epidérmico (EGF) foi capaz de modular a expressão de USP2a, interferindo na quantidade de formas ubiquitinadas de FAS. Também foi investigada neste trabalho a possível interação entre USP2a e a proteína clatrina. De acordo com resultados prévios de experimentos realizados no laboratório do Dr. Massimo Loda, no Dana-Farber Cancer Institute, a cadeia pesada de clatrina é também substrato de USP2a. Clatrina é uma proteína que participa do processo de internalização e endocitose de proteínas localizadas na membrana plasmática. Demonstramos que USP2a e a cadeia pesada de clatrina estão co-localizadas no citoplasma de células AR-iPrEC e SCC-9 e que a produção de clatrina é regulada por andrógenos em células LNCaP. Houve uma maior produção de clatrina em células que superexpressam de forma estável USP2a. Um achado interessante foi que USP2a, além de presente no citoplasma, foi também encontrada na membrana plasmática de células LNCaP e o tratamento com EGF interferiu na localização sub-celular desta DUB, como ocorre com clatrina durante a endocitose. Estes resultados sugerem que USP2a participe do processo de endocitose mediada por clatrina
Abstract: The ubiquitin (Ub)-proteasome pathway controls cellular protein turnover by degrading targeted intracellular proteins tagged with poly-Ub chains. Ubiquitination is a reversible process and the deubiquitinating enzymes (DUBs) are proteases that specifically cleave off Ub from Ub-protein conjugates. They can act in a preproteasomal level removing the poly-Ub tag from specific substrates and preventing and modulating their degradation. The DUBs USP2a and USP2b were recently identified in the prostate of men and rats. USP2a is androgen-regulated, overexpressed in prostate cancer, and interacts with and stabilizes fatty acid synthase (FAS) and the protein murine double minute (Mdm2). FAS is overexpressed in several human malignancies, including oral squamous cell carcinoma, and is correlated with a poor prognosis for some tumors. Mdm2 is an Ub-protein ligase responsible for its own ubiquitination and ubiquitination of p53, that is degraded by the proteasome. When overexpressed in nontransformed cells USP2a exhibits oncogenic behavior both in vitro and in vivo and prevents apoptosis induced by chemotherapeutic agents. Considering that USP2a stabilizes FAS and Mdm2 and then protects tumoral cells from apoptosis, the purpose of the present study was to investigate the USP2a expression and its biological role in human oral squamous carcinoma cells. mRNAs for USP2a were detected in the four studied cell lines, mainly in SCC-4 and -15. The USP2a protein levels were similar in all cell lines, being slightly higher in SCC-9 and -25. By using immunofluorescence we showed that USP2a is located in the cytoplasm of SCC-9 cells and eventually concentrated around the nuclei. No significant differences were found in the proliferative rates of USP2a overexpressing SCC-9 cells, however, cells overexpressing mutant USP2a had lower proliferative potential. In contrast with LNCaP cells, USP2a silencing by siRNA slightly induced apoptosis. The treatment with different concentrations of EGF was able to modulate the USP2a expression in SCC-9 cells and change the amount of ubiquitinated forms of FAS. We also show in the present study experiments performed in the laboratory of Dr. Massimo Loda at the Dana-Farber Cancer Institute, in which the possible interaction between USP2a and clathrin was analyzed. Clathrin is involved in the internalization and endocytosis of proteins located in at the plasma membrane. Here we show that USP2a and clathrin heavy chain colocalize in the cytoplasm of AR-iPrEC and SCC-9 cells and that clathrin protein expression is regulated by androgens in LNCaP cells. We found higher amounts of clathrin in cells that stably express USP2a than in the controls. USP2a was found at the plasma membrane in LNCaP cells and after EGF stimulation a granular positivity for USP2a was observed in the cytoplasm. These results suggest that USP2a may have a role in the clathrin mediated endocytosis
Doutorado
Patologia

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Ferraz, Lucio Fabio Caldas. "Estudo das enzimas 5 'alfa'-redutase tipo 2 e 3 'beta'-hidroxi-esteroide desidrogenase tipo 2 na ambiguidade genital e no cancer de prostata." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316603.

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Orientadores: Christine Hackel, Juergen K. V. Reichardt, Maricilda P. Mello
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: O hormônio androgênico di-hidrotestosterona (DHT) possui fundamental importância na diferenciação sexual masculina e no desenvolvimento e manutenção da próstata. Duas enzimas atuam diretamente na concentração deste andrógeno nas células: 1) com uma função anabólica, a enzima 5α-redutase tipo 2 (gene SRD5A2) é responsável pela síntese de DHT ao converter testosterona (T) em 5α-di-hidrotestosterona e 2) com uma função catabólica, a enzima 3β- hidroxi desydrogenase/Δ5-Δ4-isomerase de esteróides tipo 2 (gene HSD3B2) é responsável pela degradação do DHT, além de contribuir para síntese indireta de testosterona por uma via anabólica. Isto exposto, cenários distintos se apresentam considerando as atividades deficientes dessas enzimas: i) a deficiência congênita da enzima 5a-redutase tipo 2 conduz a uma forma específica de pseudohermafroditismo masculino (PHM) no qual a conversão de T em DHT está nula ou defeituosa, inviabilizando a virilização normal da genitália externa em indivíduos com cariótipo 46,XY e ii) em razão das propriedades bifuncionais da enzima 3β-HSD2, tanto na via de síntese quanto de degradação de andrógenos, sua deficiência congênita pode conduzir a quadros clínicos distintos de ambigüidade genital. No adulto, mutações somáticas que afetem sua atividade enzimática podem contribuir para a manifestação do câncer de próstata, pelo acúmulo do DHT. O presente trabalho aborda as duas enzimas esteroidogênicas envolvidas com o metabolismo da DHT, buscando caracterizar mutações germinativas e/ou somáticas que conduzem a deficiências enzimáticas relacionadas a diferentes condições clínicas. Com relação à deficiência em 5a-redutase tipo 2, investigou-se a presença de mutações germinativas no gene SRD5A2 em amostras de DNA 20 pacientes de sexo genético masculino com suspeita de deficiência em 5α-redutase tipo 2, pertencentes a 18 famílias brasileiras, por meio de sequenciamento direto dos produtos de PCR dos cinco exons do gene e de suas regiões flanqueadoras. Foram identificadas alterações moleculares em 18 desses pacientes, compreendendo tanto mutações não anteriormente referidas na literatura (G158R, del642T, 217_218insC e IVS3+1G>A), como mutações recorrentes já descritas em outros grupos étnicos ou em indivíduos de outras regiões geográficas. Os resultados detalhados, bem como a discussão, acham-se apresentados no Capítulo III.1, sob a forma de artigo publicado. (...continua)
Abstract: The androgenic hormone dihydrotestosterone (DHT) has fundamental relevance in normal male sexual differentiation and in prostate development and maintenance. Two enzymes act directly on the regulation of DHT concentration at cellular level: 1) with an anabolic function the steroid 5α-reductase type 2 enzyme (SRD5A2 gene) leads to DHT synthesis by converting testosterone (T) in 5α-dihydrotestosterone and 2) with a catabolic pathway the 3β-hydroxysteroid dehydrogenase/Δ5-Δ4-isomerase type 2 enzyme (HSD3B2 gene) is responsible for DHT degradation, besides contributing to indirect synthesis of testosterone in an anabolic pathway. Thus, different scenarios can be considered regarding the deficiencies in the activities of these enzymes: i) congenital steroid 5α-reductase type 2 enzyme deficiency leads to a specific form of male pseudohermaphroditism (MPH), where the conversion of T into DHT is defective or inexistent, preventing normal virilization of the external genitalia in individuals with a 46,XY karyotype; and ii) due to the bi-functional properties of the 3β-HSD2 enzyme, either at synthetic or degradation androgen pathways, its congenital deficiency can lead to distinct manifestations of genital ambiguity. Furthermore, in the adult, somatic mutations that affect 3β-HSD2 enzymatic activities could contribute to prostate cancer manifestation, due to DHT accumulation. The present work approaches these two steroidogenic enzymes involved with the DHT metabolism, aiming to characterize germinal and/or somatic mutations leading to enzymatic deficiencies related to different clinical conditions. Concerning the steroid 5α- reductase type 2 deficiency, we screened for germinal mutations on SRD5A2 gene in DNA samples of 20 patients from 18 Brazilian families with suspected SRD5A2 deficiency, by directly sequencing of the PCR products from the five exons and flanking regions of the gene. Molecular alterations were detected in 18 of these patients, comprising either mutations not previously reported in the literature (G158R, del642T, 217_218insC e IVS3+1G>A) as well as recurring mutations already described in other ethnical groups or in individuals from other geographical regions. The detailed results and corresponding discussion are presented at Chapter III.1, as a published paper. (¿to be continued)
Doutorado
Genetica Animal e Evolução
Doutor em Genetica e Biologia Molecular

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Manseck, Andreas, Christian Pilarsky, Stefan E. Froschermaier, Mario Menschikowski, and Manfred P. Wirth. "Diagnostic Significance of Prostate-Specific Antigen Velocity at Intermediate PSA Serum Levels in Relation to the Standard Deviation of Different Test Systems." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-133947.

