Rozprawy doktorskie: „Prostate”

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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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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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Birtle, A. J. "Prostate specific antigen negative prostate cancer". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444634/.

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Prostate specific antigen (PSA) has been used in the diagnosis and monitoring of prostate cancer for almost 20 years. Most men who present with metastatic prostate cancer have markedly elevated serum levels of PSA. However, approximately 1% of cases have serum PSA levels that are much lower than the tumour burden would suggest - so-called "PSA-Negative" tumours. Their diagnosis may be delayed, and management compromised. Little is known about this patient group. The aim of this study was to improve the understanding and management of "PSA-negative" prostate cancer. The clinical history and tissue from 33 patients who presented with treatment-naive metastatic prostate cancer and a serum PSA < 10 ng/ml were included in this study, the largest series so far reported. Clinical and immunohistochemical features were defined and alternative biomarkers investigated. Potential mechanisms underlying PSA-negativity were explored using prostate cancer cell lines and archival tissue. From the clinical case notes review, patients presenting with low serum PSA and metastatic prostate cancer have a similar pattern of disease to men with high PSA prostate cancer. However, response duration to first line hormonal treatment and overall survival were shorter. Immunohistochemistry performed on archival prostatic tissue has shown that the majority of the cancers are positive for PSA, despite low serum levels. The extent of PSA immunostaining is patchy and could be missed on biopsy. PSMA and AR are expressed, however, and represent alternative diagnostic aids. The study indicates that PSMA and PAP should be explored as potential serum biomarkers in this patient group. The androgen receptor (AR) remains expressed in over 90 % of these cases and therefore defects in this pathway are unlikely to explain the low serum PSA levels. Neither loss of heterozygosity nor gene methylation of AR or PSA appear to be mechanisms underlying low serum PSA levels.

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Quintal, Maisa Momesso de. "Cancer de prostata : estudo da extensão tumoral em prostatectominas radicais". [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308452.

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Orientador: Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: No estadiamento TNM 1997, os tumores de próstata órgão-confinados eram subdivididos em dois grupos: pT2a (unilaterais) e pT2b (bilaterais). Em 2002, o sistema TNM reclassificou os tumores em três grupos: pT2a (envolvimento de menos da metade de um lobo), pT2b (mais da metade de um lobo), e pT2c (envolvimento bilateral). Estudos recentes questionam a verdadeira existência de tumores pT2b, assim como diferenças relacionadas à progressão bioquímica pós-prostatectomia radical entre os estádios pT2a e pT2c. Os objetivos deste trabalho são: avaliar a extensão tumoral em espécimes de prostatectomia radical, relacionando-a com graduação histológica de Gleason, comprometimento de margens cirúrgicas, estádio clínico e patológico, PSA pré-operatório e tempo de progressão bioquímica pós-prostatectomia radical; comparar tumores localizados com comprometimento bilateral (T2c) com tumores órgão-confinados com comprometimento unilateral (pT2a) quanto aos mesmos parâmetros e verificar a existência real do estádio patológico pT2b. Foram estudados 230 homens submetidos à prostatectomia radical no período de janeiro de 1997 a julho de 2005 na Universidade Estadual de Campinas. Os espécimes cirúrgicos foram totalmente incluídos para exame histológico. A extensão tumoral foi avaliada utilizando-se um sistema de contagem de pontos. Os espécimes cirúrgicos foram estadiados segundo os critérios do TNM 2002. Os valores séricos de PSA = 0,4 ng/ml foram considerados como progressão bioquímica tumoral. Os dados foram analisados estatisticamente utilizando-se o teste de Mann-Whitney para comparação de amostras independentes e o teste exato de Fisher para avaliação de diferenças entre proporções. Foram considerados significantes os valores de p = 0,05. Para avaliação do tempo de progressão bioquímica pós-prostatectomia radical utilizou-se o produto limite de Kaplan-Meier. Utilizando os critérios TNM 2002, 29 pacientes (12,7%) eram pT2a; 139 (61,3%) eram pT2c; 30 (13,7%) eram pT3a e 28 (12,3%) eram pT3b. O mínimo e o máximo de pontos totais obtidos em tumores que envolviam apenas um lobo prostático foi de 192 e de 368 pontos, respectivamente; o maior tumor unilateral mostrou 68 pontos positivos (menos da metade do valor mínimo de pontos totais). Não foi constado nenhum caso onde a neoplasia prostática comprometesse mais da metade de um lobo, sem envolver o lobo contralateral (pT2b). A extensão tumoral apresentou relação significante e direta com PSA pré-operatório, graduação histológica de Gleason, margens cirúrgicas positivas e estádios clínico e patológico, mas não com o tempo de progressão bioquímica pós-prostatectomia radical. Não houve diferenças entre os pacientes com estádios pT2a e pT2c com relação ao PSA pré-operatório, contagem final de Gleason e tempo de progressão bioquímica, com exceção do comprometimento das margens cirúrgicas. Há relação da extensão tumoral em espécimes cirúrgicos de prostatectomia radical com PSA pré-operatório, graduação histológica de Gleason, margens cirúrgicas positivas e estádio patológico. A extensão tumoral isoladamente não parece influenciar o tempo de progressão bioquímica pós-prostatectomia radical. Este estudo questiona a real existência do estádio pT2b (tumores unilaterais que ocupam mais da metade de um lobo). Não há diferenças significativas quanto ao tempo de progressão bioquímica pós-prostatectomia radical entre os estádios patológicos pT2a e pT2c. Esses achados apóiam autores que defendem a não subdivisão do estádio pT2
Abstract: In the 1997 TNM staging system, confined-organ prostate tumors were classified in two groups: pT2a (unilateral involvement) and pT2b (bilateral involvement). In 2002, TNM staging system reclassified those tumors in three groups: pT2a (less than one half of one lobe involvement), pT2b (more than one half of one lobe involvement) and pT2c (bilateral involvement). Recent studies put in question the existence of a real pT2b tumor as well as a difference related to biochemical progression after radical prostatectomy between pT2a and pT2c tumors. The aim of this study is to verify the real existence of pT2b and evaluate tumor size comparing to Gleason score, positive surgical margins, clinical and pathological stage, preoperative PSA and time to biochemical progression after radical prostatectomy. Besides that, compare bilateral tumors (pT2c) with unilateral ones (pT2a) according to the same parameters. A total of 230 men were submitted to radical retropubic prostatectomy from July 1997 to July 2005 at Universidade Estadual de Campinas. All the surgical specimens were evaluated by complete embedding and whole mount processing. Tumor extent was evaluated through a point-count method. The surgical specimens were staged according to 2002 TNM staging system. The serum values of PSA= 0,4 ng/ml were considered biochemical progression. Mann-Whitney¿s test and Fisher¿s exact test were used to compare independent samples and different proportions. p = 0,05 was considered significant. Time to PSA progression was studied using the Kaplan-Meier¿s product limit survival estimates. Using the 2002 TNM criteria, 29 patients (12,7%) were pT2a; 139 (61,3%) were pT2c; 30 (13,7%) were pT3a and 28 (12,3%) were pT3b. The minimum and maximum total points obtained in unilateral tumors were 192 and 368 points, respectively; the biggest unilateral tumor showed 68 positive points (less than half the minimum of total point count). This study found no pT2b tumors (unilateral tumors involving greater than one-half of one prostatic lobe). Tumor extent was directly related to preoperative PSA, Gleason score, positive surgical margins, clinical and pathological stage. Alone, tumor extent does not seem to influence biochemical progression. Comparing pT2a with pT2c, there were no differences in preoperative PSA, Gleason score and biochemical progression, except positive surgical margins. There is a connection of tumor extent in radical prostatectomy specimens with preoperative PSA, Gleason score, positive surgical margins and pathological stage. Tumor extent does not seem to influence time of biochemical progression after retropubic radical prostatectomy. This study puts in question the real existence of pT2b pathological stage (unilateral tumors involving greater than one-half of one prostatic lobe). There are no significant differences between pT2a and pT2c patients in time to biochemical progression after retropubic radical prostatectomy. These findings support authors who question the subdivision of pathological stage pT2
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas

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Paes, Thais Ruano Lazzarini. "Cancer de prostata : estudo das margens cirurgicas comprometidas e invasão do colo vesical em especimes de prostatectomia radicais". [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308448.

