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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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Orientadores: Athanase Billis, Luciana Rodrigues de MeirellesDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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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
2
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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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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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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Orientador: Ubirajara FerreiraDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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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
5
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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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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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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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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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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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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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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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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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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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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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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Orientadores: Fernandes Denardi, Wagner Eduardo MatheusDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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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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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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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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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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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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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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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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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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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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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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Siadat-Pajouh, Majid. "Expression of metalloproteinases in human prostate carcinoma and their role in invasion and metastasis." Diss., The University of Arizona, 1991. http://hdl.handle.net/10150/185387.
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Twenty five surgical specimens of malignant human prostate, 3 lymph nodes with metastatic prostate carcinoma, 5 benign prostate hyperplasia (BPH), 11 normal human prostates, as well as 3 human prostate cell lines (DU-145, PC3 and LNCaP) were examined for the expression of human matrix metalloproteinase-7 gene (MMP-7) from the human collagenase family (originally called PUMP-1 for putative metalloproteinase-1) (Majid Siadat-Pajouh et al. 1991). Northern blots were prepared using total RNA extracted from 18 prostate adenocarcinomas, 4 BPH, 2 lymph nodes with metastatic prostate carcinoma and 11 normal human prostates. When the northern blots were hybridized with ³²P labeled MMP-7 cDNA probes, a 1.2 Kb mRNA was detected in 14 out 18 prostate adenocarcinomas, 1 out of 4 BPH, 1 out of 2 metastatic lymph nodes, and 3 out of 11 normal prostates. The 3 human prostate cell lines did not show any evidence of MMP-7 transcript. In situ hybridization was conducted using a ³⁵S labeled MMP-7 cRNA. In situ hybridization was carried out on seven prostate adenocarcinomas, 2 BPH, and 3 metastatic lymph nodes. In situ hybridization revealed that the MMP-7 gene was expressed in the epithelial cells of primary prostate adenocarcinoma as well as invasive and metastatic cells. MMP-7 expression was also seen focally in some benign epithelial cells but not in inflammatory cells or stroma. The combined results of northern analysis and in situ hybridization indicated that 72% of prostate adenocarcinomas, 66% of metastatic prostatic lymph nodes, 40% of BPH and 27% of normal prostate tissues express MMP-7 transcripts. Additional northern blot analysis was performed using probes to human type IV collagenase, type I collagenase and Stromelysin I in human prostate adenocarcinoma as well as normal prostate tissues. The results indicated that 6 out of 10 adenocarcinoma samples and none of the 4 normal samples were positive for type IV collagenase transcripts. None of the tissues examined for the expression of type I collagenase and stromelysin I were found to express the transcripts of interest at detectable levels. A monclonal antibody was generated against a 10 mer synthetic peptide unique to MMP-7. This antibody was reactive with the native protein in frozen prostate tissues. These data suggest that certain metalloproteinases are differentially expressed in prostatic adenocarcinoma and may play a role in invasion and metastasis.
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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 tumoralThe 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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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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Orientador: Athanase BillisDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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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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Klein, Russell David. "The regulation of matrilysin expression in prostate carcinoma cells by paracrine interactions with stromal cells." Diss., The University of Arizona, 1999. http://hdl.handle.net/10150/288940.
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Matrilysin is a matrix metalloprotease that degrades extracellular matrix and basement membrane components. Matrilysin expression is elevated in prostate cancers and is associated with increased histological grade and clinical stage of prostate cancer. We have proposed that the overexpression of matrilysin in prostate cancer cells could be due to stimulation by paracrine factors from stromal cells. Human prostate cancer cell lines were cultured with prostate-derived fibroblasts and fibroblast conditioned media (PFCM). PFCM induced matrilysin expression in three of six prostate cancer cell lines, including the cell line LNCaP. Biochemical characterization of the matrilysin inducing activity in PFCM identified fibroblast growth factors (FGFs) as candidates for this activity. Recombinant FGF-1, FGF-2, FGF-9 and FGF-10 induced matrilysin expression in LNCaP cells. The expression of these FGFs by prostate fibroblasts was verified using RT-PCR. Using a specific inhibitor of FGF receptor activation, we demonstrated that a significant portion of the matrilysin inducing activity of PFCM is dependent on activation of LNCaP cell FGF receptors. Matrilysin expression in normal prostate epithelial cells (PrEC) is not enhanced by treatment with FGFs or PFCM. Aberrant expression of FGFR-1 was observed in LNCaP cells, revealing a potential explanation for the ability of FGFs to induce matrilysin in LNCaP but not PrEC cells. Matrilysin expression is also elevated in inflamed ductile and acinar prostate epithelial cells associated with infiltrating macrophages. Therefore, the ability of monocyte secreted factors to induce matrilysin expression in prostate epithelial cells was determined. Treatment of LNCaP and PrEC cells with conditioned media from activated monocyte cultures induced matrilysin expression in these cells. The factor responsible for this induction was identified as interleukin-1β (IL-1β) using an anti-IL-1β neutralizing antibody. IL-1β induced transactivation of a reporter construct containing cis-elements from the human matrilysin promoter in LNCaP cells, indicating an effect of IL-1β on matrilysin gene transcription. An inhibitor of NF k B activity, pyrollidine dithiocarbamate (PDTC), blocked induction of matrilysin in LNCaP cells by IL-1β. This result implies a role for NFκB in the induction of matrilysin expression by IL-1β, an implication supported by evidence that IL-1β induces NFκB activity in LNCaP cells.