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Serial prostate-specific antigen (PSA) measurements (PSA velocity) as an additional instrument to detect prostatic cancer was introduced in 1992. It has previously been reported that PSA increase per year differed in the last 5 years prior to diagnosis in patients with benign prostatic hyperplasia (0.18 ng/ml/year), locally confined (0.75 ng/ml/year) and metastasized (4.4 ng/ml/year) cancer of the prostate (CaP) in contrast to healthy men (0.04 ng/ml/year). The ability of PSA velocity to detect organ-confined CaP in patients with intermediate PSA serum values depends therefore on a reliable and reproducible PSA result. The present study comprised 85 men with PSA values between 3 and 8 ng/ml (Abbott IMx). PSA measurements were repeated with Abbott IMx (n = 85 patients) and Hybritech Tandem-E (n = 59 patients) assays. The PSA serum values differed from one examination to the other from 0.02 to 2.74 ng/ml with the Abbott IMx. Standard deviation amounted to 0.35 ng/ml with the Abbott IMx PSA assay. Using the Hybritech Tandem-E assay, mean standard deviation was 1.15 ng/ml and therefore higher than with the Abbott IMx assay. The difference from one test to the other ranged from 0.05 to 4.05 ng/ml with the Hybritech Tandem-E. Using the Abbott IMx assay, 10.6% of all repeat measurements exceeded 1 ng/ml whereas in the Hybritech Tandem-E assay 62.7% of the second measurements differed >1 ng/ml from the first PSA result. An increase in PSA serum values may therefore be due to intratest variation, physiological day-to-day variation as well as prostatic disease. It is important to notice that the intra-assay variation may be greater than the PSA increase per year in a patient with CaP. Therefore, PSA velocity seems to be of limited value
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich

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Manseck, Andreas, Christian Pilarsky, Stefan E. Froschermaier, Mario Menschikowski, and Manfred P. Wirth. "Diagnostic Significance of Prostate-Specific Antigen Velocity at Intermediate PSA Serum Levels in Relation to the Standard Deviation of Different Test Systems." Karger, 1998. https://tud.qucosa.de/id/qucosa%3A27551.

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Serial prostate-specific antigen (PSA) measurements (PSA velocity) as an additional instrument to detect prostatic cancer was introduced in 1992. It has previously been reported that PSA increase per year differed in the last 5 years prior to diagnosis in patients with benign prostatic hyperplasia (0.18 ng/ml/year), locally confined (0.75 ng/ml/year) and metastasized (4.4 ng/ml/year) cancer of the prostate (CaP) in contrast to healthy men (0.04 ng/ml/year). The ability of PSA velocity to detect organ-confined CaP in patients with intermediate PSA serum values depends therefore on a reliable and reproducible PSA result. The present study comprised 85 men with PSA values between 3 and 8 ng/ml (Abbott IMx). PSA measurements were repeated with Abbott IMx (n = 85 patients) and Hybritech Tandem-E (n = 59 patients) assays. The PSA serum values differed from one examination to the other from 0.02 to 2.74 ng/ml with the Abbott IMx. Standard deviation amounted to 0.35 ng/ml with the Abbott IMx PSA assay. Using the Hybritech Tandem-E assay, mean standard deviation was 1.15 ng/ml and therefore higher than with the Abbott IMx assay. The difference from one test to the other ranged from 0.05 to 4.05 ng/ml with the Hybritech Tandem-E. Using the Abbott IMx assay, 10.6% of all repeat measurements exceeded 1 ng/ml whereas in the Hybritech Tandem-E assay 62.7% of the second measurements differed >1 ng/ml from the first PSA result. An increase in PSA serum values may therefore be due to intratest variation, physiological day-to-day variation as well as prostatic disease. It is important to notice that the intra-assay variation may be greater than the PSA increase per year in a patient with CaP. Therefore, PSA velocity seems to be of limited value.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

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16

Chang, Ching-Jey George. "Prostate, benign hypertrophy and prostatic carcinoma - a study of cell biology of prostate and chemotherapy for prostatic hypertrophy and prostatic cancer /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487856906256116.

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17

Herrera, Maria Lourdes C. "The expression of various growth factors in the normal human prostate, benign prostatic hyperplasia, and prostate carcinoma." Thesis, Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1754628X.

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18

Hellawell, Giles. "The IGF1R in human prostate cancer." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249458.

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19

Weaver, Jennifer. "Development of an in vitro model for investigating the properties of human prostate epithelial cells and prostatic carcinoma cells /." St Andrews, 2008. http://hdl.handle.net/10023/755.

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20

Weaver, Jennifer. "Development of an in vitro model for investigating the properties of human prostate epithelial cells and prostatic carcinoma cells." Thesis, University of St Andrews, 2009. http://hdl.handle.net/10023/755.

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Prostate cell lines were derived from two regions of prostate tissue from the same patient. The objective was to produce cell lines (as a useful in vitro model) from these two different regions which exhibit different properties for carcinoma development. The tissue was obtained from patients suffering from benign prostate hyperplasia undergoing trans-urethral resection. Tissue was taken from the deep (peripheral) and superficial (peri-urethral) areas. The cells were immortalised by transduction with constructs over expressing the cdk4 and hTERT genes. These cell lines were then characterised for their cellular phenotypes utilized for radiation transformation studies and utilized to investigate the role of plant derived polyphenols on normal and tumour cells. The cell line from the superficial region (P21s) was treated to fractionated doses of gamma radiation and a transformed cloned cell line was derived (P21s 40Gy (clone-a)). The cell line from the deep region (P21d) was found to consist of a mixed population of abnormal cells and a transformed cloned cell line was derived from it (P21d 0Gy (clone-a). In an attempt to obtain a normal P21d cell line cloned cell lines from early passage P21d cells were established. All seven cloned lines were abnormal with an average of 80 chromosomes per cell, invasive using a Matrigel assay and produced anchorage independent colonies. All cell lines were fully characterised with immunocytochemistry, chromosome analysis, invasion assays, and anchorage independent colony formation. P21s expressed basal cell markers (cytokeratin 5 (CK5) and 14), were positive for stem cell markers (prostate specific stem cell antigen PSCA, CK6), positive for p16, p63 and telomerase expression and negative for c-Myc expression. P21s was not invasive in a Matrigel assay and did not produce anchorage independent colony formation. P21d and P21d 0Gy (clone-a) also expressed CK5, CK14, PSCA, CK6, and telomerase but not p16 or p63 and showed an increase in expression of nuclear c-Myc, highly invasive and produced anchorage independent colonies. P21s 40Gy (clone-a) expressed CK5, CK14, PSCA, CK6, telomerase and p63, produced anchorage independent colonies, and was weakly positive for c-Myc expression. Spectral karyotyping analysis (SKY) showed P21s had a normal chromosome complement except an additional chromosome 20 whereas the P21s 40Gy (clone-a), P21d and P21d 0Gy (clone-a) cell lines had an abnormal chromosome complement with P21d and P21d 0Gy (clone-a) cell lines expressing multiple copies of every chromosome including loss of the Y chromosome. These results were echoed in the single nucleotide polymorphism chip (SNP) results which showed P21s as normal but P21d and P21d 0Gy (clone-a) to have large deletion and amplification regions that correlated with the SKY analysis. No differential cytotoxic response was noted between normal and abnormal cell lines including prostatic carcinoma cell lines LNCaP and PC-3 following treatment with strawberry polyphenol compounds. Most reports of a cytotoxic response to tumour cells in the literature did not compare the response to normal cells and used established cell lines. Human lymphocytes were also tested and all compounds were toxic in high doses. Polyphenol and ellagitannin rich polyphenol fractions were very cytotoxic and the anthocyanin rich fraction less toxic. In contrast to the lack of a direct differential cytotoxic effect, plant polyphenols did produce a protective effect to a carcinogenic insult. However a protective effect was noted via micronucleus assay with 3 hour incubation with the polyphenol rich fraction prior to radiation treatment. Finally, the expression and association of metabolic enzymes within the cells cytosol were investigated. The P21s cells were found to express both isoforms of LDH and so thought to be able to metabolise anaerobically and aerobically. P21d and P21d 0Gy (clone-a) cells were found to only express one isoform in the complex and so it was assumed that these cells favoured anaerobic metabolism of ATP in correlation to the Warburg effect. c-Myc association with compounds in the cell cytosol of P21s cells existed whereas, abnormal cells lost this association along with up-regulation of c-Myc expression and down stream targets of c-Myc in the nuclei. Thus these newly established human prostate cell lines provide a useful model system for investigating the biology of the prostate and prostate cancer.

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21

Roulson, Jo-An. "Bone marrow endothelial transmigration of prostate carcinoma cells." Thesis, University of Manchester, 2008. https://www.research.manchester.ac.uk/portal/en/theses/bone-marrow-endothelial-transmigration-of-prostate-carcinoma-cells(997acbf2-bbbc-455b-bb84-b439ffb9f839).html.

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22

Buwenge, Milly <1980&gt. "Development of a large database on prostate carcinoma." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2020. http://amsdottorato.unibo.it/9195/1/Milly%20Buwenge_TesiDottorato.pdf.