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Orientador: Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Carcinoma da próstata é uma neoplasia maligna constituída por células que se originam de ácinos e/ou ductos prostáticos, com arranjo, graus de diferenciação e comportamento biológico variáveis. A prostatectomia radical como tratamento primário para câncer prostático clinicamente localizado tem aumentado dramaticamente nesta última década devido ao PSA. A identificação de margens cirúrgicas positivas é um fator adverso no prognóstico dos pacientes submetidos à prostatectomia radical por câncer prostático. Muitos autores relatam que margens cirúrgicas positivas são fatores preditivos significantes na progressão da doença. Já outros, afirmam que a sobrevida não é afetada pelas margens cirúrgicas. O significado do envolvimento somente microscópico do colo vesical é controverso na literatura. Para alguns autores há um menor risco de progressão quando comparado ao comprometimento das vesículas seminais e para outros o risco de recorrência é maior. Os objetivos deste trabalho foram: correlacionar margens cirúrgicas comprometidas e invasão do colo vesical em espécimes de prostatectomias radicais com variáveis clínico-patológicas. Foram estudados 230 pacientes submetidos consecutivamente a prostatectomia radical no Hospital de Clínicas da Universidade Estadual de Campinas (UNICAMP), no período de janeiro de 1997 a julho de 2005. Todo o espécime cirúrgico obtido foi previamente processado por inteiro para exame histopatológico. Cada peça cirúrgica foi pesada e medida, e a superfície foi totalmente coberta por tinta Nankim. O colo vesical e a margem apical foram amputados. Os valores séricos de PSA = 0,2 ng/mL foram considerados como progressão bioquímica. Os dados foram analisados estatisticamente utilizando-se o teste de Mann-Whitney para comparação de amostras independentes e o teste exato de Fisher para avaliação de diferenças entre proporções. O tempo de sobrevida livre de progressão bioquímica foi baseado na análise do produto-limite de Kaplan-Meier e a comparação entre os grupos foi feita usando o teste do long-rank, sendo considerado significante o valor de p =0,05. Os resultados obtidos mostraram que as margens cirúrgicas comprometidas têm relação significante com PSA pré-operatório, contagem final de Gleason (no espécime cirúrgico), extensão tumoral, estádio patológico, e tempo de progressão bioquímica (PSA) pós-prostatectomia radical. Pacientes com invasão do colo vesical apresentaram relação significante com PSA pré-operatório; contagem final de Gleason tanto no espécime cirúrgico quanto na biópsia prostática de agulha correspondente; extensão tumoral; estádio patológico e margens cirúrgicas uretral e circunferencial, porém sem relação estatística com tempo de progressão bioquímica (PSA) pós-prostatectomia radical. Ao compararmos a evolução livre de progressão bioquímica (PSA) pós-prostatectomia radical entre pacientes com invasão do colo vesical, e pacientes com invasão da vesícula seminal, os achados não apóiam considerar invasão microscópica do colo vesical como sendo pT4
Abstract: Prostate cancer is a malignant neoplasia composed by cells with origin in prostatic acini and/or ducts that present variable arrangement, biologic behavior and differentiation. Radical prostatectomy as primary treatment for localized prostate cancer has been increased dramatically in the last years due to PSA. Positive surgical margin identification is an adverse prognostic factor in patients submitted to radical prostatectomy. Many authors mention that positive surgical margins are a significant predictive factor for disease progression. Others affirm that positive surgical margins or other variables do not affect prognosis. The significance of microscopic involvement of bladder neck is controversial in the literature. For some authors biochemical progression in patients with bladder neck invasion is less important than seminal vesicle involvement but not for others. The purpose of the study was to find any possible relationship of surgical margins and bladder neck invasion in radical prostatectomies to several clinicopathological variables. This study consisted in 230 patients submitted consecutively to radical prostatectomy in the University Hospital, School of Medicine, State University of Campinas (Unicamp), between January 1997 and July 2005. All specimens were whole processed for pathological examination. Each surgical fragment was weighted, measured, and painted with Nankim's ink. Bladder neck and apex were separately processed. Biochemical (PSA) progression following radical prostatectomy was considered as being = 0,2 ng/mL. The data were statistically analysed using Mann-Whitney test to compare independent samples and exact Fisher test to evaluate differences between proportions. The time to biochemical (PSA) progression was analysed by the Kaplan-Meier product-limit analysis and the comparison between groups was done using the log-rank test. A p value of <0.05 was considered statistically significant. The results showed that patients with positive surgical margins had higher preoperative PSA, higher Gleason score on the specimen, and more extensive tumors and pathologic stage. Patients with bladder neck invasion had higher preoperative PSA, higher Gleason score in biopsies and specimens, higher number of apical and circumferential positive surgical margins, and more extensive tumors and pathological stage. The time to biochemical (PSA) progression following radical prostatectomy was not statistically significant comparing patients with and without bladder neck invasion, but statistically significant when comparing patients with and without vesicle seminal invasion. This latter finding do not support considering bladder neck invasion as stage pT4
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas

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Özorak, Alper Perk Hakkı. "Prostat biyopsilerinde 6-10-12 kadran biyopsilerin prostat kanseri saptama oranları ve prostat kanseri saptanması için optimal alınması gereken parça sayısının araştırılması /". Isparta : SDÜ Tıp Fakültesi, 2007. http://tez.sdu.edu.tr/Tezler/TT00340.pdf.

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Pritchard, Colin C. "The molecular program of mouse prostate development /". Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/5041.

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Almeida, Neto Adauto 1977. "Abordagem quantitativa da expressão do gene WFDC1 e sua isoforma delta 3 = Quantitative approach of the expression of WFDC1 gene and its isoform delta 3". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317579.

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Orientadores: Hernandes Faustino de Carvalho, Paulo Roberto Eleutério de Souza
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: A próstata é alvo de afecções severas que comprometem a função urinária, a qualidade de vida e que consistem em risco de vida aos indivíduos do sexo masculino, particularmente com o avançar da idade. Interações dinâmicas entre o epitélio prostático e o estroma, regulam vários aspectos do desenvolvimento, da função e das patologias prostáticas. O gene WFDC1 é expresso pelas células musculares lisas do estroma prostático normal e tem função na regulação do comportamento do epitélio, na organização da matriz extracelular e na regulação da angiogênese. Dois transcritos principais são oriundos de splicing alternativo do transcrito primário: um com todos os éxons (WFDC1) e outro sem o éxon 3 (Delta 3). Neste trabalho, investigamos as relações quantitativas entre estas duas variantes, com emprego de qRT-PCR (Taqman) e sondas para as junções dos éxons 2-3 e 2-4, em amostras de hiperplasia prostática benigna (BPH) e de câncer de próstata (PCA) provenientes de bancos de tecidos. A expressão do gene marcador MYH11 foi utilizada como estimativa do conteúdo de células musculares lisas nas amostras. Os resultados demonstraram que as amostras puderam ser dividas em dois grupos com expressão diferencial da MYH11(um com baixa expressão e outro com alta miosina, sendo o primeiro correspondente ao quartil inferior da distribuição dos valores de expressão). Foi demonstrada correlação entre a expressão de WFDC1 e MYH11 em BPH, mas não em PCA, enquanto não houve correlação entre Delta 3 e WFDC1 e nem com MYH11. O conteúdo de Delta 3 variou em cinco ordens de magnitude em comparação ao de WFDC1. A razão entre as duas variantes apresentou variação exponencial, distribuições discretas e intercaladas das amostras de BPH e de PCA, que se distribuíram em populações que preservaram as relações 10:1; 1:1 e 1:3. Poucas amostras estiveram livres de cada uma destas variantes. Em conclusão, a expressão do gene WFDC1 e de sua variante WFDC1 correlaciona-se com a diferenciação das células musculares lisas, mas não está condicionada a ela, enquanto a expressão de Delta 3 é completamente independente deste parâmetro e tem correlação positiva com o progressão do PCA, quando o sistema de classificação de Gleason (Gleason 1 + Gleason 2) foi considerado. Adicionalmente, fatores independentes da idade, incidência de BPH ou PCA, são mais influentes na determinação da quantidade total e da proporção entre as duas variantes
Abstract: The prostate gland is intimately related with reproductive and urinary functions, commonly disturbed by a series of diseases. Besides reducing the quality of life, they consist in serious life risk particularly to the aging men. Dynamic interactions between the epithelium and stroma in the gland regulate various aspects of development, function and pathologies. The WFDC1 gene is expressed by smooth muscle cells in the prostate stroma and its product ps20 was shown to control epithelial cell behavior, extracellular matrix organization and angiogenesis. It is supposed to function as a serine protease inhibitor, as other members of its family do. Two transcripts are produced as a result of alternative splicing. The first (WFDC1) retains all exons and the second (Delta 3) lacks the exon 3. In this work, we investigated the quantitative relationship among these two splicing variants, using qRT-PCR (Taqman) probing the junctions between exons 2-3 and 2-4, in benign prostatic hyperplasia (BPH) and prostate cancer (PCA) samples from tissue banks. The expression of the MYH11 gene was used to estimate the content of smooth muscle cells in the samples. The results demonstrate that the samples could be divided in two groups with low or high expression of MYH11, the first corresponding to the lower quartile of expression values). WFDC1 and MYH11 expression were correlated in the BPH samples. Delta 3 expression was independent of both WFDC1 and from WFDC1. The ratio between the variants WFDC1 and Delta 3 varied exponentially in five orders of magnitude. The the ratio between the two variants also varied exponentially, with BPH and PCA samples arranged in discrete and intercalated subgroups. The distribution of populations with different expression levels preserved the ratios 10:1, 1:1 and 1:3. Either variant was absent in only a few samples. In conclusion, the expression of WFDC1 and it WFDC1 variant correlates with but is not conditioned to the differentiation of smooth muscle cells, while Delta 3 is completely independent and is positively correlated with PCA grade (as assessed by the summed Gleason score). Unknown factors independent of age, BPH or PCA incidence are likely influencing Delta 3 expression
Doutorado
Biologia Celular
Doutor em Biologia Celular e Estrutural

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Holt, Jim. "Prostate Cancer". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6456.

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Ambrosini, Gina L. "Dietary risk factors for prostate cancer and benign prostatic hyperplasia". University of Western Australia. School of Population Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0135.