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Mesihää, M. (Markus). "Mass spectrometric characterization of urinary fibrinogen-derived peptides in prostate cancer and renal cell carcinoma." Master's thesis, University of Oulu, 2015. http://urn.fi/URN:NBN:fi:oulu-201512082282.
Full textAbstract:
In previous studies we have found that urinary fibrinogen-derived peptides are potential tumor markers for renal cell carcinoma. These peptides occur at low concentrations in urine.
Identification of a low-abundant tumor marker requires optimal sample preparation and a highly sensitive analyzer. In this work different chromatographic and mass spectrometric methods were compared and evaluated for tumor marker discovery. We used urine samples from patients with renal cell carcinoma and prostate cancer.
Our main targets were peptides derived from fibrinogen beta with unknown sequence that are produced by differential proteolysis. With our optimized workflow we discovered 26 fibrinogen beta derived peptides that have not been identified in urine previously.
30
Alhabhbeh, Ammar, Purva Sharma, Mohammad Ali Khan, Koyamangalath Krishnan, and Devapiran Jaishanker. "Adenocarcinoma of Prostate with Small Cell Differentiation Presenting As Refractory Hypokalemia." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/asrf/2020/presentations/29.
Full textAbstract:
Prostate cancer is among the most common malignancies in males in the United States and adenocarcinoma accounts for 95% of all malignancies of prostate. Rarely prostate cancer can also present as small cell carcinoma. Pure small cell carcinoma is rare at time of initial diagnosis (<2%) however neuroendocrine differentiation into small cell carcinoma may emerge in men who have had previous treatment with ADT for prostate adenocarcinoma. These tumors, sometimes called treatment-related neuroendocrine prostate cancers or aggressive-variant prostate cancers, are increasingly recognized in the castration-resistant phases of disease progression. They account for less than 1% of all prostate cancers. A 73-year-old otherwise male had routine health screening in May 2018. Prostate specific antigen (PSA) level was elevated at 9.53 ng/mL. He had not had a screening PSA for at least two prior years but this was a significant change from prior levels. Patient was asymptomatic however the abnormal laboratory evaluation prompted consultation with Urology. Biopsy of prostate gland confirmed prostatic adenocarcinoma with Gleason's score of 5+ 4 = 9 with bilateral gland involvement. Imaging studies including CT scan of abdomen and pelvis, a bone scan and a PET scan showed no clear evidence of metastatic disease. Patient's clinical stage was determined to be IIIC with T2c N0 M0 disease. Patient began treatment with androgen deprivation therapy and received definitive radiation treatment with external bean radiation therapy from July to September 2018. PSA was 0.08 ng/ml at the end of radiation treatment. Patient did well for about 15 months, after which he had multiple hospital admissions for dyspnea, fluid retention and lower extremity edema. He was also found to have refractory hypokalemia. Patient underwent MRI brain which revealed numerous small enhancing calvarial and skull base lesions consistent with bony metastasis in the skull. Patient also underwent PET/CT scan which showed numerous thoracic spine bony lesions, numerous to count bony metastasis throughout the lumbar spine and pelvis, as well as multiple hepatic lesions. Patient underwent biopsy of right hepatic lobe lesion and pathology was consistent with small cell carcinoma with positive neuroendocrine markers including CD56, synaptophysin and TTF-1. Interestingly patient’s PSA was only 0.09ng/dL. Given refractory hypokalemia, paraneoplastic syndrome was suspected and further work-up was initiated. Serum cortisol levels were elevated at 119.6 mcg/dL (3.7-19.4) and ACTH level was 333 pg/mL (7.2 - 63.3). Aldosterone level was <1 ng/dL (0 - 30.0). Patient was diagnosed with paraneoplastic Cushing syndrome. Given aggressive nature of this small cell transformation, patient was started on treatment with systemic chemotherapy with Carboplatin/Etoposide during the hospital stay, with stabilization of potassium levels. Prostate small cell carcinoma poses a challenge for diagnosis and treatment. In contrast to adenocarcinoma of the prostate, serum prostate-specific antigen (PSA) is not predictive of disease severity, nor is it a useful tumor marker for monitoring progression or surveillance. Patients with prostate small cell cancer presents with more diverse symptoms than any other prostate cancer since it tends to metastasize early. Also paraneoplastic syndromes are more common in prostate small cell cancers as well.