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The main aim of this study was to analyze the prognostic impact on outcome and toxicity of patients with prostate cancer [PCa] treated with radiotherapy [RT] in three different settings [curative, adjuvant, and salvage RT] based on a comprehensive analysis of parameters related to tumor, patients, and treatment characteristics. Furthermore, we aimed to develop simple risk stratification systems, based on real life data from a large patient population including the three different RT settings. Data on 2526 patients were collected. In the “curative RT” group we designed a prognostic model of the 5-year biochemical outcome using three PSA categories and 5 GS categories to define 15 different groups of patients. We arranged these 15 groups in only 4 categories based on 5-year bRFS values: group 1: very low-risk [bRFS > 90%], group 2: low risk [bRFS: 80-90%], group 3: intermediate risk [bRFS: 60-79.9%], group 4: high risk [bRFS < 60%]. In the “adjuvant RT” group we designed a predictive model of biochemical outcome using two age categories, two nodal stage categories, and four PSA categories to define 16 different groups of patients. These 16 groups were arranged in only 3 categories based on 5-year bRFS values: group 1: very low-risk [bRFS > 95%], group 2: low-intermediate risk [bRFS: 76-95%], group 3: high risk [bRFS: < 76%]. In the “salvage RT” group we designed a prognostic model using 4 GS categories, 2 nodal stage categories, and 2 nodal irradiation categories to define 16 different groups of patients. These 16 groups were arranged in only 4 categories based on 5-year bRFS values: group 1: low-risk [bRFS > 80%], group 2: intermediate risk [bRFS: 60-80%], group 3: high risk [bRFS: 40-< 59.9%], and group 4: very high risk [bRFS: < 40%].

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23

MENCACCI, CECILIA. "Identification of candidate prostate cancer biomarkers in prostate needle biopsy." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/1142.

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Il carcinoma della prostata è uno dei tumori più frequenti e rappresenta quasi il 30% di tutti i tumori di nuova diagnosi nel sesso maschile. La concomitanza di fattori quali l'elevata mortalità, la tardività della diagnosi clinica abituale ed i benefici della diagnosi precoce hanno negli ultimi tempi suscitato un notevole interesse per iniziative sistematiche di diagnosi precoce e di screening. La ricerca di una o più sostanze potenzialmente utili per identificare i pazienti con un cancro della prostata o per stabilire la prognosi della neoplasia non ha messo in evidenza fin’ora un marker completamente soddisfacente. Circa il 20-30% dei tumori della prostata non sono associati ad elevati livelli di PSA. Il PSA, infatti, si innalza anche in caso di infiammazione della prostata o di ipertrofia prostatica benigna, e in caso di massaggio o manipolazione prostatica. Lo studio del profilo genico del tessuto prostatico permette di identificare biomarcatori specifici utili nella diagnosi. Il tessuto prostatico è stato ottenuto da 30 pazienti sottoposti a biopsia prostatica. Il livello sierico di PSA è compreso tra 2,68 ng/ml e 100ng/ml. Tramite Real Time PCR, abbiamo determinato l’espressione dei geni ODC1, DPP4, IMPDH1 e 2, ZIP1, ZIP2, ZIP3, ZIP4. La valutazione quantitativa è stata ottenuta tramite Light Cycler 1.5. Dal nostro studio è emerso chiaramente che in caso di PCa è presente una down-regulation dell’espressione dei geni ZIP, trasportatori dello zinco. Questo dato potrebbe risultare utile nella diagnosi e prognosi del tumore della prostata ed i geni ZIP potrebbero essere utili in qualità di biomarcatori tumorali.
Prostate cancer is the most common cancer among men and it is a significant cause of morbidity and mortality worldwide. Screening for prostate specific antigen has led to earlier detection of prostate cancer. However PSA is neither tissue specific. Thus the serum PSA screening is characterized by poor specificity as well as poor sensitivity. This low specificity of PSA is a reason of marker improvement. Therefore it is of prime interest to develop clinical markers with a superior specificity for prostate cancer lesions for use in the initial diagnosis. Characterization of gene expression profiles that molecularly distinguish prostatic neoplasms may identify genes involved in prostate carcinogenesis. For this study, we determined the expression level of ODC1, DPP4, IMPDH1, IMPDH2, ZIP1, ZIP2, ZIP3 & ZIP4 by means of Real-Time PCR (qPCR). Quantitative detection of human genes was performed with a Light-Cycler 1.5 Instrument. Prostate tissue specimens were obtained from 30 patients undergoing prostate needle biopsy. These included 14 patients who were diagnosed for Adenocarcinoma, 14 who had a diagnosis of benign prostate hyperplasia (BPH), and 2 of prostatic intraepithelial neoplasia (PIN). The serum PSA levels of these patients were determined and all patients had a range between 2,68ng/ml and 100ng/ml (mean PSA value=13,95ng/ml). The mean age of the selected patients was between 43 and 80 years (mean age= 65,3years) and Gleason score between 0 and 8 ( mean score =3,1). Our results clearly establish that Zip1, Zip2, and Zip3 mRNA are down regulated in malignant prostate glands and up regulated in BPH. This is the first report that identifies the expression of Zip1, Zip2, Zip3 and Zip4 in human prostate needle biopsy. The down regulation of these transporters in the malignant cells is essential for the cellular depletion of zinc to prevent the anti tumor effects of zinc. These findings are consistent with the concept that Zip1, Zip2 and Zip3 are tumor-suppressor genes in prostate cancer. The identification of new prostate cancer specific genes such as ZIP genes would represent a considerable advance in the improvement of diagnostics tests for prostate cancer.

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24

Kehinde, Elijah Oladunni. "Regulation of prostatic carcinoma by growth factors." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29556.

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The present study was designed to test the hypothesis that non-androgenic growth factor inhibitors have a role to play in the management of patients with metastatic hormone-resistant prostate cancer.;The effects of the growth factor inhibitors, Somatostatin 201-995 (SMS 201-995), Estramustine phosphate (EMP) alone and in combinations on the cellular proliferation of established human prostate cancer cell lines LNCaP, DU145 and PC3 and on cells obtained by primary culture from patients with various stages of prostate cancer were assessed using 3H thymidine incorporation assay.;Suramin (0-270 ug/ml), SMS 201-995 (0-20 ug/ml), and EMP (0-50 ug/ml) produced dose dependent growth inhibition on both hormone dependent (LNCaP) and hormone independent (PC3) prostate cancer cells and cells obtained by primary culture of prostate cancer epithelial cells. Suramin and EMP combination produced statistically significant synergism on established prostate cancer cell lines, but not on prostate cancer cells obtained by primary culture.;In a preliminary clinical trial, patients with metastatic hormone-resistant prostate cancer were randomised into two treatment groups, Group A received EMP (280 mg twice daily) while Group B received EMP (280 mg twice daily) and low dose intravenous Suramin (1 gm weekly for 6 weeks). There were 6 patients in each treatment group. The control group, made up of 6 patients, continued on maximal androgen blockade namely castration and Flutamide (250 mg three times daily) or Cyproterone acetate (100 mg three times daily). At the end of 6 months of treatment, there was statistical significant reduction of serum levels of prostate specific antigen and better pain control for patients on EMP and Suramin compared to patients who received EMP alone (P < 0.01) or patients on EMP and Suramin compared to controls (P < 0.001) (Kruskal-Wallis test).;Suramin, a non-androgen growth factor inhibitor has been shown in this study to produce significant in vitro and in vivo inhibition of the proliferation of prostate cancer cells. Its use as a novel chemotherapeutic agent for hormone-resistant prostate cancer patients alone or in combination with EMP deserves further study.

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25

Haq, Mahmudul. "Host-tumor interactions in skeletal metastasis of prostate carcinoma." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56996.

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Approximately 70% of patients with prostatic cancer develop bone metastases. Metastatic prostate adenocarcinomas are associated with high mortality rates and represent a leading cause of cancer-related deaths among males. To study the host-tumor interactions underlying the predilection of prostate cancer cells for skeletal bone, an experimental model was developed using rat Dunning carcinoma Mat-LyLu cells. Inoculations of these cells into the left ventricle of the heart led to the development of spinal metastases in 100% of inoculated animals. A subline of Mat-LyLu (Mat-LyLu-B5) was subsequently selected through sequential inoculation of bone marrow derived carcinoma cells into the left ventricle of the heart and was found to have an increased metastatic potential compared to the parental line. The possible role of tumor cell adhesion to host cells in the process of bone marrow colonization was then investigated in vitro using the metastatic line and primary cultures of rat bone marrow-derived stromal cells. It was found that the adhesion of the metastatic Mat-LyLu cells to a bone marrow stromal cell culture highly enriched for endothelial cells (BMEC) was significantly higher than the adhesion to other bone-derived cells including non-endothelial BM stromal cells (3x) and osteoblasts (1.4x). It was also significantly higher than the adhesion to rat fibroblasts (5.5x) and to hepatic endothelial cells (7x). The results suggest that the adhesion of prostate carcinoma cells to the bone marrow endothelium may play a role in their metastasis to bone.

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26

Bulmer, Bronwyn. "Prostate specific antigen-like expression in renal cell carcinoma." Thesis, Queensland University of Technology, 2002.

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27

Gulkesen, Kemal Hakan. "A Patient-oriented Decision Support Framework And Its Application To Biopsy Decision For Prostatic Carcinoma." Phd thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/12610510/index.pdf.