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[Truncated abstract] This thesis examines the potential role of dietary intake in the development of two common conditions affecting the prostate gland; prostate cancer and benign prostatic hyperplasia (BPH). Diet is of interest as a potential risk factor for prostate cancer because of geographical variations in prostate cancer incidence and increased prostate cancer risks associated with migration from Asian to western countries. Some geographical variation has been suggested for BPH, but this is less certain. However, both prostate cancer and BPH have potential links with diet through their positive associations with sex hormone levels, metabolic syndrome, increased insulin levels and chronic inflammation. In addition, zinc is an essential dietary micronutrient required for semen production in the prostate gland. The original work for this thesis is presented in six manuscripts of which, four have been published in peer-reviewed journals (at the time of thesis completion). BPH investigated in this thesis is defined as surgically-treated BPH. The following hypotheses were investigated. Regarding foods, nutrients and the risk of prostate cancer and BPH: 1. Increasing intakes of fruits, vegetables and zinc are inversely associated with the risk of prostate cancer and BPH 2. Increasing intakes of total fat and calcium are positively associated with the risk of prostate cancer and BPH. 3. Dietary patterns characterised by high meat, processed meat, calcium and fat content are positively associated with the risk of prostate cancer and BPH. 4. Dietary patterns characterised by high fruit and vegetable and low meat content are inversely associated with the risk of prostate cancer and BPH. v Regarding methodological issues related to the study of diet-disease relationships: 5. Dietary patterns (overall diet) elicited from principal components analysis yield stronger diet-disease associations than when studying isolated nutrients. 6. Remotely recalled dietary intake is reliable enough to be used in studies of chronic disease with long latency periods, such as prostate cancer and BPH. Methods: Data from two studies was used to address the hypotheses above. ... Based on the literature reviewed and the original work for this thesis, the most important dietary risk factors for prostate cancer and BPH appear to be those common to western style diets, i.e. diets high in red meat, processed meat, refined grains, dairy products, and low in fruit and vegetables. This type of diet is likely to result in marginal intakes of antioxidants and fibre, excess intakes of fat and possibly, moderate intakes of carcinogens associated with processed meat and meat cooked at high temperatures. These dietary factors have been linked with biomarkers of inflammation, and they support the hypotheses that chronic inflammation is involved in the development of both prostate cancer and BPH. In addition, this work builds on evidence that zinc is an important factor in prostate health. There is scope for more investigation into the reliability of dietary patterns and the use of nutrient patterns as an alternative to focussing on single food components. Further studies on the reliability of remote dietary intake would also be useful. Because of the latency of chronic disease, it can be theorised that remote dietary recall may uncover more robust diet-disease relationships.

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Khan, Humera. "Determinants of prostate cancer : the Birmingham Prostatic Neoplasms Association study". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3170/.

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This Birmingham Prostatic Neoplasms Association Study (BiPAS) was initiated to investigate determinants of prostate cancer. The study recruited 314 prostate cancer patients, 381 active surveillance patients, 201 hospital controls and 175 population controls. By comparing groups of varying risk, the aetiology of the disease was investigated. Within the BiPAS dataset, sun exposure, physical activity and obesity were analysed. The association with occupation was assessed by performing a meta analysis of 7, 762 cases and 20, 634 controls. Finally, a replication study on genetic polymorphisms on 8q24 using 277 cases and 282 controls from the Netherlands Cohort Study (NLCS) is presented. A protective effect was observed for high sun exposure in early adulthood and high intensity exercise. An increased risk was observed for low intensity exercise and men classed as obese at age 20. The meta analysis suggested moderately increased and decreased risks associated with a number of job titles, however none were statistically significant. The results for allele A on the single nucleotide polymorphism rs1447295 were replicated; however a decreased risk was detected for allele -8 on the microsatellite DG8S737. No significant difference was detected for analysis comparing prostate cancer or high PSA cases.

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Lexander, Helena. "Protein expression in prostate cancer /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-617-4/.

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Souza, Felipe Gonçalves Schröder e. 1983. "Perfil dos pacientes submetidos à biópsia de próstata = Profile of patients who undergo prostate biopsy". [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312937.

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Orientador: Miriam Dambros Lorenzetti
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Introdução: A neoplasia de próstata é a segunda mais prevalente entre os homens, com estimativa de cerca de 68 mil casos novos no Brasil em 2014. Além disso, é a segunda causa de morte no sexo masculino por neoplasias. O câncer de próstata raramente causa sintomas em seus estágios iniciais, por isso existe a necessidade do diagnóstico precoce. Atualmente a forma de rastreamento desta neoplasia ainda é controverso, porém quando realizado, baseia-se em exame digital retal da próstata e na mensuração sérica dos níveis do PSA. Estudos de rastreamento populacional mostraram uma diminuição de 41% no casos de neoplasia avançada de próstata e risco de diagnóstico de câncer 46% maior, quando comparados a grupos não submetidos a rastreamento. O PSA não é câncer específico, então, os refinamentos do PSA (relação do PSA livre/total, densidade do PSA e velocidade do PSA) aparecem como métodos para melhorar sua especificidade, na tentativa de diminuir o número de biópsias desnecessárias. Quando existe suspeita diagnóstica, é indicada uma biópsia guiada por ultrassonografia transretal, procedimento que não é isento de complicações, principalmente as infecciosas. Objetivos: Avaliar a positividade para adenocarcinoma de próstata em biópsias guiadas por ultrassonografia transretal, e estratificá-la de acordo com a idade, com o valor do PSA total, com a densidade do PSA e com a relação entre a fração livre do PSA e o PSA total. Materiais e Métodos: Analisamos retrospectivamente os resultados obtidos no serviço de urologia do Hospital Municipal Dr. Mário Gatti com relação à positividade das biópsias estratificadas pela idade, PSA total, percentual da fração livre do PSA e densidade do PSA, comparando-os com os dados descritos na literatura. Resultados: Foram realizadas 314 biópsias no período de janeiro de 2011 à novembro de 2012. A média de idade dos pacientes foi de 65,2 (± 8,32) anos e a positividade foi de 44,9%. A positividade das biópsias foi maior com o aumento da idade (p<0,001), com o aumento do PSA (p<0,001), com o aumento da densidade (p<0,001) e com a diminuição da relação do PSA (p=0,002) Conclusão: A neoplasia prostática correlacionou-se significativamente com o aumento da idade, do PSA total, da densidade do PSA, e com a diminuição da relação entre o PSA livre sobre o PSA total
Abstract: Introduction: Prostate neoplasia is the second most prevalent neoplasia in men and about 68 thousand new cases were estimated in 2014 in Brazil. In addition, it is the second most common cause of cancer related death in men. Prostate cancer rarely causes symptoms at an early stage, hence the need of an early diagnosis. Although there is still no consensus about how to screen this neoplasia, it is done through digital rectal examination and measurement of PSA levels. Population screening trials showed a decrease of 41% in new cases of advanced prostate neoplasia. The risk of a cancer diagnosis increased 46% when compared to the group who was not screened. PSA is not cancer specific. Therefore, PSA features (relation between free PSA and total PSA, PSA density, PSA velocity) are used to increase its specificity, attempting to reduce the number of unnecessary biopsies. Once there is a cancer suspicion, a biopsy guided by transrectal ultrasonography is indicated, which is not a complication free procedure, mainly infection. Objective: to assess the positiveness of prostatic adenocarcinoma in transrectal ultrasonography guided biopsies and to evaluate it according to age, total PSA value, PSA density, and the relation between free PSA and total PSA. Materials and Methods: This is a retrospective study with patients who underwent prostatic biopsy guided by transrectal ultrasonography done by the urology team from Hospital Municipal Dr. Mário Gatti. Collected data included patient¿s age, total PSA value, PSA density and the relation between free PSA and total PSA. Results: 314 prostatic biopsies guided by transrectal ultrasonography were analyzed between January 2011 and November 2012. Patient¿s mean age was 65.2 (+/-8.32) years. A positive biopsy to adenocarcinoma was found in 44.9% of the patients. The number of positive biopsies was higher among older patients (p<0.001). It was also higher the higher the PSA (p<0.001) and the higher the PSA density (p<0.001). It was inversely related to PSA relation (p=0.002). Conclusion: There is a direct correlation between prostatic neoplasia and age, value of PSA and PSA density. Additionally, prostatic neoplasia is inversely proportional to the relation of free PSA over total PSA
Mestrado
Fisiopatologia Cirúrgica
Mestre em Ciências da Cirurgia

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Pang, See-Tong. "A functional genomics approach to study prostate disorders /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-640-5/.

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Alonso, João Carlos Cardoso 1972. "Açao da dutasterida no tecido prostático humano normal : papel dos receptores hormonais esteroides como possíveis marcadores clínicos". [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313128.

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Orientadores: Wagner Eduardo Matheus, Ubirajara Ferreira
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Introdução: Os andrógenos, além de desempenhar um papel importante no desenvolvimento e no crescimento da próstata, também são responsáveis pelo surgimento e progressão de lesões prostáticas. Portanto, as ações desses hormônios podem ser antagonizadas impedindo a conversão irreversível de testosterona em dihidrotestosterona, por meio da inibição da 5?-redutase. Neste contexto, os objetivos deste estudo foram caracterizar os efeitos clínicos e morfofuncionais da dutasterida, um inibidor de 5?-redutase, em receptores de hormônios esteroides no tecido da próstata humana normal, bem como para verificar a viabilidade desses receptores como potenciais marcadores para o manejo clínico dos pacientes em uso de dutasterida. Métodos: estudo prospectivo, duplo-cego e randomizado que avaliou 49 homens com idades entre 45 e 70 anos, sem alterações no exame de toque retal e com dosagens de PSA entre 2,5 e 4,0 ng/ml. Estes pacientes foram submetidos a biópsia de próstata guiada pelo ultrassom transretal, e após ter sido descartada neoplasia de próstata, foram divididos em dois grupos recebendo dutasterida (n=25) ou placebo (n=24). Os pacientes foram avaliados clinicamente a cada trimestre e, ao final de 12 meses, submetidos a novos testes laboratoriais e análise histopatológica por nova biópsia da próstata. Resultados: Os resultados não mostraram variações significativas nos níveis de estrógeno, testosterona séricos e índice de massa corporal em ambos os grupos, bem como de ER? (receptor estrogênico ?). No entanto, a imunorreatividade para AR (receptor androgênico) e ER? (receptor estrogênico ?) foram significativamente maiores no grupo dutasterida em relação ao grupo placebo, acompanhado por uma redução significativa do volume da próstata e dos níveis de PSA séricos no grupo dutasterida. Além disso, ambos os índices de proliferação e apoptose também foram significativamente maiores no grupo dutasterida, porém a razão proliferação/apoptose foi significativamente menor neste grupo, indicando assim predominância de apoptose. Conclusão: O tratamento com dutasterida mostrou distintas reatividades no tecido prostático normal, apontando a importância da ativação de ER? no mecanismo apoptótico, propiciando efeito protetor no tecido prostático normal, indicando ser este receptor um importante mediador para o seguimento clínico de pacientes em uso de dutasterida
Abstract: Introduction: The androgens, besides playing an important role in prostate development and growth, are also responsible for the development and progression of prostatic lesions. Therefore, preventing the irreversible conversion of testosterone into dihydrotestosterone by inhibiting 5?-redutase can antagonize the actions of these hormones. In this context, the aims of this study were to characterize the clinical and morphofunctional effects of 5?-redutase inhibitor, dutasteride, on steroid hormone receptors in the human normal prostate tissue, as well as to verify the viability of these receptors as potential markers to clinical management of patients on dutasteride use. Methods: Prospective, randomized and double-blind study, evaluating 49 men with ages between 45 and 70 years, no alterations in digital rectal examination and PSA levels between 2.5 and 4.0 ng/ml. These patients underwent prostate biopsy guided by transretal ultrasound (TRUS) with prostate neoplasia ruled out and it has divided into two groups receiving dutasteride (n=25) or placebo (n=24). Patients were clinically assessed every three months and at the end of 12 months undergoing new laboratory tests, prostate rebiopsy, histopathological and clinical analysis. Results: The results did not show significanty variations in serum estrogen and testosterone levels and body mass index in both dutasteride and placebo groups, as well as their ER? (? estrogen receptor). However, AR (androgen receptor) and ER? (? estrogen receptor) immunoreactivity were significantly higher in the dutasteride group in relation to placebo group, followed by a significant reduction in prostate volume performed by TRUS and total serum PSA levels in the dutasteride group when compared to placebo group. Furthermore, both proliferative and apoptotic indices were significantly higher in the dutasteride group in relation to placebo group. However, the proliferation/apoptotic ratio was significantly lower in the dutasteride group, indicating predominance of apoptotic process. Conclusion: The dutasteride treatment led to distinct reactivities in the normal prostate tissue, indicating different signals to the dynamics of the prostate and pointed out the importance of ER? pathways in the activation of apoptosis. Taken together, these data demonstrated that dutasteride treatment exerted protective effect in the normal prostate via ER?, indicating this receptor as important mediator to clinical management of patients on dutasteride use
Mestrado
Fisiopatologia Cirúrgica
Mestre em Ciências