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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.
Full textAbstract:
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&rsquos 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.
32
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/.
Full textAbstract:
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.
33
Traeger, Lara N. "Cognitive Predictors of Health-related Quality of Life in Localized Prostate Cancer: A Lifespan Perspective." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/248.
Full textAbstract:
Research on aging indicates that older adults do not, as a group, report decreased health-related quality of life (HRQOL) despite age-related declines in physical health status. Several cognitive adaptation strategies have been suggested to underlie HRQOL stability in this population. Studies of older cancer patients nevertheless show substantial variance in post-treatment HRQOL outcomes, although cognitive mechanisms for individual differences have received little attention. The current study expanded on a developmental adaptation of self-regulation theory in which aging influences both self-vulnerability and perceptions of disease. A model was tested in which older age was hypothesized to predict better HRQOL via less severe illness perceptions in men treated for localized (Stage I and II) PC. Results indicated that age was not directly associated with HRQOL. However, older age was indirectly associated with better HRQOL via less severe PC perceptions. Further, this indirection association helped account for the positive association between age and HRQOL that three risk factors (income, comorbid disease burden, and sexual function) were shown to suppress. Perceptions of PC may promote HRQOL stability by mitigating age-related declines in health and income status. Disease perceptions thus represent critical components of health assessments and interventions for PC survivors of all ages, but particularly for men facing difficulties adapting to complex health profiles or normative lifespan challenges.
34
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.
Full textAbstract:
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 recommendableHintergrund: 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
35
Binneman, Brigitte. "Selective induction of apoptosis by 7- methyljuglone, its derivatives and isolated compounds from foeniculum vulgare Mill. on human cancer cells." Diss., Pretoria : [s.n.], 2009. http://upetd.up.ac.za/thesis/available/etd-06112009-173251/.
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Häggström, Christel. "Metabolic factors and risk of prostate, kidney, and bladder cancer." Doctoral thesis, Umeå universitet, Urologi och andrologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-83947.
Full textAbstract:
Background: Prostate cancer is the most common cancer in Sweden with around 10,000 new cases every year. Kidney and bladder cancer are less common with 1,000 and 2,000 new cases annually, respectively. The incidence of these cancer sites is higher in developed, than in developing countries, suggesting an association between lifestyle and cancer risk. The aims of this thesis were to investigate body mass index (BMI), blood pressure, and blood levels of glucose, total cholesterol, and triglycerides as risk factors for prostate, kidney, and bladder cancer. Furthermore, we aimed at assess probabilities of prostate cancer and competing events, all-cause death, for men with normal and high levels of metabolic factors. Material and methods: This thesis was conducted within the Metabolic Syndrome and Cancer project (Me-Can), a pooled cohort study with data from 578,700 participants from Norway, Sweden, and Austria. Data from metabolic factors were prospectively collected at health examinations and linked to the Cancer and Cause of Death registers in each country. Results: High levels of metabolic factors were not associated with increased risk of prostate cancer, but high levels of BMI and blood pressure were associated with risk of prostate cancer death. The probability of prostate cancer was higher for men with normal levels of metabolic factors compared to men with high levels, but the probability of all-cause death, was higher for men with high levels than for those with normal levels. For both men and women, high levels of metabolic factors were associated with increased risk of kidney cancer (renal cell carcinoma). Furthermore, blood pressure for men and BMI for women were found as independent risk factors of kidney cancer. High blood pressure was associated with an increased risk of bladder cancer for men. Conclusions: High levels of metabolic factors were associated to risk of kidney and bladder cancer and to death from kidney, bladder, and prostate cancer. Compared to men with normal levels, men with high levels of metabolic factors had a decreased probability of prostate cancer but an increased probability of all-cause death.Ytterligare forskningsfinansiärer: World Cancer Research Fund (2007/09) och Wereld Kanker Onderzoek Fonds (R2010/247)
Me-Can
37
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.
Full textAbstract:
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.
38
Kaewsakhorn, Thattawan. "Roles of calcitriol and its analog on canine transitional cell carcinoma in vitro and in vivo, and in normal canine prostate tissue explaints." The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1181937183.
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Litvin, Isnard Elman. "Invasão de nervos pelo carcinoma da próstata em biópsias transretais." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2004. http://hdl.handle.net/10183/10371.