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Serum PSA (Prostate Specific Antigen) level is used for prediction of prostatic carcinoma, but it suffers from weak sensitivity and specificity. We applied logistic regression, artificial neural networks, decision tree, and genetic algorithm to prostate cancer prediction problem to design a model for Turkish population. A hybrid model of logistic regression and decision tree has been designed. The model could prevent 33 biopsies (4.4% of our patients who have PSA level between 0 and 10) from our data set without a loss from sensitivity. The prepared online decision support tool and a questionnaire were published on a website. Fifty urologists have completed the questionnaire. Cronbach&rsquo
s alpha was 0.770. On a five graded Likert scale, the mean score of &ldquo
attitude to computer use in healthcare&rdquo
(ACH) was 4.2. The mean of eight responses related to the online tool (Attitude to Decision Support Tool
ADST), was 3.7. ADST was correlated with ACH (r=0.351, p=0.013). Physicians who have positive attitude to computer use in healthcare tend to use the tool (r=0.459, p=0.001). The first factor influencing the opinions of the urologists was the attitude of the user to computer use in healthcare, the other factor was the attitude of the user to the decision support tool itself. To increase the acceptance, education and training of physicians in the use of information technologies in healthcare, informing users about the logic of the decision support tool, and redesigning the system according to user feedback may be helpful.

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28

Amiry, Naeem. "Investigating the role of TFF1 in mammary and prostate carcinoma." Thesis, University of Auckland, 2011. http://hdl.handle.net/2292/6480.

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Trefoil Factor-1 (TFF1) belongs to the family of trefoil factor peptides. Trefoil factors protect the gastrointestinal tract against mucosal injury. Trefoil peptides are upregulated and secreted in an autocrine and paracrine fashion in response to gastrointestinal injury. They facilitate cell migration and prevent anoikis. TFF1 is also expressed in various tissues and regulated by multiple cellular processes. Several studies have also demonstrated increased expression of TFF1 in a high percentage of mammary and prostate carcinoma cases. However, the functional role of autocrine TFF1 in mammary and prostate carcinoma has not been previously elucidated. Herein, I demonstrate that forced expression of TFF1 in mammary carcinoma cells resulted in increased total cell number as a consequence of increased cell proliferation and survival. Forced expression of TFF1 enhanced anchorage-independent growth and promoted scattered cell morphology with increased cell migration and invasion. Moreover, forced expression of TFF1 increased tumor size in xenograft models. Conversely, depletion of TFF1 by RNA interference (RNAi) in mammary carcinoma cells significantly reduced anchorageindependent growth and migration. Furthermore, neutralization of secreted TFF1 protein by polyclonal antibody decreased mammary carcinoma cell viability in vitro and resulted in regression of mammary carcinoma xenografts. In prostate carcinoma cell lines utilized herein, I demonstrate that forced expression of TFF1 did not affect proliferation and anchorage-independent growth. However, forced expression of TFF1 enhanced prostate carcinoma cell migration and invasion. Additionally, functional inhibition of TFF1 by RNAi or polyclonal antibody abrogated prostate carcinoma cell invasion. I have therefore demonstrated that TFF1 possesses oncogenic functions in mammary carcinoma cells and enhances prostate carcinoma cell invasion. Functional antagonism of TFF1 can therefore be considered as a novel therapeutic strategy for mammary carcinoma.

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29

Slaibi, Jinani Elias. "Targets of Hsa-miR-488* In Human Prostate Carcinoma Cells." Cleveland State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=csu1273843449.

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30

Tran, Nhan Le. "Molecular characterization of cadherin expression and function in prostate carcinoma." Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/279962.

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The epithelial cytoarchitecture and function in the prostate gland are maintained in part by the E-cadherin/catenin complex. In human prostate adenocarcinoma, an association between the loss of E-cadherin, increased Gleason score, and extracapsular dissemination has been observed. Further characterizations of human prostate carcinoma cell lines show loss of E-cadherin and expression of N-cadherin in poorly differentiated prostate carcinoma cell lines. N-cadherin expression correlates with an invasive phenotype in cancer cells and mediates the interactions between malignant tumor cells and N-cadherin expressing cells, such as prostate stromal fibroblasts. Additionally, N-cadherin-mediated intercellular adhesions generate a compensatory mechanism that promotes anchorage-independent growth and suppresses apoptosis through a phosphatidylinositol 3-kinase/Akt/protein kinase B survival pathway. Activated Akt results in the phosphorylation of two downstream substrates, Bad and CREB, to regulate Bcl-2 protein stability and bcl-2 transcription, respectively. Under serum deprivation, N-cadherin intercellular adhesion stimulates a 4-fold increase in bcl-2 mRNA expression resulting in a 3.5-fold increase in Bcl-2 protein expression, while the cellular level of proapoptotic protein Bax remains constant. Following N-cadherin homophilic adhesion the phosphatidylinositol 3-kinase p85 subunit is found in immunoprecipitates of the N-cadherin/catenin complex. The recruitment of phosphatidylinositol 3-kinase is dependent on both N-cadherin homophilic adhesion and N-cadherin binding to an intact actin cytoskeleton. These results suggest that the association of the N-cadherin/catenin complex with the actin cytoskeleton acts as a scaffold to localize the activation of phosphatidylinositol 3-kinase/Akt signaling pathway at adherens junctions. The identification of outside-in signal transduction mediated by N-cadherin adhesion provides new information on anti-apoptotic cell-cell adhesion mechanisms enhancing the activity of the phosphatidylinositol 3-kinase/Akt cell survival pathway in metastatic prostate carcinoma. Collectively, these observations indicate that alterations in cadherin expression play a role in prostate cancer progression that may have a profound affect on metastatic cell survival.

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31

Davis, Tracy Lynn. "Alterations of the α6β4 and α6β1 integrins in prostate carcinoma". Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/290157.

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The (140 kD) α6 integrin is an essential gene product in epithelial cell maintenance and remodeling of the stratified epithelium. The prostate gland is an example of a glandular epithelium. In prostate cancer, alterations of integrins are observed. Specifically, a shift from α6β4 to persistent expression of α6β1 integrin occurs. Accompanying the loss of polarized α6β4 is loss of its extracellular ligand, laminin-5. Using immunofluorescence staining human prostate, breast and colon tissues, were examined for β4 integrin and laminin-5 expression. Loss of β4 and laminin-5 was apparent beginning in PIN lesions and was absent in prostate carcinoma, differing from retained expression in breast and colon carcinoma. These data suggested progressive loss of β4 integrin and laminin-5 occurs and that this combined defect is unique to prostate cancer progression. A novel 70 kD (non-reduced) variant of the α6 integrin, called α6p for the latin word parvus (small), was identified on the cell surface of normal epithelial and carcinoma cell lines. The α6p variant paired with either β1 or β4 subunits and retained sequences corresponding to the extracellular 'stalk region' and the cytoplasmic tail of the α6 integrin. The β-propeller domain postulated to mediate ligand binding, was missing from this variant. Protein levels of α6p increased three fold during calcium-induced terminal differentiation in a normal mouse keratinocyte model system. Production of the α6p variant was dependent upon an intact actin cytoskeleton. Cell surface α6p was less responsive to changes in the actin cytoskeleton, relative to that observed for α6 and β1 integrins, suggesting α6p did not participate in the focal contact. Additionally, inhibition of serine/threonine phosphatases decreased α6 integrin protein levels, but not α6p integrin, again suggesting the variant functioned as an inactive subunit for signaling. Finally, α6, but not α6p integrin co-immunoprecipitated with hemidesmosome components: laminin-5 and CD151. Preliminary data demonstrated adhesion to synthetic peptide integrin antagonists resulted in a 65 kD form of the alpha6p variant with no alteration of α6 integrin. Together the presented data were consistent with differential regulation of alpha6 and α6p integrins and suggested the α6p variant functioned as an inactive receptor.

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32

Dimitrije, Jeremić. "Značaj određivanja koncentracije D vitamina u evaluaciji karcinoma prostate." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2015. https://www.cris.uns.ac.rs/record.jsf?recordId=100043&source=NDLTD&language=en.