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Lundberg, Kajsa. "On immunotherapy against prostate cancer". Stockholm : Karolinska institutet, 2010. http://diss.kib.ki.se/2010/978-91-7409-805-1/.

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Wang, Wanzhong. "Inflammation and prostatic carcinogenesis : a morphological study of the human prostate /". Göteborg : Dept. of Urology, Institute of Clinical Sciences, Sahlgrenska University Hospital, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/9634.

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

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

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Holt, Jim, i Fereshteh Gerayli. "Prostate Cancer Screening". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6471.

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Whether to screen for prostate cancer in aging men is a topic that is fairly well researched, but recommendations are controversial, because the evidence supporting any recommendation is equivocal. The evidence clearly does not support routine screening of all average-risk men, but for men aged 55 to 69 years, either not routinely screening, or engaging each man in shared decision making for his individual preference on screening, is reasonable and consistent with the evidence. Many organizations, including the American Cancer Society, have not yet reassessed their guidelines, in response to the US Preventative Services Task Force revised guideline.

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Herrala, A. (Annakaisa). "Human prostate-specific antigen and glandular kallikrein 2:production and characterization of the recombinant proteins, and association with prostate cancer". Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514267702.

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Abstract Human prostate-specific antigen (hPSA, KLK3) and glandular kallikrein 2 (hK2, KLK2), two members of a large human tissue kallikrein enzyme family, were produced as recombinant mature proteins for the first time and characterized. Furthermore, their association with prostate cancer was studied. Both proteins were produced with baculovirus expression vector system in pilot-scale using bioreactors. Recombinant hPSA was either active with chymotrypsin-like activity or inactive with incorrect processing of N-terminus. The molecular weight of active recombinant hPSA was 31 kD and it formed stable complexes with serine protease inhibitors, α1-antichymotrypsin (ACT) and α2-macroglobulin (2αM). Two polymorphic forms of KLK2, Arg226hK2 and Trp226hK2, were found. The recombinant Arg226hK2 had trypsin-like activity, while recombinant Trp226hK2 was inactive. The Arg226hK2 was labile with low production yields. The molecular weights of hK2 polymorphic forms were 33 kD. hPSA isoforms secreted by prostate cancer cells, LNCaP, were isolated and characterized. These proteins were N-terminally heterogeneous: 10-60% of LNCaP-PSAs were correctly processed. Molecular modeling suggested that the additions or deletions of two or four N-terminal amino acids could affect the three-dimensional structure and reduce the activity of LNCaP-PSA. Active isoforms had chymotrypsin-like activity and formed stable complexes with ACT and 2αM. The expression of hPSA and hK2 was studied with in situ hybridization and immunohistochemistry techniques in benign and cancerous prostate tissue. hK2 mRNA was expressed at a significantly higher level in prostate cancer tissue than in benign prostate tissue (P < 0.0005). The hPSA mRNA expression levels were reversed (P = 0.06). In benign tissue, the mean level of hK2 mRNA was 82% of the respective value of hPSA (P < 0.003), whereas in tumor tissue the mean hK2 expression level was 21% higher than that of hPSA (P < 0.01). The results at protein level supported the mRNA findings. There was a correlation between hPSA and hK2 mRNA levels in both benign (r = 0.735; P < 0.01) and malignant (r = 0.767; P < 0.01) prostate tissue. It was shown with competitively differential PCR that the KLK2 gene was amplified in prostate tumor tissue, while the KLK3 gene was not. These results suggest that hK2 and hPSA have a diverse value in the diagnosis of prostate cancer.

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Staples, Margaret Patricia. "A population-based family study of prostate cancer in an era of prostate-specific antigen testing /". Connect to thesis, 2005. http://eprints.unimelb.edu.au/archive/00001431.

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Dilmen, Cem Perk Hakkı. "Prostat kanserli hastalarda leptin düzeylerinin araştırılması /". Isparta: SDÜ Tıp Fakültesi, 2004. http://tez.sdu.edu.tr/Tezler/TT00200.pdf.

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Knight, Kellie Ann. "Daily Image Guided Radiation Therapy for Prostate Cancer: An assessment of treatment plan reproducibility". Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1628.

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It is well documented that for prostate cancer patients undergoing radiation therapy there is a correlation between target volume displacement and changes in bladder and rectal volumes. However, these studies have used a methodology that has captured only a subset of all treatment positions. This research used daily Computer Tomography (CT) imaging to comprehensively assess organ volumes, organ motion and their effect on dose, something that has never been performed previously, thus adding considerably to the understanding of the topic. Daily CT images were obtained using a Siemens Primus Linear Accelerator equipped with an in-room Somatom CT unit in the accelerator suite, marketed as ‘Primatom’, to accurately position the patient prior to treatment delivery. The internal structures of interest were contoured on the planning workstation by the investigator. The daily volume and location of the organs were derived from the computer to assess and analyse internal organ motion. The planned dose distribution was then imported onto the treatment CT datasets and used to compare the planned dose to i) the actual isocentre, where the isocentre was actually placed for that fraction, ii) the uncorrected isocentre, by un-doing any on-line corrections performed by the treatment staff prior to treatment delivery, and iii) the future isocentre, by placing the isocentre relative to internal organ motion on a daily basis. The results of this study did not confirm a statistically significant decrease in rectum volumes over time (hypothesis 1), however large fluctuations in bladder volume were confirmed (hypothesis 2). Internal organ motion for the rectum and bladder was demonstrated to be related to organ filling. Ideal planning volumes for these organs have been reported to minimise systematic and random uncertainty in the treatment volumes. An observed decrease in prostate volume over time, a systematic uncertainty in the location of the prostate at the time of the planning CT scan and a significant relationship between prostate centre of volume and rectum and bladder volumes has resulted in a recommendation that patients should be re-scanned during treatment to ensure appropriate clinical target volume coverage. A significant relationship between rectal and bladder volumes and the dose delivered to these organs was found (hypothesis 3). The dose delivered to the planning target volume was not related to the rectal or bladder volumes, although it was related to the motion of these organs. Despite these results only minimal effects on the dose delivered to any of the three isocentres occurred, indicating that the planned dose was accurately delivered using the methodology presented here (hypothesis 4). However the results do indicate that the patient preparation instructions need to be improved if margins are to be reduced in the future. It is unrealistic to assume that Image Guided Radiation Therapy will ever become routine practice due to infrastructure costs and time limitations. This research will inform radiation therapy centres of the variables associated with prostate cancer treatment on a daily basis, something that has never before been realistically achievable. As a result centres will be able to devise protocols to improve treatment outcomes.

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Knight, Kellie Ann. "Daily Image Guided Radiation Therapy for Prostate Cancer: An assessment of treatment plan reproducibility". University of Sydney, 2006. http://hdl.handle.net/2123/1628.