Full textAbstract:
Introdução e Objetivo: A invasão de nervos pelo carcinoma da próstata, em biópsias por agulha, pode ser um preditor independente de extensão extra-prostática e pode influenciar no manejo cirúrgico. Nervos são, algumas vezes, difíceis de serem visualizados em biópsias por agulha da próstata coradas pela técnica da hematoxilina e eosina. É possível que, utilizando-se a técnica da imuno-histoquímica com o anticorpo para a proteína S-100, os nervos e a invasão de nervos sejam mais facilmente detectados, reduzindo-se a quantidade de falso-negativos. Material e Método: Foram examinados 101 exames de biópsias por agulha, correspondendo a setenta pacientes, com carcinoma da próstata, através de lâminas coradas pela técnica da hematoxilina e eosina, selecionados a partir de 500 exames consecutivos. Obtiveram-se novos cortes dos mesmos blocos de parafina que foram corados pela técnica imuno-histoquímica, utilizando o anticorpo policlonal para a proteína S-100. O número total de nervos, o número de nervos invadidos pelo carcinoma da próstata, o número de nervos por área de tecido, o número de nervos invadidos por área de carcinoma e o diâmetro dos nervos invadidos pelo carcinoma foram determinados por dois investigadores, nas duas técnicas de coloração. Resultados: Dos 70 pacientes avaliados 31 (44,3%) apresentaram invasão de nervo pelo carcinoma no HE e 43 (61,4%) apresentaram invasão de nervo com a técnica imunohistoquímica da proteína S-100 (p<0,001). Na área de carcinoma foram detectados mais nervos invadidos no S-100 do que no HE (p<0,001). O diâmetro do menor nervo invadido pelo carcinoma foi menor no S-100 do que no HE (p=0,007). Conclusão: A coloração com a técnica imuno-histoquímica com o anticorpo para a proteína S-100 aumenta a sensibilidade para reconhecer nervos em material de punção-biópsia da próstata por agulha. Também, com o S-100 se reconhecem mais invasões de nervos pelo carcinoma da próstata, as quais não eram visualizadas quando coradas com o HE. Desta forma reduziu-se a quantidade de casos falso-negativos e demonstrou-se que o exame criterioso de espécimes corados com o HE não é suficiente para detectar todas as invasões de nervos pelo carcinoma da próstata.Background: The identification of perineural invasion in prostate needle biopsies may be an independent predictor of extraprostatic extension of prostatic carcinoma and may also affect surgical management. Nerves are often difficult to recognize on hematoxylin and eosin stained prostate needle biopsies. Perhaps using an immunohistochemical stain for S-100 protein, nerves and the presence of perineural invasion, may be more easily detected. Methods: We examined 101 (70 patients) cases of prostatic carcinoma by routine HE stain to determine perineural invasion and nerves. Step sections were immunostained for S- 100 protein (polyclonal antibody). The total nunmber of nerves, the number of nerves showing perineural invasion, the number of nerves per square millimeter of tissue, the number of nerves showing perineural invasion per square millimeter of prostatic carcinoma and the diameter of perineural invasion were determined by two investigators on the HE and S-100 stained prostate needle biopsies. Results: Among the 70 patients, perineural invasion was detected in 31 (44,3%) patients on HE stained sections and in 43 (61,4%) on S-100 stained sections (p<0,001). The prostate needle biopsies on median showed more perineural invasion on S-100 stained than on HE (P<0,001). The minimum diameter of perineural invasion was smaller on S-100 stained than on HE (p=0,007). Conclusions: S-100 staining increases the sensivity with which nerves are recognized in prostate needle biopsies. More significantly, S-100 staining reveals perineural invasion by prostatic carcinoma that is often unrecognized in HE stained sections. These results support that careful examination of routine HE-stained specimens is not sufficient to detect all important nerve invasion.
40
Thomasson, Marcus. "Expression and prognostic value of LRIG1 and the EGF-receptor family in renal cell and prostate cancer." Doctoral thesis, Umeå : Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-29865.
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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.
Full textAbstract:
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 valueDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
42
Miller, Michael Raymond. "Effects and regulation of dystroglycan glycosylation in cancer." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/3146.
Full textAbstract:
The interplay between cancer cells and the extracellular matrix (ECM) remains a critical regulator of both normal tissue organization and cancer cell invasion. Proteins that function as ECM receptors function to link the cell with the ECM. Abberations in either the structure of the ECM or the expression of ECM receptors leads to disrupted interaction and downstream signaling effects. Dystroglyan (DG) is an ECM receptor that is expressed in a variety of tissue types and functions to mediate sarcolemma stability, epithelial polarity, and is critical in the early formation of basement membranes. However, DG has primarily been studied in muscle where loss of its function is linked to a host of muscular dystrophies. In the epithelium, the role of DG remains enigmatic. While DG has repeatedly been shown to lose function during cancer development and progression, the mechanism and functional consequence of its loss are currently unknown.