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Анотація:

Vitamin D ima antiproliferativno, proapoptotsko i prodiferencijaciono dejstvo. Dokazi o dejstvu na ćelije adenokarcinoma prostate su malobrojni i nekonzistentni. Cilj ispitivanja je određivanje stepena povezanosti između nivoa vitamina D, stadijuma adenokarcinoma prostate, prostata specifičnog antigena, Gleason grade i progresije oboljenja. Ispitivanje je prospektivno, sprovedeno na 120 ispitanika (90 pacijenata sa dijagnostikovanim karcinomom prostate i 30 kontrolnih, zdravih subjekata). Pacijenti sa dijagnostikovanim adenokarcinomom prostate podeljeni su prema stadijumu bolesti u dve grupe: lokalizovano (pT2cN0M0, prostata specifični antigen ≤ 20 ng/ml, Gleason 2-7) i metastatsko oboljenje (pT3-4, N1, M 0,1(a,b,c), prostata specifični antigen ≥ 20 ng/ml, Gleason ≥ 8), dok su prema ordiniranoj terapiji podeljeni u tri grupe: pacijenti koji su hemijski kastrirani, hirurški kastrirani i grupa kod koje je urađena radikalna prostatektomija. Uzorci za analizu nivoa vitamina D i prostata specifičnog antigen uzeti pre ordinirane terapije a nakon toga posle 6 i 12 meseci. Kako ne postoje definisane vrednosti unosa vitamina D i kalcijuma za ispitivano podneblje formirani smo Upitnik kojim smo evaluirali dnevni unos kod 90 zdravih subjekata muškog pola starijih od 50 godina koji nisu učestvovali u ispitivanju. Da bismo uočili ispitanike koji su hranom ili životnim navikama drastično uticali na vrednost vitamina D isti Upitnik su ispunili svi ispitanici uključeni u ispitivanje. Ustanovljena je očuvana godišnja oscilacija vitamina D kod ispitanika te smo statističkim modelom korigovali ovu varijablu. Rezultati pokazuju da grupa obolelih nema apsolutno niske vrednosti vitamina D i da su vrednosti kod obolelih niže u odnosu na kontrolne subjekte (64.12 nmol/l vs. 74.45 nmol/l). Nije uočena razlika u nivou vitamina D kod pacijenata sa lokalizovanim i metastatskim oboljenjem (62.90 nmol/l vs. 64,65 nmol/l). Odnos između prostata specifičnog antigena i vitamina D posmatran tokom perioda ispitivanja pokazuje da je kod obolelih pacijenata koji su hemijski ili hirurški kastrirani i kod pacijenata kod kojih je urađena radikalna prostektomija postoji pozitivna korelacija pre ordinirane terapije u sve tri grupe, nakon ordinirane terapije možemo uočiti inverznu korelaciju. Konrolna grupa ispitanika pokazuje stalnu pozitivnu korelaciju između nivoa vitamina D i prostata specifičnog antigena. Pacijenti kod kojih je došlo do progresije imaju niže vrednosti nivoa vitamina D u odnosu na pacijente kod kojih nije došlo do progresije. Nije ustanovljena korelacija između vremenskog intervala do progresije oboljenja i nivoa vitamina D.
Vitamin D has antiproliferative, proapoptotic and prodifferentiational actions. There is a limited number of studies asessing influence of vitamin D on prostate cancer. Results of those available studies are inconsistent. This study hypothesizes with correlation of vitamin D, prostate cancer stage, prostate specific antigen, Gleason grade, stage, and disease progression. This prospective study included 120 subjects (90 subjects with diagnosed prostate cancer and 30 healthy, age adjusted controls). Patients with diagnosed prostate cancer formed two groups by criterion of disease advancement: localized (≤pT2cN0M0, prostate specific antigen ≤ 20 ng/ml, Gleason 2-7) and metastatic (≥pT3-4, N1, M 0,1(a,b,c), prostate specific antigen ≥ 20 ng/ml, Gleason ≥ 8. According to applied therapy subjects were devided in three groups: surgicaly castrated, medicamentous castrated and radical prostatectomy treated. Samples were obtained before therapy and after 6 and 12 months. As no defined value for vitamin D and calcium intake could be found we formed Questionnaire for vitamin D and calcium intake. Data were obtained from 90 healthy, age adjusted subjects, not included in this study. All subjects included in this study filed the Questionnarie and subjects with unusual vitamin D and calcium intake were excluded. Annual oscilation of vitamin D was observed, so we applied statistical model that excluded this variable. Subjects with diagnosed prostate cancer didn't have absolutely low vitamin D level. This level was lower in group of subjects whith diagnosed prostate cancer comparing to controls (64.12 nmol/l vs. 74.45 nmol/l). No differences in vitamin D level was observed in groups of patients with localised and metastatic disease (62.90 nmol/l vs. 64,65 nmol/l).Correlation of vitamin D and prostate specific antigen during 12 months period showed that castrated subjects and subjects in radical prostatectomy group showed possitive correlation before surgical treatment and inverse, negative correlation, after treatment. Control group showed possitive correlation of vitamin D and prostate specific antigen in all three measurements. Subjects with progression have significantly lower vitamin D level comparing to subjects without progression. No correlation between time to progression and vitamin D have been observed.

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33

Manseck, Andreas, K. Guhr, Oliver Hakenberg, Karsten Rossa, and Manfred P. Wirth. "Clinical Significance of the Echogenicity in Prostatic Ultrasound Findings in the Detection of Prostatic Carcinoma." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135178.

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Background: Transrectal ultrasound is commonly performed in the clinical evaluation of the prostate. Ultrasound-guided randomized sextant biopsy became the standard procedure for the diagnosis of carcinoma of the prostate (CaP). A guided biopsy of sonographically irregular lesions of the prostate is not performed in randomized biopsies. An almost generally accepted opinion is that hypoechoic lesions are suspicious for the presence of CaP. However, the role of prostatic lesions with an echogenicity other than iso- or hypoechoic, e.g. hyperechoic or irregular lesions in relation to CaP is not clear. The intention of the present prospective study was to clarify the role of different prostatic ultrasound findings with a new-generation ultrasound probe in regard to their relevance concerning the presence of cancer. Material and Methods: 265 patients who were referred for prostatic evaluation because of an elevated PSA serum level or a positive digital rectal examination were enrolled in a prospective study. All patients had a systematic ultrasound-guided sextant biopsy of the prostate and a 4-core biopsy of the transition zone. All biopsy cores taken were guided by transrectal ultrasound. In case of a sonographically suspicious lesion, biopsy was always directed into this area. The predominant ultrasound appearance was separately recorded for each core. Results: Carcinoma of the prostate was detected in 87 (32.8%) of the 265 patients. Biopsy cores with isoechoic ultrasound findings revealed CaP in 7.6%. The data for hypoechoic, hyperechoic, mixed-echoic and anechoic lesions were 34.5, 26.9, 21.1 and 0%, respectively. Hypoechoic ultrasound findings were less frequently found in the transition zone of the prostate, but the rate of CaP detection was the same as in the peripheral zone of the prostate. Conclusions:The transrectal ultrasound pattern of the prostate yields important information about the presence of carcinoma of the prostate. Especially hypoechoic lesions indicate the presence of CaP in a significant proportion of cases. However, hyperechoic lesions and lesions of mixed or irregular echogenicity were found to contain cancer in significant numbers as well, and should therefore be considered to be suspicious for cancer when performing transrectal ultrasound of the prostate. Directed biopsy of irregular ultrasound patterns in the prostate seems therefore to be recommendable
Hintergrund: Der transrektale Ultraschall ist die häufigste bildgebende Untersuchung zur klinischen Beurteilung der Prostata. Zur Diagnostik des Prostatakarzinoms (PCa) hat sich die ultraschallgesteuerte Sextanten-Biopsie als Standardverfahren etabliert. Eine gezielte Biopsie irregulärer Ultraschallbezirke ist hier nicht vorgesehen. Es ist jedoch bekannt, daß sonographisch echoarm erscheinende Areale suspekt für die Präsenz eines PCa sind. Die Wertigkeit nicht einheitlicher oder echoreicher Ultraschallmuster ist jedoch bisher nicht zweifelsfrei geklärt. Ziel der vorliegenden Arbeit war es, mit einem Ultraschallgerät der neuesten Generation die Bedeutung der verschiedenen Ultraschallmuster bezüglich des Vorhandenseins von Prostatakarzinomen zu klären. Material und Methoden: 265 Patienten mit erhöhten PSA-Serumwerten oder suspekten Tastbefunden der Prostata wurden in die prospektive Untersuchung eingeschlossen. Bei allen Patienten wurden systematische, ultraschallgesteuerte Prostatabiopsien, wie in der Sextantenbiopsie vorgesehen, und 4 Zylinder aus der Transitionalzone entnommen. Bei der Biopsie wurde jedoch gezielt die Punktion in Bereichen von – falls vorhanden – irregulärem Ultraschallmuster vorgenommen und das entsprechende Ultraschallbild dokumentiert. Ergebnisse: Bei 87 der 265 Patienten (32,8%) wurden Prostatakarzinome nachgewiesen. Biopsiezylinder aus isodensen Bereichen wiesen in 7,6% ein Prostatakarzinom auf. Die Karzinomhäufigkeit bei Biopsie von echoarmen und echoreichen Arealen sowie von Arealen mit unterschiedlichen Echomustern und von zystischen Arealen wurde mit 34,5, 26,9, 21,1 bzw. 0% ermittelt. Echoarme Befunde wurden seltener in der Transitionalzone nachgewiesen, waren jedoch dort in etwa gleicher Häufigkeit mit einem Karzinom verbunden wie in der peripheren Zone. Schlußfolgerungen: Das transrektale Ultraschallmuster in der Prostata liefert wichtige Hinweise auf das Vorhandensein eines Prostatakarzinoms. Insbesondere echoarme Läsionen deuten auf ein PCa hin. Echoreiche Läsionen und solche mit unterschiedlichen Echomustern enthielten jedoch Karzinome in so bedeutender Anzahl, daß diese Läsionen ebenfalls als karzinomverdächtig eingestuft werden müssen und auch eine gezielte Biopsie dieser Areale im Rahmen der Sextantenbiopsie empfehlenswert erscheint
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich

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34

Scortegagna, Eduardo. "Comportamento das celulas musculares lisas nos carcinomas da prostata humana : variações fenotipicas ultraestruturais." [s.n.], 2000. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317549.