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Doctor of Health Science
It is well documented that for prostate cancer patients undergoing radiation therapy there is a correlation between target volume displacement and changes in bladder and rectal volumes. However, these studies have used a methodology that has captured only a subset of all treatment positions. This research used daily Computer Tomography (CT) imaging to comprehensively assess organ volumes, organ motion and their effect on dose, something that has never been performed previously, thus adding considerably to the understanding of the topic. Daily CT images were obtained using a Siemens Primus Linear Accelerator equipped with an in-room Somatom CT unit in the accelerator suite, marketed as ‘Primatom’, to accurately position the patient prior to treatment delivery. The internal structures of interest were contoured on the planning workstation by the investigator. The daily volume and location of the organs were derived from the computer to assess and analyse internal organ motion. The planned dose distribution was then imported onto the treatment CT datasets and used to compare the planned dose to i) the actual isocentre, where the isocentre was actually placed for that fraction, ii) the uncorrected isocentre, by un-doing any on-line corrections performed by the treatment staff prior to treatment delivery, and iii) the future isocentre, by placing the isocentre relative to internal organ motion on a daily basis. The results of this study did not confirm a statistically significant decrease in rectum volumes over time (hypothesis 1), however large fluctuations in bladder volume were confirmed (hypothesis 2). Internal organ motion for the rectum and bladder was demonstrated to be related to organ filling. Ideal planning volumes for these organs have been reported to minimise systematic and random uncertainty in the treatment volumes. An observed decrease in prostate volume over time, a systematic uncertainty in the location of the prostate at the time of the planning CT scan and a significant relationship between prostate centre of volume and rectum and bladder volumes has resulted in a recommendation that patients should be re-scanned during treatment to ensure appropriate clinical target volume coverage. A significant relationship between rectal and bladder volumes and the dose delivered to these organs was found (hypothesis 3). The dose delivered to the planning target volume was not related to the rectal or bladder volumes, although it was related to the motion of these organs. Despite these results only minimal effects on the dose delivered to any of the three isocentres occurred, indicating that the planned dose was accurately delivered using the methodology presented here (hypothesis 4). However the results do indicate that the patient preparation instructions need to be improved if margins are to be reduced in the future. It is unrealistic to assume that Image Guided Radiation Therapy will ever become routine practice due to infrastructure costs and time limitations. This research will inform radiation therapy centres of the variables associated with prostate cancer treatment on a daily basis, something that has never before been realistically achievable. As a result centres will be able to devise protocols to improve treatment outcomes.

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Xiao, Hong. "Distribution of Metal Ions in Prostate and Urine during Prostate Carcinogenesis". University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1310410436.

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Orakpo, W. Nnamdi. "Does Prostate Cancer Begin in the Prostate? Key Predictors of Diagnosis". Thesis, University of North Texas, 2011. https://digital.library.unt.edu/ark:/67531/metadc84262/.

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The purpose of this exploratory study was to identify the key predictors of prostate cancer; such study may lead to the development of appropriate interventions and prevention. Previous epidemiological studies have found these following factors to be key predictors for being diagnosed with hormone-associated carcinoma such as prostate cancer: age, ethnicity, physical activity, family history, diet, sleep amount, marital status, and having another form of carcinoma. Many studies have included results only for men over the age of 65, however, prostate cancer is claiming the lives of many African American, Hispanic and White American men over the age of 35, and younger men are more likely to battle it if they are genetically predisposed. The sample population (N =21,646) was selected because men aged 35 or over have the highest prevalence of prostate cancer. Of this sample, 619 reported having prostate cancer, and 1,401 reported having some other type of cancer. This study employs a logistic regression model using SAS® and utilizes the National Health Interview Survey data set and a multivariate analysis of the years 2006, 2007, and 2008. To improve the quality of future research the methods need modification, the subpopulation being studied should be larger, and the studies should be longitudinal. This particular study found the aforementioned factors to be critical in predicting prostate cancer. Maximum sun exposure was found to be also related to having prostate cancer. Key predictors for prostate cancer diagnosis are age, ethnicity, having some other cancer and maximum sun exposure, and education. Though previous studies have found physical activity, sleep amount, and occupation to be beneficial in reducing the risk for prostate cancer, it was not confirmed in this particular study.

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Esser, Alison K. "The role of dystroglycan in the prostate epithelium and prostate cancer". Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/2696.

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Interactions between cells and the extracellular matrix are essential to the organization and maintenance of tissue architecture and function. ECM receptors serve as a link between the cell and the ECM. Through interactions with various matrix molecules and activation of intracellular signaling pathways, ECM receptors allow cells to sense and respond to their microenvironment. The matrix receptor dystroglycan (DG) has been shown to have roles in tissue morphogenesis, basement membrane formation as well as in the regulation of cell proliferation, differentiation and survival. DG is expressed in many tissues but has primarily been studied in muscle. The function of dystroglycan within the epithelium is currently unknown. To gain insight into the role of dystroglycan in the prostate epithelium, we generated individual prostate luminal cell (Probasin Cre) and basal cell (Keratin 5 Cre) specific DG knockout mice. DG was not required for maintenance of the basement membrane, polarity or cellular homeostasis in the prostate. Furthermore, gland morphology and ability to regenerate following androgen depletion were normal. These studies indicate DG may have more subtle roles within the epithelium. Disruption of cell/ECM interactions is a hallmark of cancer and contributes to cancer progression. DG expression is lost in many carcinomas including prostate yet the molecular mechanism behind loss of expression and the functional consequences remain unclear. To elucidate the molecular mechanism in prostate cancer, we examined DG expression in metastatic prostate cancer cell lines. alpha-DG was heterogeneously glycosylated across the cell line panel. Surprisingly, we show that LARGE2 is able to functionally glycosylate alpha-DG and loss of LARGE2 expression is a mechanism for DG hypoglycosylation in prostate cancer. Additionally, initial results suggest that oncogene expression modulate alpha-DG glycosylation status through regulation of LARGE2 expression. This work has shown a novel mechanism for alpha-DG hypoglycosylation in prostate cancer. In summary, these studies have contributed new information on the role of DG in the prostate epithelium. Furthermore, we have shown a novel mechanism for loss of alpha-DG glycosylation in prostate cancer and have provided initial data suggesting oncogene expression modulates alpha-DG glycosylation. These insights may lead to advances in the treatment of prostate cancer.

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Peters, Helene. "Expressão do Reck, um inibidor de metaloproteinases de matriz, no desenvolvimento pos-natal e na regressão prostatica pos-castração". [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317570.

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Orientador: Hernandes Faustino de Carvalho
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: A próstata tem merecido crescente atenção devido à maior incidência de câncer prostático e outras afecções do órgão, que resultam do aumento na longevidade dos indivíduos do sexo masculino em todo o mundo. Além disto, o desenvolvimento e crescimento prostático normal apresenta regulação androgênica e está sujeito a uma série de disruptores endócrinos que afetam o seu crescimento e função, assim como predispõem ao desenvolvimento tumoral. Nosso interesse reside principalmente na remodelação prostática seguida à castração e nas interações epitélio estroma que ocorrem neste órgão. Neste trabalho, investigamos a expressão do inibidor de metaloproteinases (MMPs) RECK, em nível de RNAm, procurando correlacioná-Io com o desenvolvimento pós-natal e com a regressão prostática seguida à castração. Para isto, foram utilizadas técnicas de RT-PCR semiquantitativo, Real time RT-PCR e de hibridação in situ,pareados sempre que possível com a expressão do RNAm e com a atividade de algumas MMPs. Os resultados demonstram que o gene RECK é expresso na próstata ventral de ratos, que existe uma significativa redução na sua expressão ao longo do desenvolvimento pós-natal, que há mecanismos diferenciados controlando a expressão dos pares RECKlMMP-2 e MMP-7/MMP-14. Foi observado também um crescente aCÚInulo da forma ativa da MMP-9, conforme o animal se aproxima da idade adulta. Utilizando RT-PCR semiquantitativo, pudemos determinar que o conteúdo relativo do RNAm para o RECK após a castração não muda, embora haja uma inversão no balanço entre a expressão epitelial (células epiteliais) e estromal (células musculares lisas e fibroblastos), nesta situação. No conjunto, os resultados sugerem que o RECK é expresso por diferentes tipos celulares da próstata ventral de ratos, com mecanismos de regulação complexos provavelmente oriundos da existência de diferentes compartimentos no órgão, ao contrário do que se observa para células isoladas
Abstract: The prostate has deserved increasingly attention due to the growing incidence of prostatic cancer and other prostatic diseases, which can be related to the longevity increase of men around the world. Besides, the normal prostatic development is under androgen regulation and as so is subject to a series of endocrine disruptors which affect its growth and function and predisposes to prostate cancer. Our interest resides on the prostatic remodelling following castration and on the epithelial-stromal relationships known to occur in the organ. In this work, we have investigated the expression of the matrix metalloproteinase inhibitor RECK, at the rnRNA leveI, trying to correlate its expression with the post natal prostatic development and regression after castration, using semiquantitative RT-PCR, Real time RT-PCR and in situ hybridization, paralleled with the determination of some MMPs expression and activity. Tbe results demonstrate that RECK is expressed in the rat ventral prostate, that there is a significative reduction in its expression during the post natal development, which is paralleled by the expression of some MMPs and that the mechanisms controling the pairs RECKJMMP-2 and MMP-7/MMP-14 are different. It was also observed an increased proportion of the active form of MMP-9, as the animal approaches adulthood. Using semiquantitative RT-PCR, we could determine that the relative content ofRECK rnRNA remains unchanged by castration, spite detecting an inversion in the balance between the epithelial (epithelial cells) and stromal (smooth muscle cells and fibroblasts) in this situation. Taken together, the results indicate that RECK is expressed by different cell types of the rat ventral prostate, with regulatory mechanisms appearing more complex, likely resulting ftom the existence of different compartments in the organ opposing what was seen for isolated cells
Mestrado
Biologia Celular
Mestre em Biologia Celular e Estrutural

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29

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 Meirelles
Dissertação (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

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30

Noronha, Marcelo Ramos. "Adenocarcinoma da próstata = estudo de fatores clinicopatológicos preditivos de progressão bioquímica (PSA) pós-prostatectomia radical". [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310489.