In order to increase our understanding of DG in cancer development, we analyzed its expression and glycosylation, a functional requirement for DG, in a range of prostate cancer cell lines. Previous work has shown DG to be downregulated in prostate cancer, but the mechanism by which this occurs has remained largely unclear. We found that DG expression is maintained while its glycosylation was heterogeneous in the cell lines. Further investigation revealed that lines with hypoglycosylated DG strongly associated with the loss of expression of the glycosyltransferase LARGE2. Further this enzyme is frequently downregulated in human cancers and appears to serve as a required enzyme in DG glycosylation within prostate epithelium. This is the first work to demonstrate the functional requirement of LARGE2 for DG, and the only work to implicate loss-of-function of LARGE2 in cancer progression.
To determine whether loss of LARGE2 is found in other tumor types, we analyzed human clear cell renal cell carcinoma (ccRCC) samples by immunohistochemistry and via in silico analysis with the Cancer Genome Atlas (TCGA). Our work demonstrated a frequent and significant downregulation of LARGE2 expression and its association with DG hypoglycosylation. Additionally, we found the loss of LARGE2 strongly associated with increased mortality. Thus, we again demonstrated a functional requirement of LARGE2 but also found a clinical correlate with increased mortality.
Finally, we examined the functional outcome of DG hypoglycosylation or loss of expression in both a mouse model of prostate cancer and a variety of cell lines models. We found that while loss of DG expression does not increase prostate cancer growth or metastasis in one model of cancer, loss of its glycosylation does seem to mediate downstream metabolic changes within cells. The mechanism for this change remains unclear.
In summary, these studies have contributed to our understanding of DG glycosylation and function in both prostate and renal carcinoma. Additionally, we have shown a novel mechanism by which DG glycosylation is lost with downregulation of LARGE2 expression. Finally, while we were unable to demonstrate a clear mechanism by which signaling changes arose, we were able to demonstrate a strong correlation between DG hypoglycosylation and increased mortality in ccRCC. These insights could be used to improve treatment of multiple cancer types as our understanding of DG function continues to improve.
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Aarab-Terrisse, Safae. "Impact de l'axe microbiome-thymus sur l'efficacité de la déprivation androgénique et sur le renforcement de l’immuno-surveillance dans le cancer de la prostate Immunodynamics of Explanted Human Tumors for Precision and Personalized Immuno-Oncology Gut Bacteria Composition Drives Primary Resistance to Cancer Immunotherapy in Renal Cell Carcinoma Patients." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL025.
Full textAbstract:
La déprivation androgénique est la pierre angulaire du traitement du cancer de la prostate (CaP), mais la plupart des patients deviendront réfractaires à la castration (CRPC). En outre, les immunothérapies par inhibiteurs de points de contrôle immunitaire ne sont pour l’instant pas un standard dans la prise en charge de ce cancer en raison de son environnement immunosuppresseur. Notre hypothèse est que pour accroître la sensibilité des patients aux traitements immuno-modulateurs (déprivation androgénique, inhibiteurs des points de contrôle immunitaire et autres), il faudrait restaurer l’environnement immunitaire systémique de l’hôte, et rétablir ainsi un microenvironnement intra-tumoral immuno-reactif de manière plus précoce dans la prise en charge de la maladie.Étant donné que les patients atteints d'un cancer avancé peuvent présenter une dysbiose intestinale, qu’on sait que la composition du microbiote intestinal joue un rôle essentiel dans le succès de tout traitement immuno-modulateur, nous avons donc analysé l'impact du système immunitaire, de la composition du microbiote intestinal et la relation entre les deux composants sur la durée de l’hormono-sensibilité chez les patients atteints de CaP et dans un modèle murin de cancer de la prostate (Lignées Myc-CaP).Tout d'abord, en utilisant des anticorps depletant les lymphocytes CD4 ou CD8 et des souris nudes- athymiques, nous avons démontré le rôle clé des lymphocytes T dans le temps jusqu’à résistance à la castration. Ensuite, à l'aide d'expériences d'antibiotiques à large spectre, de « cohousing », de transplantation microbienne fécale (FMT) et d’utilisation de probiotiques immunogènes nous avons dévoilé le rôle fondamental du microbiote intestinal de l’hôte dans le contrôle de la croissance des tumeurs pendant la suppression androgénique. Troisièmement, la métagénomique des fèces couplées aux analyses métabolomiques sanguines ont mis en évidence des changements significatifs associés à la castration et aux manipulations du microbiote. Enfin, l’intégrité du thymus semble être compromise par la présence du cancer de la prostate, que la castration ne restaure pas. Néanmoins, un microbiote sain restaurerait la thymopoïèse et l'émigration des lymphocytes matures associés à une immunosurveillance anticancéreuse efficace. Dans l'ensemble, nous démontrons que la déprivation androgénique permet d'obtenir une efficacité anti-cancéreuse optimale et de longue durée, de manière dépendante des lymphocytes T lorsque la dysbiose intestinale est compensée par la FMT d’individus sains ou par des probiotiques immunogènes. Par ailleurs ce renforcement du tonus immunitaire de l’hôte permettrait de sensibiliser le cancer de la prostate aux traitements ultérieurs par immunothérapieAndrogen deprivation therapy (ADT) is the backbone treatment for Prostate cancer (PCa), but most patients will become refractory to castration (CRPC). In addition, immune checkpoint blockade may not be an option for CRPC. Given that advanced cancer patients may exhibit a gut dysbiosis and the pivotal role of the intestinal microbiota composition in dictating the success of chemo-and immuno-therapy, we analyzed the role of the immune system, the impact of the gut microbiota and the