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Анотація:

Orientadores: Hernandes Faustino de Carvalho, Sebastião Roberto Taboga
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: As células musculares lisas da próstata humana foram estudadas ao microscópio eletrônico de transmissão, a partir de amostras obtidas por prostatectomia radical em casos de carcinoma da próstata. As células musculares lisas apresentam-se comumente formando feixes, nos quais elas aparecem intimamente associadas com as vizinhas, sendo que as membranas basais de células adjacentes mostram-se únicas. Com o desenvolvimento tumoral, nas áreas de proliferação epitelial em tumores com graus intermediários de diferenciação glandular, inicia-se um acúmulo de matriz extracelular entre as células vizinhas, sendo que as membranas basais tomam-se únicas para cada célula, refletindo a perda dos contatos homotípicos. Com a invasão tumoral, nos tumores altamente indiferenciados, as células musculares lisas apresentaram três fenótipos distintos: atrófico, ativado e degenerado. As células atróficas possuem uma proporção núcleo/citoplasma elevada, com notada diminuição do componente contrátil e com membrana basal menos desenvolvida e comumente interrompida. O fenótipo ativado mostra acúmulo de material vesicular nas regiões periféricas e intenso pregueamento da superfície celular em regiões de íntimo contato com elementos fibriJares da matriz extracelular. Em algumas células nota-se um aumento na proporção de organelas como retículo endoplasmático granular e Golgi, em detrimento do cito esqueleto. O fenótipo degenerado possui citoplasma bastante reduzido, com núcleo colapsado e com espaço perinuclear expandido, sendo que a membrana basal está interrompida. Uma série de prováveis conversões entre estes fenótipos das células musculares lisas é proposta. As modificações das células musculares lisas parecem decorrer da perda da sinalização proveniente do epitélio e também a partir da degradação da membrana basal por enzimas produzidas pelas células tumorais
Abstract: The smooth muscle cells of the human prostate were studied at the electron microscopy level from samples of radical prostatectomy in cases of prostate carcinomas. The smooth muscle cells are found in bundies, in which they are intimately associated to each other and with fused basement membrane. With the tumor progression, in the areas of glandular proliferation in the intermediary graded tumors, there is an accumulation of extra cellular matrix between the smooth muscle cells, which loose the homotypic contacts and acquire individualized basement membranes. With the stromal invasion by the epithelial cancer cells, the smooth muscle cells show three different phenotypes: atrophic, activated and degenerated cells. The atrophic cells show a diminished cytop1asmlnucleus ratio, with a marked loss of the contractile component and showing a reduced and frequently disrupted basement membrane. The activated phenotype shows an accumulation of vesicular material at the cell periphery and intense folding of the cell surface in regions of intimate contact with extracellular fibrillar components. Some cells had an increase in the amount of organelles such as the rough endoplasmic reticulum and Golgi while the cytoskeleton is diminished. The cells of the degenerated phenotype have a reduced cytoplasm, collapsed nuclei and expanded perinuclear spaces. The basement membrane around these cells is disrupted A series of conversions between these smooth muscle cell phenotypes is proposed. The modifications observed in this study seem to occur by the lack of a proper stimulation by the epithelium and or from the degradation of the basement membrane by proteolytic enzymes produced by the tumor cells
Mestrado
Biologia Celular
Mestre em Biologia Celular e Estrutural

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35

Herrmann, Valerie Laura [Verfasser]. "Immunotherapy of Prostate Carcinoma with biodegradable PLGA Microspheres / Valerie Laura Herrmann." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1115726641/34.

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36

Naccarato, Angela Maria Elizabeth Piccolotto 1955. "Estudo demográfico e aspectos psicológicos de pacientes sob rastreamento de carcinoma prostático." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309275.

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Анотація:

Orientadores: Fernandes Denardi, Wagner Eduardo Matheus
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-16T00:00:51Z (GMT). No. of bitstreams: 1 Naccarato_AngelaMariaElizabethPiccolotto_M.pdf: 3567933 bytes, checksum: bf53ae2ff5454c30b3dd914c045af6a8 (MD5) Previous issue date: 2010
Resumo: Introdução: O câncer de próstata (CaP) é a segunda causa de morte em homens, estudos recentes tem confirmado a eficácia do toque retal (TR) e seus benefícios no diagnóstico precoce. Objetivo: Avaliar aspectos demográficos e psicológicos de homens submetidos ao TR durante consulta para rastreamento do CaP. Pacientes e Métodos: Estudo realizado com 345 pacientes submetidos ao TR pela primeira vez entre Fevereiro 2006 a Dezembro 2007, que foram avaliados quanto às impressões sobre o TR. Dados sobre etnia, idade, escolaridade, profissão e as motivações para o rastreamento foram colhidos e a correlação entre variáveis descritivas e aspectos psicológicos dos pacientes foi realizada. Resultados: A média de idade foi de 52.8 anos. Sentiram medo 40.94% (sendo medo do exame 15.94% e medo do diagnóstico 25%), vergonha 26.45% e 48.26% referiram não pensar em nada. A correlação entre faixa etária, nível de escolaridade e reações emocionais não apresentou diferença significativa. 52.35% consideraram o exame melhor do que imaginavam, dos quais 41.81% eram analfabetos/1º grau incompleto, 4.12% uma experiência ruim e 96.8% fariam o teste novamente. O convencimento em se consultar foi em 50.14% por decisão própria, 26,67% encaminhados por médicos, 18,55% pela esposa, 7,83% por familiares ou amigos, 6,67% através da mídia e 24.06% tiveram consulta marcada pelas parceiras. Embora 85,47% soubessem da importância do exame, 80,81% consideram-se mais esclarecidos após a consulta. A falta de informação sobre o exame foi mais freqüente dentre os pacientes de menor escolaridade e 52.38% com decisão própria em se consultar tinham conhecimento prévio à consulta sobre a importância do exame. Conclusão: Medo e vergonha frente ao TR desempenham papel significativo na resistência ao se submeter ao exame, porem a maioria absoluta dos pacientes achou menos desagradável do que imaginava e repetirá o exame futuramente
Abstract: Introduction: Prostate cancer (PCa) is the second leading cause of death in men. Recent studies have confirmed the effectiveness of the digital rectal examination (DRE) in early diagnosis. Aim: To evaluate the psychological and demographic aspects of men who received DRE during the PCa screening in an outpatient clinical setting. Patients and Methods: Patients (345) who underwent DRE for the first time from February 2006 to December 2007 were evaluated for their psychological reactions and feelings after the examination. Data on age, race, education, profession and the motivations for the screening were gathered. Correlation of descriptive and psychological aspects of patients under PCa screening was done. Results: The average age of the patients was 52.8 years; 40.94% had felt fear (examination fear 15.94%, and diagnosis fear 25%), 26.45% shame and 48.26% indicated they were not thinking about anything. There was no correlation between age, educational level and emotional reactions. Most patients (96.8%) would undergo a DRE again and 52.35% had considered it better than they had imagined. Of these patients, 41.81% were illiterate/incomplete elementary school. Only 4.12% described having a negative experience. The factors that persuade the patient to book an appointment were: 50.1% made their own decision, 26.67% were recommended by a physician, 18.55% family/friends and 6.67% were influenced by the media. Wives booked 24.06% of the consultations. Although 85.47% of patients had some previous knowledge about the examination, 80.81% felt they had further clarification afterward. Lower educational level was related to lack of information about DRE, while 52.38% who made their own decision had previous knowledge of the importance of DRE. Emotional aspects and access to information play significant roles in the decision to undergo PCa screening and must be considered in educational campaigns. Conclusion: The majority of the patients found DRE less awkward than what they had imagined it to be and would repeat the examination in the future. Fear and shame before the examination are baseless, but are a barrier to the DRE
Mestrado
Pesquisa Experimental
Mestre em Cirurgia

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37

Forsyth, Leigh James. "Identification of DNA sequences involved in the metastatic phenotype of human prostatic carcinoma cells." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269601.

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38

Manseck, Andreas, K. Guhr, Oliver Hakenberg, Karsten Rossa, and Manfred P. Wirth. "Clinical Significance of the Echogenicity in Prostatic Ultrasound Findings in the Detection of Prostatic Carcinoma." Karger, 2000. https://tud.qucosa.de/id/qucosa%3A27626.