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Orientadores: Luciana Rodrigues de Meirelles, Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O adenocarcinoma de próstata é a segunda neoplasia maligna que afeta homens, sendo precedida somente pelo cancer de pele. A prostatectomia radical continua sendo a mais aceita estratégia terapêutica para os casos confinado a próstata. Alguns achados clinicopatológicos em pacientes submetidos a prostatectomia radical são controvertidos como tendo valor preditivo de progressão bioquímica pós-cirurgia. O monitoramento da progressão da moléstia pós-prostatectomia radical é feito através de dosagem do PSA sérico cujo aumento pode significar recidiva local e/ou metástases. O valor de corte do PSA sérico indicando progressão é variável entre os autores. Há uma recomendação recente da Associação Americana de Urologia para que este valor seja ?0,2ng/mL com um segundo valor >0,2ng/mL. Não está estabelecido se pacientes mais jovens ou de raça negra mostram taxa de recidiva bioquímica maior. O PSA pré-operatório é um dado de grande importância preditiva, mas não está estabelecido a validade da estratificação dos valores em 3 categorias: 4-10ng/mL, 10-20ng/mL e >20ng/mL. Margens cirúrgicas comprometidas no espécime cirúrgico estão na categoria I (valor preditivo comprovado). É controvertido se a contagem final de Gleason 3+4=7 é semelhante ou não a 4+3=7 como fator preditivo de progressão bioquímica pós-prostatectomia radical. O estudo foi retrospectivo e os dados foram coletados dos prontuários médicos de 300 pacientes submetidos consecutivamente à prostatectomia radical no Hospital de Clínicas da Universidade Estadual de Campinas, no período de janeiro de 1997 a maio de 2007. O objetivo principal do trabalho foi avaliar a progressão bioquímica (PSA) pós prostatectomia radical de acordo com: raça, idade, margens cirúrgicas comprometidas, invasão microscópica do colo vesical, contagem final de Gleason, extensão do tumor, estádio patológico e PSA pré-operatório. Os dados obtidos foram analisados estatisticamente utilizando-se o teste de Mann-Whitney, o produto limite de Kaplan-Meier utilizando-se o teste do log-rank para comparação entre os grupos e o método de Cox para avaliar risco do tempo de progressão bioquímica (PSA) pós-prostatectomia radical. O nível de significância considerado para rejeição da hipótese nula foi p<0,05 bicaudal. Os resultados mais importantes neste trabalho foram: diferença estatisticamente significante quanto ao tempo de progressão bioquímica de pacientes com PSA pré-operatório ?10ng/mL, margens cirúrgicas comprometidas, invasão microscópica do colo vesical, Gleason 4+3=7, tumores mais extensos e tumores não confinados à próstata. Não houve associação da idade e raça com progressão bioquímica. Em análise univariada, os fatores preditivos significantes do tempo e risco de progressão pós-prostatectomia radical foram o PSA pré-operatório, as margens cirúrgicas positivas, a invasão das vesículas seminais, a invasão microscópica do colo vesical e o Gleason 4+3=7. Em análise multivariada, somente PSA pré-operatório, margens positivas e invasão das vesículas seminais mostraram-se fatores preditivos independentes do tempo e risco de progressão bioquímica pós-prostatectomia radical
Abstract: Adenocarcinoma of the prostate is the second malignancy that affects men, being preceded only by skin cancer. Radical prostatectomy remains the most widely accepted treatment strategy for cases confined to the prostate. Some clinical and pathological findings in patients undergoing radical prostatectomy are at issue as having predictive value of biochemical progression after surgery. The monitoring of disease progression after radical prostatectomy is done by measuring concentrations of PSA which can mean increased local recurrence and/or metastases. The cutoff of PSA indicating progression varies among authors. There is a recent recommendation of the American Urological Association that this value is ?0.2ng/mL with a second value >0.2ng/mL. It has not been established whether younger or black patients show higher rate of biochemical recurrence. The preoperative PSA is an important predictive factor for biochemical recurrence, but it has not been established the validity of the stratification of values in three categories: 4-10ng/mL, 10-20ng/mL, and >20ng/mL. Positive surgical margins in the surgical specimen are in category I (proven predictive value). It is controversial whether the final Gleason score 3+4=7 is similar or not to 4+3=7 as a predictor of biochemical progression after radical prostatectomy. The study was based on 300 whole-mount consecutive radical prostatectomies. The aim of this study was to analyse the risk and time for biochemical progression after surgery, according to race, age, positive surgical margins, bladder neck invasion, Gleason score, tumor extension, pathological stage and serum PSA preoperative levels. Time to biochemical progression-free outcome was compared using the Kaplan-Meier product-limit analysis using the log-rank to compare the groups. To assess individual variables for risk and time to biochemical progression, we created a univariate Cox proportional hazards model, and to assess the influence of several variables simultaneously, we developed a final multivariate Cox proportional hazards model of the statistically significant covariates. The most important results were: There was a significant association to time of progression of patients with preoperative PSA ?10ng/mL, positive surgical margins, microscopic invasion of the bladder neck, Gleason 4+3=7, more extensive tumors and non confined tumors. No association of race and age to biochemical progression following radical prostatectomy. On univariate analysis, the significant predictive variables for risk and time to biochemical progression were: preoperative PSA, positive surgical margins, seminal vesicle invasion, microscopic invasion of the bladder neck, and Gleason 4+3=7. On multivariate analysis, only positive surgical margins and seminal vesicle invasion were independent predictive variables
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas

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31

Sieh, Weiva. "Genetic susceptibility to prostate cancer : the androgen receptor and prostate-specific antigen loci /". Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/10875.

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Піддубний, Артем Михайлович, Артем Михайлович Поддубный, Artem Mykhailovych Piddubnyi, Микола Сергійович Линдін, Николай Сергеевич Лындин, Mykola Serhiiovych Lyndin, Юлія Василівна Москаленко i in. "The effect of prostatic stones on the immunophenotype of prostate cancer cells". Thesis, Lithuanian University of Health Sciences, 2019. http://essuir.sumdu.edu.ua/handle/123456789/73112.

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Background.Prostate cancer (PGC) is leading the way in the structure of cancer morbidity around the world. The presence of prostatic concretions (PC) and skeletal metastases significantly reduces the patients’ life quality and worsens the prognosis of the disease. However, the phenomenon of osteotropic tumor metastases is not sufficiently studied. Aim.To define the impact of PC on the development of prostate cancer metastasis to the bones. Methods.10 samples of PGC with PC, 10 intact PGC specimens, and PGC metastasis tissue to lymph node were analysed. Histology (staining with hematoxylin-eosin), histochemistry (von Kossa reaction, alizarin red), immunohistochemistry (OSN, Col I, Col II, Bax, Casp3, MPO, CD68), SEM, EDS. Results.All PC samples had the calcium hydroxyapatite origin with a slight deviation from the stoichiometric composition and admixture of extraneous elements. Assessment of apoptotic potential (Вах and Саsp3) and inflammatory infiltration (MPO and CD68) revealed the significantly higher rates of these processes in PGC tissue with PC (p <0.01). We suggest that the combined effect of these factors predetermines the development of a specific phenotype of cancer cells. This phenomena is manifested by the significantly higher OSN and Col I osteoblastic markers expression in PGC with PC and metastatic tissue (p <0.05). Conclusions.The determination of osteoblastic markers expression in PGC can be used as criterion for evaluation of probability of bone metastases development. The presence of PC in PGC tissue can be an important prognostic information for clinicians.The presence of these pathological inclusions, namely the PC, promotes the expression of osteoblastic markers in PGC tissue, which helps the tumor cells to recognize a favorable microenvironment. Acknowlegments.This research has been performed with the financial support of grants of the Ministry of Education and Science of Ukraine No. 0117U003937 “The development of tumor diagnosis method of reproductive system organs using cellular adhesion molecules of cancerembryonic antigen” and No. 0118U003570 “The efficiency of “liquid biopsy” and tissue biopsy in the diagnosis and treatment of malignant tumors”.

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Abdul-Rahman, T., Артем Михайлович Піддубний, Артем Михайлович Поддубный, Artem Mykhailovych Piddubnyi, Владислав Володимирович Сікора, Владислав Владимирович Сикора, Vladyslav Volodymyrovych Sikora, Роман Андрійович Москаленко, Роман Андреевич Москаленко i Roman Andriiovych Moskalenko. "Prostatic сalculi сauses reduction of heat shock proteins expression in prostate cancer". Thesis, The Romanian National Library, 2020. https://essuir.sumdu.edu.ua/handle/123456789/81897.

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Heat shock proteins (Hsp) have an important role in tumor cells. Unfortunately, there is no data on the effect of intraluminal inclusions (IIn) on the expression of Hsp in prostate cancer (PCa) cells. The aim of our study was to detect the association between IIn and expression of Hsp in PCa tissue.

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34

Hallung, Linda, i Carl-Oscar Scotting. "Upplevelser av biverkningarna vid prostatacancerbehandling". Thesis, Högskolan Väst, Avdelningen för omvårdnad - grundnivå, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:hv:diva-9117.

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Background: Prostate cancer is the most common type of cancer in Sweden. The three primary treatment types for prostate cancer are prostatectomy, radiotherapy and different types of endocrine therapy. With all treatments mentioned above comes adverse effects that may have big effects on the person treated. Aim: The aim of this study was to highlight men´s experiences of the adverse effects that comes with the treatment for prostate cancer. Method: The research method employed was a literature study based on eleven qualitative articles. The method of analysis was done according to Friberg five-step analysis of qualitative articles and through the analysis, six themes emerged. Results: The themes were A feeling of emotional imbalance, Not prepared enough, The experience of loosing control, Feeling of diminished masculinity, The experience of a feminized body and An altered identity. Conclusion: The result showed that men experience adverse effects of the prostate cancer treatment as difficult in many ways. The changes to the body and mental well-being tend to be difficult to deal with, and the men need relevant information prior to treatment to give them time to adjust to their new life.

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Bui, Loan Thuy. "Localisation of kallikreins in the prostate and association with prostate cancer progression". Thesis, Queensland University of Technology, 2006. https://eprints.qut.edu.au/16276/1/Loan_Bui_Thesis.pdf.