inter-relationship between both components in the time to CRPC in PCa patients and in a mouse model of prostate cancer (MyC-CaP cell line). First, using CD4 or CD8 depleting antibodies and athymic nude mice, we demonstrated the key role of T lymphocytes in the time to progression during ADT. Secondly, using cohousing experiments, fecal microbial transplantation and broad spectrum antibiotics, we unveiled the seminal role of the host microbiota in governing tumor growth control during ADT. Third, metagenomics coupled with metabolomics analyses highlighted significant changes associated with ADT, their physiological relevance being currently investigated. Finally, while the development of PCa compromises the thymus integrity despite ADT; healthy microbiota restores thymopoiesis and the emigration of mature lymphocytes associated with effective anticancer immunosurveillance. Altogether, ADT mediates a full blown T cell-dependent anti-PCa cancer efficacy when intestinal dysbiosis is compensated by FMT or immunogenic probiotics
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Sheppard, Sarah (Sarah Elizabeth). "The effect of temperature on the bystander effect as examined in human prostate carcinoma cells with alpha particle irradiation." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/41596.
Full textAbstract:
Thesis (S.B.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2006."June 2006."
Includes bibliographical references (p. 30-32).
The bystander effect is seen when irradiated cells release a factor that can produce damage or death in neighboring "bystander" cells that are not actually hit by any radiation. One proposed mechanism involves the irradiated cells releasing a soluble factor into the medium that can cause damage to the non-irradiated cells. Previous studies in the Coderre lab showed that the soluble factor released by DU-145 human prostate carcinoma cells was a short-lived, free radical species (Wang and Coderre, Rad. Res., 164, 711-722, 2005). This thesis examined the effect of temperature on the bystander effect. A co-culture system was used to create irradiated and bystander DU-145 cells in the same medium. This thesis showed that a decrease in temperature lessens or prevents the bystander effect. Researching the bystander effect will allow a better understanding of a process that may already be occurring during alpha-particle based therapies such as boron neutron capture therapy (BNCT) and tumor radioimmunotherapy and could provide a means to improve these therapies.
by Sarah Sheppard.
S.B.
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Silva, Luciana Sanches. "Pesquisa de células tumorais circulantes em pacientes com câncer de próstata por método de filtração celular." Botucatu, 2018. http://hdl.handle.net/11449/155896.
Full textAbstract:
Orientador: Adriana Polachini ValleResumo: Introdução: O câncer de próstata (CP) é o mais incidente entre os homens em todas as regiões do Brasil. A detecção e caracterização de células tumorais circulantes (CTCs) tem sido apontada como uma alternativa para melhor compreensão da biologia dos tumores, incluindo câncer de próstata. Objetivo: Este estudo tem como objetivo avaliar a detecção de CTCs em pacientes com tumor de próstata localizado e metastático por teste rápido de filtração celular. Metodologia: Foram incluídos pacientes com diagnóstico anatomopatológico de câncer de próstata ou neoplasia intraepitelial prostática. Os dados demográficos, laudos anatomopatológicos e de Cintilografia Óssea e valores do antígeno prostático especifico ( PSA) foram obtidos pelo estudo dos prontuários médicos dos pacientes. Os pacientes foram classificados como portadores de tumor metastático quando apresentavam evidência de imagem metastática pela Cintilografia Óssea. As CTS foram isoladas por teste rápido de filtração celular com posterior imunocitoquímica utilizando-se anticorpos monoclonais anti-PSA para caracterização câncer de próstata específica das células. Resultados: As CTCs foram detectadas em 9 dos 21 pacientes (43%) com positividade de 60% no grupo metastático e 36% no grupo de tumor localizado. Não foram observadas associações entre os valores de PSA e tratamento instituído com a detecção de CTCS. Discussão: A positividade das CTCs no presente estudo mostrou-se semelhante aos dados da literatura, embora possam ser ci... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Introduction: Prostate cancer (PC) is the most frequent among men in all regions of Brazil. The detection and characterization of circulating tumor cells (CTCs) has been pointed out as an alternative for a better understanding of the biology of tumors, including prostate cancer. Objective: This study aims to evaluate the detection of CTCs in patients with localized and metastatic prostate tumor by rapid cell filtration test. Methodology: Patients with anatomopathological diagnosis of prostate cancer or prostatic intraepithelial neoplasia were included. Demographic data, anatomopathological and bone scintigraphy reports and prostate specific antigen (PSA) values were obtained by the study of patients' medical records. Patients were classified as having metastatic tumor when they presented evidence of metastatic image by Bone Scintigraphy. The CTS were isolated by rapid cell filtration test with subsequent immunocytochemistry using anti-PSA monoclonal antibodies for cell-specific prostate cancer characterization. Results: CTCs were detected in 9 of the 21 patients (43%) with 60% positivity in the metastatic group and 36% in the localized tumor group. No associations were observed between PSA values and treatment established with CTCS detection. Discussion: The positivity of the CTCs in the present study was similar to the data in the literature, although some limitations of the study may be cited, such as a small number of patients included, difficulties encountered by research... (Complete abstract click electronic access below)
Mestre
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Chen, Jia. "Identification of tumor-associated proteins in human prostatic epithelial cell lines & squamous cell carcinoma of head and neck by proteomic technology." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31519362.