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Анотація:

Background: Transrectal ultrasound is commonly performed in the clinical evaluation of the prostate. Ultrasound-guided randomized sextant biopsy became the standard procedure for the diagnosis of carcinoma of the prostate (CaP). A guided biopsy of sonographically irregular lesions of the prostate is not performed in randomized biopsies. An almost generally accepted opinion is that hypoechoic lesions are suspicious for the presence of CaP. However, the role of prostatic lesions with an echogenicity other than iso- or hypoechoic, e.g. hyperechoic or irregular lesions in relation to CaP is not clear. The intention of the present prospective study was to clarify the role of different prostatic ultrasound findings with a new-generation ultrasound probe in regard to their relevance concerning the presence of cancer. Material and Methods: 265 patients who were referred for prostatic evaluation because of an elevated PSA serum level or a positive digital rectal examination were enrolled in a prospective study. All patients had a systematic ultrasound-guided sextant biopsy of the prostate and a 4-core biopsy of the transition zone. All biopsy cores taken were guided by transrectal ultrasound. In case of a sonographically suspicious lesion, biopsy was always directed into this area. The predominant ultrasound appearance was separately recorded for each core. Results: Carcinoma of the prostate was detected in 87 (32.8%) of the 265 patients. Biopsy cores with isoechoic ultrasound findings revealed CaP in 7.6%. The data for hypoechoic, hyperechoic, mixed-echoic and anechoic lesions were 34.5, 26.9, 21.1 and 0%, respectively. Hypoechoic ultrasound findings were less frequently found in the transition zone of the prostate, but the rate of CaP detection was the same as in the peripheral zone of the prostate. Conclusions:The transrectal ultrasound pattern of the prostate yields important information about the presence of carcinoma of the prostate. Especially hypoechoic lesions indicate the presence of CaP in a significant proportion of cases. However, hyperechoic lesions and lesions of mixed or irregular echogenicity were found to contain cancer in significant numbers as well, and should therefore be considered to be suspicious for cancer when performing transrectal ultrasound of the prostate. Directed biopsy of irregular ultrasound patterns in the prostate seems therefore to be recommendable.
Hintergrund: Der transrektale Ultraschall ist die häufigste bildgebende Untersuchung zur klinischen Beurteilung der Prostata. Zur Diagnostik des Prostatakarzinoms (PCa) hat sich die ultraschallgesteuerte Sextanten-Biopsie als Standardverfahren etabliert. Eine gezielte Biopsie irregulärer Ultraschallbezirke ist hier nicht vorgesehen. Es ist jedoch bekannt, daß sonographisch echoarm erscheinende Areale suspekt für die Präsenz eines PCa sind. Die Wertigkeit nicht einheitlicher oder echoreicher Ultraschallmuster ist jedoch bisher nicht zweifelsfrei geklärt. Ziel der vorliegenden Arbeit war es, mit einem Ultraschallgerät der neuesten Generation die Bedeutung der verschiedenen Ultraschallmuster bezüglich des Vorhandenseins von Prostatakarzinomen zu klären. Material und Methoden: 265 Patienten mit erhöhten PSA-Serumwerten oder suspekten Tastbefunden der Prostata wurden in die prospektive Untersuchung eingeschlossen. Bei allen Patienten wurden systematische, ultraschallgesteuerte Prostatabiopsien, wie in der Sextantenbiopsie vorgesehen, und 4 Zylinder aus der Transitionalzone entnommen. Bei der Biopsie wurde jedoch gezielt die Punktion in Bereichen von – falls vorhanden – irregulärem Ultraschallmuster vorgenommen und das entsprechende Ultraschallbild dokumentiert. Ergebnisse: Bei 87 der 265 Patienten (32,8%) wurden Prostatakarzinome nachgewiesen. Biopsiezylinder aus isodensen Bereichen wiesen in 7,6% ein Prostatakarzinom auf. Die Karzinomhäufigkeit bei Biopsie von echoarmen und echoreichen Arealen sowie von Arealen mit unterschiedlichen Echomustern und von zystischen Arealen wurde mit 34,5, 26,9, 21,1 bzw. 0% ermittelt. Echoarme Befunde wurden seltener in der Transitionalzone nachgewiesen, waren jedoch dort in etwa gleicher Häufigkeit mit einem Karzinom verbunden wie in der peripheren Zone. Schlußfolgerungen: Das transrektale Ultraschallmuster in der Prostata liefert wichtige Hinweise auf das Vorhandensein eines Prostatakarzinoms. Insbesondere echoarme Läsionen deuten auf ein PCa hin. Echoreiche Läsionen und solche mit unterschiedlichen Echomustern enthielten jedoch Karzinome in so bedeutender Anzahl, daß diese Läsionen ebenfalls als karzinomverdächtig eingestuft werden müssen und auch eine gezielte Biopsie dieser Areale im Rahmen der Sextantenbiopsie empfehlenswert erscheint.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

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39

Siddall, J. K. "A multivariate analysis of factors influencing the evolution of prostatic carcinoma." Thesis, University of Leeds, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384682.

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40

Ajayi, A. A. "Investigation of a tumour suppressor gene at chromosome 10q23.3 in prostate carcinoma." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445295/.

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Using various molecular genetic techniques, attempts have been made to identify a tumour suppressor gene (TSG) in prostate carcinoma. This gene will act as a genetic marker to identify patients at risk of disease progression from prostate cancer. The region at chromosome 10q23-24 is postulated to contain a TSG that plays an important role in the development and progression of tumours as it is deleted in a number of cancers including glioblastomas, endometrial and prostate cancer. In glioblastomas, chromosome 10 is partially or entirely deleted in approximately 90% of tumours. The TSG called Pten has been identified on chromosome 10 in the region 10q23.3. The significance of loss of the Pten gene in prostate cancer is unknown. In this thesis, the clinical significance of single nucleotide polymorphisms (SNP'S) in the chromosomal region 10q23-24 was evaluated. Comparisons in the distribution of polymorphisms between Ninety-five prostate cancer patients and forty-three non-prostate cancer patients were made. Three intronic polymorphism markers within the Pten gene were used: a single-base A >G substitution in intron A, 96 bp upstream of exon 2. A 5-bp ATCTT insertion / deletion in intron D, 110 bp downstream of exon 4 and a single-base T >G substitution in intron H, 32 bp downstream of exon 8. This study did not isolate any particular trend in polymorphism distribution in the Pten gene when comparisons were made between the two study groups. The significance of loss of Pten gene in thirty-four prostate cancer patients was evaluated using four highly informative microsatellite markers: D10S541, D10S2492, D10S1765 and AFMa086wg9 located within and around the Pten locus. DNA was extracted from prostate cancer cells following microdissection of archival paraffin embedded radical prostatectomy specimens. Loss of heterozygousity (LOH) studies was performed on matching blood/tissue DNA using these four microsatellite markers. For these case specimens, frequency of allele loss of 48% was found at the D10S541 locus 39% at D10S1765 32% at D10S2492 and 22% at the AFMa086wg9 locus. At all four microsatellite, the mean (range) LOH was 35.25% (22%-48%). Of the 34 case specimens 17(50%) showed LOH in at least one of the informative marker sites. Correlating the significance of this region of LOH with pathological staging and known prognostic indicators in prostate cancer showed that the loss of the Pten gene was associated with late stage disease and likely to be involved in disease progression in prostatic adenocarcinoma.

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41

Stratton, Mimi Suzanne. "Regulation of the matrix metalloproteinase matrilysin in human prostate carcinoma in vitro." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/279914.

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Prostatic carcinoma is the most frequently diagnosed cancer in men in the United States, however, its etiology is largely unknown. The mechanisms of invasion and metastases of prostate carcinoma are currently topics of intense study. Our research focused on IL-1β induced expression of the matrix metalloproteinase, matrilysin, in the prostate. Matrilysin is suspected to be involved with invasive and/or metastatic properties of prostate carcinoma cells and has been shown to be up regulated in prostate cancer. Inhibition of NFκB completely abrogated IL-1β induced promatrilysin expression, however, inhibition of protein synthesis with cyclohexamide completely blocked induction of IL-1β stimulated matrilysin mRNA which indicated that synthesis of one or more signaling factors was required for potentiation of promatrilysin expression by IL-1β. IL-1β also induced expression of IL-6 by LNCaP cells; and, recombinant IL-6 stimulated promatrilysin expression. Cyclohexamide did not inhibit induction of promatrilysin by IL-6 indicating that IL-6 induced promatrilysin expression was direct and did not require new protein synthesis. In addition, our data revealed that inhibition of IL-6 activity with a neutralizing antibody directed against the IL-6 ligand, blocked IL-1β induced promatrilysin expression. Further investigation of this pathway suggested that STAT3 acts downstream to regulate IL-6 induced matrilysin expression. Dominant negative STAT3 inhibited both IL-1β and IL-6 induced activity of a co-transfected matrilysin-luciferase reporter construct. Because of their relevance to prostate cancer, we next examined the effect of androgens on IL-1β induced promatrilysin expression. We found that the androgens, testosterone and dihydrotestosterone blocked IL-1β induced promatrilysin and IL-6 expression through inhibition of NFκB. Androgens showed no effect on IL-6 induced promatrilysin expression indicating that STAT3 is not regulated by androgens in our system. Therefore, our data indicate that IL-1β induced promatrilysin expression is regulated by NFκB mediated synthesis of IL-6 and STAT3 signaling; and, through inhibition of NFκB, androgens can block IL-1β induced promatrilysin. Degradation of the extracellular matrix by MMPs is thought to play a role in prostate cancer invasion and metastatasis. These data provide evidence that IL-1β and IL-6 mediated expression of matrilysin may be involved in prostate cancer progression.

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42

von, Bredow Dorothea Charlotte Minka Erika 1966. "The function of matrilysin and other matrix metalloproteinases in human prostate carcinoma." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/290681.