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At present, prostate cancer is a significant public health issue throughout the world and is the second leading cause of cancer deaths in older men. The prostate specific antigen or PSA (which is encoded by the kallikrein 3/KLK3 gene) test is the current most valuable tool for the diagnosis and management of prostate cancer. However, it is insufficiently sensitive and specific for early diagnosis, for staging of prostate cancer or for discriminating between benign prostatic hyperplasia (BPH) and prostate cancer. Recent research has revealed another potential tumour marker, glandular kallikrein 2 (KLK2 gene/hK2 protein), which may be used alone or in conjunction with PSA to overcome some of the limitations of the PSA test. Twelve new kallikrein gene family members have been recently identified and, like hK2 and PSA, many of these genes have been suggested to be involved in carcinogenesis. In this study, the cellular localisation and level of expression of several of these newer kallikreins (KLK4, KLK5, KLK7, KLK8 and KLK11) was examined in prostate tissue, to provide an understanding of the association of their expression with prostatic diseases and their potential as additional biomarkers. Like PSA and hK2, the present observation indicated that each of these proteins, hK4, hK5, hK7, hK8 and hK11, was detected within the cytoplasm of the secretory cells of the prostate glands. For the first time, all of these newly-identified proteins were shown to be expressed in prostatic intraepithelial neoplasia (PIN) lesions, in comparison to normal glands and cancer lesions. In addition to cytoplasmic secretory cell expression, the localisation of hK4 to the basal cells and nuclei in prostatic lesions was intriguing. The intensity of hK4 staining in prostate tissue was strongest in comparison to the other newly-identified kallikrein proteins (hK5, hK7, hK8 and hK11). Therefore, KLK4/hK4 expression was characterised further to define this cellular localisation and examined in non-prostatic tissue and also in a larger number of prostate tissues in an attempt to determine its potential value as a biomarker for prostate disease. Three hK4 antipeptide polyclonal antibodies, derived against N-terminal, mid-region and C-terminal hK4 amino acid sequences, were used. The hK4 N-terminal antipeptide antibody was used to demonstrate the cellular localisation of hK4 in kidney, salivary glands, liver, testis, colon carcinoma, heart, endometrium and ovarian cancer, for the first time. The presence of hK4 in these non-prostate tissues was consistent with the previous reports using RT-PCR. The dual cytoplasmic and nuclear localisation of hK4 observed in the prostate above was also seen in these tissues. Although hK4 was found widely expressed in many human tissue types, indicating that it is not prostate specific in its expression, the highest expression level of hK4 was seen in the prostate. Therefore, detailed expression patterns and levels of KLK4 mRNA and hK4 protein in the normal prostate and prostatic diseases and histopathological lesions were investigated and reported for the first time in this study. Twelve benign prostatic hyperplasia (BPH), 19 adenocarcinoma (Gleason grade 2-5) and 34 bone metastases from prostate cancer were analysed. Using in situ hybridisation, the expression of KLK4 mRNA was detected in the cytoplasm of the secretory cells of both normal and diseased prostate tissue. KLK4 mRNA was also noted in both secretory and basal cells of PIN lesions, but the basal cells of normal glands were negative. Using the hK4 N-terminal and mid-region antipeptide antibodies, hK4 was predominantly localised in the cytoplasm of the secretory cells. The intensity of hK4 staining appeared lowest in normal and BPH, and increased in PIN lesions, high Gleason grade prostate cancer and bone metastases indicating the potential of hK4 as a histopathological marker for prostatic neoplasias. Further studies are required with a larger cohort to determine its utility as a clinical biomarker. Small foci of atypical cells, which were found within normal glands, were also intensely stained. Surprisingly, hK4 protein was found in the nucleus of the secretory cells (but not the basal cells) of high grade PIN and Gleason grade 3 prostate cancer. The detection of KLK4 mRNA and hK4 protein in PIN lesions and small foci of atypical cells suggests that up-regulation of KLK4 expression occurs early in the pathology of prostate carcinogenesis. The finding of basal cell expression is not typical for the kallikreins and it is not clear what role hK4 would play in this cell type. With the use of the hK4 C-terminal antipeptide antibody, the staining was mainly localised in the nuclei of the secretory cells of the prostate glands. Although the nuclear localisation was readily noted in more than 90% of epithelial cells of the prostate gland with the C-terminal antibody, no difference in staining intensity was observed among the histopathological lesions of the prostate. The prominent nuclear localisation with the C-terminal antipeptide antibody was also shown to be distributed throughout the nucleus by using confocal microscopy. Further, by using gold-labelled particles for electron microscopy, the intracellular localisation of these hK4 antipeptide antibodies was reported here for the first time. Similar to the immunohistochemical results, the cytoplasm was the major site of localisation with the N-terminal and mid-region antipeptide antibodies. To further characterise the involvement of KLK4/hK4 in human prostate cancer progression, the transgenic adenocarcinoma mouse prostate (TRAMP) model was used in this study. In this study, mouse KLK4 (also known as enamel matrix serine protease -1, EMSP-1) was shown to be expressed in the TRAMP prostate for the first time. Previous studies had only shown the developing tooth as a site of expression for EMSP-1. The level of EMSP-1 mRNA expression was increased in PIN and prostate cancer lesions of the TRAMP model, while negative or low levels of EMSP-1 mRNA were seen in normal glands or in control mouse prostate tissue. The normal mouse prostate did not stain with any the three hK4 antipeptide antibodies. hK4 N-terminal and mid-region antipeptide antibodies showed positive staining in the cytoplasm of the epithelial cells of PIN and cancer lesions of the mouse prostate. The C-terminal antipeptide antibody showed distinctively nuclear staining and was predominantly localised in the nuclei of the glandular cells of PIN and cancer lesions of the mouse prostate. The expression patterns of both the mRNA and protein level for mouse KLK4 strongly supported the observations of KLK4/hK4 expression in the human prostate and further support the utility of the TRAMP model. Overall, the findings in this thesis indicate a clear association of KLK4/hK4 expression with prostate cancer progression. In addition, several intriguing findings were made in terms of cellular localisation (basal as well as secretory cells; nuclear and cytoplasmic) and high expression in atypical glandular cells and PIN, perhaps indicating an early involvement in prostate disease progression and, additionally, utility as basal cell and PIN histological markers. These findings provide the basis for future studies to confirm the utility of hK4 as a biomarker for prostate cancer progression and identify functional roles in the different cellular compartments.

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36

Bui, Loan Thuy. "Localisation of kallikreins in the prostate and association with prostate cancer progression". Queensland University of Technology, 2006. http://eprints.qut.edu.au/16276/.

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At present, prostate cancer is a significant public health issue throughout the world and is the second leading cause of cancer deaths in older men. The prostate specific antigen or PSA (which is encoded by the kallikrein 3/KLK3 gene) test is the current most valuable tool for the diagnosis and management of prostate cancer. However, it is insufficiently sensitive and specific for early diagnosis, for staging of prostate cancer or for discriminating between benign prostatic hyperplasia (BPH) and prostate cancer. Recent research has revealed another potential tumour marker, glandular kallikrein 2 (KLK2 gene/hK2 protein), which may be used alone or in conjunction with PSA to overcome some of the limitations of the PSA test. Twelve new kallikrein gene family members have been recently identified and, like hK2 and PSA, many of these genes have been suggested to be involved in carcinogenesis. In this study, the cellular localisation and level of expression of several of these newer kallikreins (KLK4, KLK5, KLK7, KLK8 and KLK11) was examined in prostate tissue, to provide an understanding of the association of their expression with prostatic diseases and their potential as additional biomarkers. Like PSA and hK2, the present observation indicated that each of these proteins, hK4, hK5, hK7, hK8 and hK11, was detected within the cytoplasm of the secretory cells of the prostate glands. For the first time, all of these newly-identified proteins were shown to be expressed in prostatic intraepithelial neoplasia (PIN) lesions, in comparison to normal glands and cancer lesions. In addition to cytoplasmic secretory cell expression, the localisation of hK4 to the basal cells and nuclei in prostatic lesions was intriguing. The intensity of hK4 staining in prostate tissue was strongest in comparison to the other newly-identified kallikrein proteins (hK5, hK7, hK8 and hK11). Therefore, KLK4/hK4 expression was characterised further to define this cellular localisation and examined in non-prostatic tissue and also in a larger number of prostate tissues in an attempt to determine its potential value as a biomarker for prostate disease. Three hK4 antipeptide polyclonal antibodies, derived against N-terminal, mid-region and C-terminal hK4 amino acid sequences, were used. The hK4 N-terminal antipeptide antibody was used to demonstrate the cellular localisation of hK4 in kidney, salivary glands, liver, testis, colon carcinoma, heart, endometrium and ovarian cancer, for the first time. The presence of hK4 in these non-prostate tissues was consistent with the previous reports using RT-PCR. The dual cytoplasmic and nuclear localisation of hK4 observed in the prostate above was also seen in these tissues. Although hK4 was found widely expressed in many human tissue types, indicating that it is not prostate specific in its expression, the highest expression level of hK4 was seen in the prostate. Therefore, detailed expression patterns and levels of KLK4 mRNA and hK4 protein in the normal prostate and prostatic diseases and histopathological lesions were investigated and reported for the first time in this study. Twelve benign prostatic hyperplasia (BPH), 19 adenocarcinoma (Gleason grade 2-5) and 34 bone metastases from prostate cancer were analysed. Using in situ hybridisation, the expression of KLK4 mRNA was detected in the cytoplasm of the secretory cells of both normal and diseased prostate tissue. KLK4 mRNA was also noted in both secretory and basal cells of PIN lesions, but the basal cells of normal glands were negative. Using the hK4 N-terminal and mid-region antipeptide antibodies, hK4 was predominantly localised in the cytoplasm of the secretory cells. The intensity of hK4 staining appeared lowest in normal and BPH, and increased in PIN lesions, high Gleason grade prostate cancer and bone metastases indicating the potential of hK4 as a histopathological marker for prostatic neoplasias. Further studies are required with a larger cohort to determine its utility as a clinical biomarker. Small foci of atypical cells, which were found within normal glands, were also intensely stained. Surprisingly, hK4 protein was found in the nucleus of the secretory cells (but not the basal cells) of high grade PIN and Gleason grade 3 prostate cancer. The detection of KLK4 mRNA and hK4 protein in PIN lesions and small foci of atypical cells suggests that up-regulation of KLK4 expression occurs early in the pathology of prostate carcinogenesis. The finding of basal cell expression is not typical for the kallikreins and it is not clear what role hK4 would play in this cell type. With the use of the hK4 C-terminal antipeptide antibody, the staining was mainly localised in the nuclei of the secretory cells of the prostate glands. Although the nuclear localisation was readily noted in more than 90% of epithelial cells of the prostate gland with the C-terminal antibody, no difference in staining intensity was observed among the histopathological lesions of the prostate. The prominent nuclear localisation with the C-terminal antipeptide antibody was also shown to be distributed throughout the nucleus by using confocal microscopy. Further, by using gold-labelled particles for electron microscopy, the intracellular localisation of these hK4 antipeptide antibodies was reported here for the first time. Similar to the immunohistochemical results, the cytoplasm was the major site of localisation with the N-terminal and mid-region antipeptide antibodies. To further characterise the involvement of KLK4/hK4 in human prostate cancer progression, the transgenic adenocarcinoma mouse prostate (TRAMP) model was used in this study. In this study, mouse KLK4 (also known as enamel matrix serine protease -1, EMSP-1) was shown to be expressed in the TRAMP prostate for the first time. Previous studies had only shown the developing tooth as a site of expression for EMSP-1. The level of EMSP-1 mRNA expression was increased in PIN and prostate cancer lesions of the TRAMP model, while negative or low levels of EMSP-1 mRNA were seen in normal glands or in control mouse prostate tissue. The normal mouse prostate did not stain with any the three hK4 antipeptide antibodies. hK4 N-terminal and mid-region antipeptide antibodies showed positive staining in the cytoplasm of the epithelial cells of PIN and cancer lesions of the mouse prostate. The C-terminal antipeptide antibody showed distinctively nuclear staining and was predominantly localised in the nuclei of the glandular cells of PIN and cancer lesions of the mouse prostate. The expression patterns of both the mRNA and protein level for mouse KLK4 strongly supported the observations of KLK4/hK4 expression in the human prostate and further support the utility of the TRAMP model. Overall, the findings in this thesis indicate a clear association of KLK4/hK4 expression with prostate cancer progression. In addition, several intriguing findings were made in terms of cellular localisation (basal as well as secretory cells; nuclear and cytoplasmic) and high expression in atypical glandular cells and PIN, perhaps indicating an early involvement in prostate disease progression and, additionally, utility as basal cell and PIN histological markers. These findings provide the basis for future studies to confirm the utility of hK4 as a biomarker for prostate cancer progression and identify functional roles in the different cellular compartments.