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Alves, Carlos Eduardo Fonseca. "Avaliação epigenética dos genes NKX3.1 E CDH1 e expressão do C-MYC, NKX3.1 e E-Caderina por imuno-histoquímica em microarranjo de tecido (TMA) de lesões pré-neoplásicas e neoplásicas na próstata de cães." Botucatu, 2016. http://hdl.handle.net/11449/143108.
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Orientador: Renée Laufer AmorimResumo: A próstata canina é um bom modelo para estudos comparados entre o cão e o homem, uma vez que essas duas espécies desenvolvem espontaneamente carcinoma de próstata (CP). Para melhor caracterização do CP canino, a presente pesquisa foi dividia em quatro capítulos que avaliam diferentes aspectos dos CPs em cães. A atrofia inflamatória proliferativa (PIA) é uma lesão pré-neoplásica descritas em humanos e pouco estuda em cães. Nós caracterizamos essa lesão em cães e identificamos uma forte relação entre a localização topográfica da PIA com os CPs. Além disso, foi identificada a perda de expressão gênica e proteica de PTEN e AR na PIA. Esses fatores associados corroboram com o potencial pré-neoplásico desta lesão em cães. Um achado interessante foi a alta expressão de P63 na PIA e em um grupo de CP caninos. Para melhor caracterizar este grupo, foi avaliada a expressão imuno-histoquímica de diferentes citoqueratinas e outras proteínas relacionadas ao desenvolvimento do CP em humanos. Os carcinomas que apresentam expressão de P63 apresentaram padrões morfológicos com escore de Gleason alto e um fenótipo mais agressivo quando comparado à tumores que não apresentação expressão de P63. Posteriormente, a expressão gênica e proteica de E-caderina, NKX3.1 e C-MYC foi avaliada em CP como marcadores nas diferentes lesões. Além disso, nós avaliamos a metilação como mecanismo regulatórios dos genes CDH1 e NKX3.1. Foi possível identificar a perda de E-caderina e NKX3.1 nos tumores, comparado à ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The canine prostate gland can be used as a model to human prostatic disease since dogs and men are the only species that spontaneously develop prostate carcinoma (PC). To better characterize the canine PC, this research was divided into four chapters that evaluated different aspects of the PC in dogs. The proliferative inflammatory atrophy (PIA) is a pre-neoplastic lesion described in humans and few studies in dogs describe it as a preneoplastic lesion. This study characterized PIA in dogs and identified a strong relationship between the PIA topography with PC. In addition, we identified the loss of PTEN and AR expression in PIA. These findings demonstrated the potential of PIA as a preneoplastic lesion in dogs. An interesting finding in this research was the high expression of P63 in PIA and a group of PC. This study found a group of PC showing P63 positive expression in neoplastic epithelial cells. Thus, these tumors were selected to better characterize them using immunohistochemistry. These tumors had an aggressive phenotype and presented high expression of AKT and C-MYC and loss of NKX3.1. Further, we selected a usual group of PC and evaluate the expression of E-cadherin, NKX3.1 and C-MYC. In addition, we evaluated the methylation as a regulatory mechanism of CDH1 and NKX3.1 genes. We have identified loss of E-cadherin and NKX3.1 in PC compared to normal prostate and C-MYC overexpression. The expression of E-cadherin was related to overall survival and Gleason score. The ... (Complete abstract click electronic access below)
Doutor
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Rodrigues, Marcela Marcondes Pinto. "Imunomarcação de COX-2 e TGF-beta nas lesòes proliferativas da próstata do cão /." Botucatu : [s.n.], 2007. http://hdl.handle.net/11449/86628.