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Matrix metalloproteinases (MMPs) are involved in many normal and pathological processes that require remodeling of the extracellular matrix. In this dissertation, the distribution of MMPs in human prostate tissue was determined. Matrilysin localized to epithelial cells in prostate ducts surrounded by inflammatory cells, and was focally expressed in carcinoma and prostatic intraepithelial neoplasia, but not in normal glands. Gelatinase A was detected in both benign and malignant prostate tissue in similar amounts. MT-MMP1, an activator of progelatinase A, was present in 100% of the carcinomas, in 88% of the cases with PIN lesions, but only in 34% of the normal glands. Matrilysin converted gelatinase/TIMP-complexes and free gelatinase B into polypeptides with gelatinolytic activity. In contrast, matrilysin was unable to proteolytically cleave gelatinase A/TIMP2 complex, but led to a transient increase in gelatinolytic activity of the proenzyme. Active matrilysin did not enhance the autocatalytic conversion of its own proform. Using indirect immunofluorescence microscopy, degradation of the fibronectin fibrils produced fibroblasts by matrilysin was demonstrated. Fibronectin fibrils represent a major component encountered by tumor cells during invasion. Removal of matrilysin resulted in regrowth of the fibrils, suggesting that matrilysin was not cytotoxic. Stable fragments derived from the gelatin-binding, the heparin-binding, and the cell attachment domains, respectively, of fibronectin, were identified. Their isolation may allow further studies on their influence on cell migration, attachment and signal transduction which are expected to be different from the effects of undegraded fibronectin. Effects of matrilysin on integrins were also investigated. Incubation of beta4, but not of alpha6 or beta1, with matrilysin, resulted in complete degradation in vitro. Thereby a specific fragment of 90 kD was generated, which was not observed with calpain or trypsin. Two putative cleavage sites for matrilysin at residues 107 (isoleucine) and 417 (leucine) located within the extracellular domain of the beta4 were identified by sequence comparisons with known substrates. Degradation of beta4 by matrilysin may partly explain the loss of beta4 integrin in prostate carcinoma. Taken together, the data presented here demonstrate effects of matrilysin on a variety of processes important in carcinogenesis.

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43

Puyhardy, Anne-Marie. "Sensibilité, spécificité et valeur prédictive des signes histologiques élémentaires dans les adénomes et les carcinomes prostatiques." Bordeaux 2, 1991. http://www.theses.fr/1991BOR2M124.

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44

CAPAIA, MATTEO GINO LINO. "Rivalutazione dell’etoposide come farmaco nelle forme avanzate di carcinoma prostatico." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1043145.

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45

Cyrta, Joanna. "A Pleiotropic Role of the SWI/SNF Complex in Cancer – Insights From Two Tumor Types : Small Cell Carcinoma of the Ovary, Hypercalcemic Type and Prostatic Carcinoma Role of Specialized Composition of SWI/SNF Complexes in Prostate Cancer Lineage Genomic Correlates of Clinical Outcome in Advanced Prostate Cancer." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL045.

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Le complexe de remodelage de la chromatine SWI/SNF est un régulateur épigénétique majeur impliqué dans le développement embryonnaire et dans la différentiation cellulaire. De plus, les gènes qui encodent les sous-unités de SWI/SNF sont altérés dans au moins 20% de cancers. Bien que le complexe SWI/SNF soit le plus souvent considéré comme suppresseur des tumeurs, il existe des preuves croissantes que le rôle de SWI/SNF dans le cancer peut dépendre du type de tissu et du contexte.Dans la première partie de cette dissertation, nous présentons la caractérisation moléculaire d’une cohorte indépendante de carcinomes à petites cellules de l’ovaire de type hypercalcémiant (SCCOHT), comme exemple d’un cancer sous-tendu par des altérations perte-de-fonction de la sous unité catalytique de SWI/SNF, SMARCA4. Dans la deuxième partie, nous explorons le rôle du SWI/SNF dans le cancer de la prostate (CP), y compris ses formes les plus agressives : le CP résistant à la castration et le carcinome neuroendocrine. Alors que les mutations des gènes de SWI/SNF sont très rares dans le CP, nous montrons que l’expression de certaines sous-unités peut être dérégulée et qu’une haute expression de SMARCA4 est associée à des CP agressifs. De plus, nous montrons que plusieurs lignées cellulaires de CP dépendent de SWI/SNF pour leur croissance.Au total, ces deux exemples supportent l’hypothèse que SWI/SNF peut jouer des rôles différents dans le cancer en fonction du type tumoral
The SWI/SNF chromatin remodeling complex is a major epigenetic regulator involved in embryonic development and in cell differentiation. In addition, genes encoding components of SWI/SNF are altered in at least 20% of cancers. Even though the SWI/SNF complex is usually regarded as a tumor suppressor, there is increasing evidence that the role of SWI/SNF in cancer may be tissue type- and context-dependent.In the first part of this dissertation, we present the molecular characterization of an independent cohort of small cell carcinomas of the ovary, hypercalcemic type (SCCOHT), as an example of a malignancy driven by loss-of-function alterations of the catalytic subunit of SWI/SNF, SMARCA4. In the second part, we explore the role of SWI/SNF in prostate cancer (PCa), including its most aggressive forms: castration-resistant prostate cancer and neuroendocrine prostate cancer. We show that while SWI/SNF mutations are exceedingly rare in PCa, the expression of several SWI/SNF subunits can be deregulated and that high SMARCA4 expression is associated with aggressive PCa. In addition, we show that many PCa cell lines are dependent on SWI/SNF for their growth.Taken together, these two examples further support the hypothesis that SWI/SNF can play different roles in cancer, depending on the tumor type

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46

LeRoy, Bruce E. "Effects of normal and neoplastic canine prostate tissue on bone formation and investigations on the origin of canine prostate carcinoma /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486463321625278.

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47

Levy, Isra Gabriel. "An investigation into the rising incidence of carcinoma of the prostate in Canada." Thesis, University of Ottawa (Canada), 1993. http://hdl.handle.net/10393/6689.

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Objectives. The purpose of this study was to analyze prostate cancer trends in Canada, determine whether the observed trends are associated with earlier detection, assess the association between prostatectomy rates and prostate cancer incidence rates and assess other possible reasons to explain the observed trends. Conclusions. Correlations between prostate cancer incidence rates and prostatectomy rates suggest that increased surgical treatment of benign prostatic disease contributed to the increase in incidence rates through increased detection of latent cancers. This hypothesis is supported by the chart review, which is the first work to show an association, other than an ecological one, between TURPs and the increased detection of prostate cancer. The increase in early stage cancers, especially incidentally discovered cancers, and the discovery of increased scrutiny of surgical specimens by histopathological staff, corroborates the ecological data. Although elevations in unestablished risk factors may have contributed to the observed increase in incidence, much of the increase can be attributed to an increase in rates of localised disease. This suggests that the increases may be due to early detection and not risk elevation. (Abstract shortened by UMI.)

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Macintosh, Catherine Anne. "An analysis of the role of human chromosome 8 in carcinoma of the prostate in vivo and in vitro." Thesis, University of York, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263671.

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Iughetti, Paula. "Identificação de marcadores moleculares associados com a susceptibilidade ao desenvolvimento do carcinoma de próstata em pacientes brasileiros." Universidade de São Paulo, 2001. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-08112001-103646/.

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No mundo inteiro, o carcinoma de próstata ocupa o quinto lugar entre as neoplasias malignas de maior mortalidade. No Brasil, estima-se para o ano de 2001 que, entre os tumores malignos no sexo masculino, o carcinoma de próstata terá a segunda maior taxa de mortalidade e a primeira taxa de incidência (Estimativa da incidência e mortalidade por câncer no Brasil 2001 INCA). Uma vez que a taxa de mortalidade por carcinoma de próstata na população brasileira tem aumentado significativamente nos últimos anos, a presente tese se propôs a investigar regiões polimórficas em genes conhecidos que poderiam estar associadas a um aumento na predisposição a esta forma de câncer. Assim sendo, estudamos as regiões polimórficas CAG e GGC do gene do receptor de andrógeno; o polimorfismo C1171T do gene do receptor de vitamina D; o polimorfismo D104N do gene da endostatina; o polimorfismo Pro72Arg do gene p53 e a região polimórfica AAAAC localizada na região 3 não traduzida do gene MXI1.
In the worlds population prostate carcinoma is the fifth most commom male cancer-related death malignancy. In Brazil, among all male invasive cancers it is expected that prostate carcinoma will have the second highest death rate and the highest incidence rate (Estimativa da incidência e mortalidade por câncer no Brasil, 2001). As the prostate carcinoma death rate in brazilian population has been increasing over the last several years we proposed to investigate polymorphic regions of known genes that might be associated with prostate carcinoma predisposition. We studied the androgen receptor CAG and GGC polymorphic regions, the vitamin D receptor C1171T polymorphism, the endostatin D104N polymorphism, the p53 Pro72Arg polymorphism and the MXI1 AAAAC polymorphic region.

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Miet, Sophie. "Analyse d'échantillons multiples de carcinomes prostatiques : identification d'altérations génétiques précoces." Lyon 1, 1999. http://www.theses.fr/1999LYO1T130.

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Дисертації з теми "Carcinoma Prostata"

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