Full textAbstract:
Orientador: Renée Laufer AmorimBanca: Veridiana Maria Brianezi Dignani De Moura
Banca: Sérgio Luis Felisino
Resumo: As lesões prostáticas em cães vêm sendo cada vez mais estudadas, uma vez que esta espécie é considerada modelo experimental para afecções prostáticas no homem. As principais são a hiperplasia prostática benigna (HPB), prostatites, cistos e o adenocarcinoma. Recentemente tem se dado atenção às lesões pré-neoplásicas, dentre elas a neoplasia intra-epitelial prostática (PIN) e a atrofia inflamatória proliferativa (PIA). Alguns marcadores imunoistoquímicos são utilizados com o objetivo de avaliar o desenvolvimento de câncer prostático a partir de lesões pré-neoplásicas. A cicloxigenase-2 (COX-2) apresenta papel fundamental na resposta inflamatória e, esta pode ter relação com o desenvolvimento do câncer, além de induzir estímulos mitogênicos, enquanto que o fator de crescimento transformador-ß (TGF-ß) induz a angiogênese e inibe a proliferação celular, sendo considerado um mediador do crescimento prostático. No presente trabalho estes marcadores foram utilizados com o objetivo de correlacionar lesões não neoplásicas, pré-neoplásicas e neoplásicas. Os resultados obtidos mostram que as neoplasias e as lesões pré-neoplásicas expressam grande quantidade de COX-2 e TGF-ß, o que permite afirmar o papel destas proteínas no desenvolvimento do câncer prostático em cães.
Abstract: Prostatic lesions in dogs are being studied more and more, since the dogs are considered na experimental model for prostatic diseases in humans. The main prostatic diseases are benign prostatic hyperplasia (BPH), prostatic inflammation, cysts and adenocarcinoma. Pre neoplastic lesions are being studied, among them prostatic intra epithelial neoplasia (PIN) and prostatic inflammatory atrophy (PIA). Immunohistochemistry markers are used to evaluate prostatic cancer from pre neoplastic lesions. COX-2 has the main role in inflammatory response and can be involved in cancer development, because induces mitosis, and TGF-ß) induces angiogenesis and inhibits cellular proliferation, and is considered a prostatic growth mediator. In this study, these markers were used to correlate non neoplastic lesions, pre neoplastic lesions and prostatic cancer. Our results show that neoplastic and pre neoplastic lesions express high amounts of COX-2 and TGF-ß, witch allows us to confirm the involvement of these proteins in prostatic cancer development in dogs.
Mestre
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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.
Full textAbstract:
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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Hawkins, William Tressel II. "Combinatorial Modulation of Multiple Signaling Pathways to Gain Therapeutic Response in Breast and Prostate Cell Carcinomas." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/1043.
Full textAbstract:
Our laboratory is primarily interested in novel pharmacological intervention of cell proliferation and survival pathways expressed in various types of cancer. These cyto-protective pathways can be activated in response to growth factor stimulation, toxic insult and radiation. In our studies, we utilized novel drug combinations with and without radiation to enhance breast & prostate tumor cell death both in vitro and in vivo. Previous studies from our group have shown that UCN-01 and MEK1/2 inhibitors interact to cause tumor cell death in transformed cell lines in vitro. We extended this observation to an in vivo animal model system using the estrogen dependent breast cell carcinoma line MCF-7 and the estrogen independent breast cell carcinoma line MDA-MB-231. This drug combination was shown to profoundly reduce tumor cell proliferation in vivo and also exhibited the ability to significantly reduce ex-vivo tumor cell colony formation 30 days after cessation of the combination drug treatment. In addition, tumor cell death coincided with decreased ERK112 phosphorylation, reduced immunoreactivity of Ki67 and CD31. Overall, these studies demonstrate that UCN-01 and MEK112 inhibitors have the potential to suppress mammary tumor growth in vivo which is independent of p53 status, estrogen dependency, caspase-3 levels or oncogenic K-RAS expression. In our LnCap prostate carcinoma cell studies we demonstrated the impact of hCG and lovastatin in combination with ionizing radiation to radiosensitize and enhance tumor cell lethality. This enhancement was attributed to the hCG-induced activation of ERBB1 via a GPCR, MEK112 and metalloprotease dependent paracrine mechanism which was further enhanced by radiation. This enhanced cell killing effect was shown to involve prolonged activation of PARP1 which could be suppressed by inhibition of ERBB1, MEKl , PI3 kinase or PARP1. Therefore, the combination of hCG, lovastatin and radiation may represent a novel approach to kill prostate cancer cells and potential new therapy.