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Morris, Emma Victoria. "Investigating the role of iASPP in normal prostate development and prostate tumourigenesis". Thesis, University of Oxford, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606228.

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Loss of TP63 expression in the prostate epithelium is a hallmark of invasive prostate cancer. An inability of prostate epithelial cells to undergo apoptosis, a process regulated by both TP63 and TP53, is a feature of their malignant transformation. p53 mutations in prostate cancer are uncommon, being mainly associated with advanced metastatic disease. Therefore it is likely that the inability of wild-type p53 to initiate and execute apoptosis is due to molecular alterations elsewhere in the apoptotic pathway. iASPP is an inhibitory member of the ASPP family of proteins and is known to inhibit p53-mediated apoptosis and regulate p63 function. In this work we have investigated how iASPP can affect normal prostate development and prostate tumourigenesis. By utilising an iASPP-deficient mouse model, we show that iASPP plays a key role in normal prostate development and homeostasis by maintaining the TP63-positive basal cell lineage of the prostate epithelium. The loss of iASPP is associated with alterations in differentiation, proliferation and apoptosis, resulting in a smaller organ size. Furthermore, by using both benign and malignant human prostate tissue we show that changes in iASPP expression have prognostic value. Nuclear and c)1.oplasmic iASPP expression are significantly increased in prostate cancer and associate with poor clinical outcome. Increased nuclear iASPP associates with cells that express high levels of TP53, suggesting that iASPP cooperates with mutant p53 to enhance its gain-of-function activity. Analysis of iASPP expression in both the mouse and human prostate epithelium led to the identification of iASPP as a novel junctional protein. In vitro studies suggest that membranous iASPP functions to add strength and stability to cell-to-cell contacts, and its' reduction increases cellular invasion and motility. Finally, iASPP significantly reduces chemosensitivity of prostate cancer cells, given the evident dual functionality of iASPP as both an oncoprotein and a tumour suppressor, depending on cellular localisation, targeting this protein to improve therapy efficacy may be challenging.

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38

Wirth, Manfred P., i Michael Fröhner. "Adjuvant Hormonal Treatment for Prostate Cancer: The Bicalutamide Early Prostate Cancer Program". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-133551.

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Adjuvant hormonal therapy has been demonstrated to be able to delay disease progression in nonmetastatic prostate cancer. To date, however, a favorable impact on survival has only been demonstrated in lymph-node-positive disease and in external-beam radiotherapy series with locally advanced and probably mainly micrometastatic tumors. The Bicalutamide Early Prostate Cancer Program is the largest study under way to define the role of adjuvant treatment in early prostate cancer and identify subgroups of patients likely to benefit from immediate hormonal therapy. At the time of the most recently published analysis, the risk of objective clinical progression was significantly reduced in the bicalutamide arm (hazards ratio 0.58, 95% confidence interval 0.51–0.66, p < 0.0001). However, further maturation of data is needed to see whether this difference will lead to a survival advantage
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich

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39

Wirth, Manfred P., i Michael Fröhner. "Adjuvant Hormonal Treatment for Prostate Cancer: The Bicalutamide Early Prostate Cancer Program". Karger, 2003. https://tud.qucosa.de/id/qucosa%3A27515.

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Adjuvant hormonal therapy has been demonstrated to be able to delay disease progression in nonmetastatic prostate cancer. To date, however, a favorable impact on survival has only been demonstrated in lymph-node-positive disease and in external-beam radiotherapy series with locally advanced and probably mainly micrometastatic tumors. The Bicalutamide Early Prostate Cancer Program is the largest study under way to define the role of adjuvant treatment in early prostate cancer and identify subgroups of patients likely to benefit from immediate hormonal therapy. At the time of the most recently published analysis, the risk of objective clinical progression was significantly reduced in the bicalutamide arm (hazards ratio 0.58, 95% confidence interval 0.51–0.66, p < 0.0001). However, further maturation of data is needed to see whether this difference will lead to a survival advantage.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

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40

Ilyuk, I. I. "Metastatic prostate cancer. Prostate specific antigen as a screening marker of metastasing". Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18163.

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41

Guimarães, Marbele Santos. "Cancer da prostata : estudo da graduação de Gleason em biopsias de agulhas e especimes de prostatectomia radical". [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308453.

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Orientador: Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-09T07:48:22Z (GMT). No. of bitstreams: 1 Guimaraes_MarbeleSantos_M.pdf: 9766799 bytes, checksum: 89baad38db3ebd410ea20926179eb1b9 (MD5) Previous issue date: 2007
Resumo: Há evidências mostrando que a graduação de Gleason para carcinoma da próstata é um dos mais importantes fatores prognósticos de comportamento biológico e um dos mais influentes fatores para determinar o tratamento do câncer da próstata. Este trabalho tem por finalidade comparar: a graduação de Gleason nas biópsias de agulha com a graduação nas prostatectomias radicais correspondentes; correlacionar a graduação de Gleason nas biópsias de agulha com a extensão tumoral nas prostatectomias radicais correspondentes; correlacionar a graduação de Gleason na prostatetomia radical com extensão tumoral, margens cirúrgicas comprometidas e estádio patológico; e, comparar a progressão bioquímica (PSA) da moléstia (recorrência e/ou metástase) pós-prostatectomia radical entre pacientes com: Gleason grau baixo/intermediário (contagem final < 7) vs grau alto (contagem final=7); contagem final 3+4 vs 4+3; e, grau predominante 4 ou 5 vs grau predominante menor que 4. Trata-se de um estudo retrospectivo baseado em 200 espécimes de prostatectomias radicais e de biópsias correspondentes provenientes de pacientes operados no Hospital das Clínicas da FCM-Unicamp no período de 1997 a 2004. A extensão tumoral foi estimada por um método semiquantitativo de contagem de pontos. A progressão bioquímica (recorrência e/ou metástase) da moléstia pós-prostatectomia radical estabelecida pelo Serviço de Urologia do Hospital das Clínicas da Unicamp é o valor de PSA igual ou maior que 0,5 ng/mL. Os dados foram analisados estatisticamente utilizando Statistica 5.5 (StatSoft,Inc., Tulsa, OK, USA). Foi considerado significante o valor de p =0,05. Houve exata correspondência em 47,1% dos casos quando comparada contagem final de Gleason na biópsia de agulha com a contagem final na prostatectomia correspondente. A contagem de Gleason foi subestimada em 40,6% dos casos e superestimada em 12,3% nas biópsias de agulha. A correlação entre contagem final de Gleason nas biópsias de agulha com a extensão tumoral nas prostatectomias radicais correspondentes mostrou-se altamente significante (p<0.001). A correlação da graduação histológica de Gleason na prostatectomia radical foi altamente significante com extensão tumoral (p<0,001), margens cirúrgicas positivas (p<0,001) e estádio patológico (p<0,001). O tempo de recorrência bioquímica (PSA) livre de doença comparando pacientes com Gleason contagem final < 7 vs contagem final >7 (log-rank, p=0,2674); contagem final 3+4 vs 4+3 (log-rank, p=0. 3207); e, grau predominante 4 ou 5 vs grau predominante menor que 4 (log-rank, p=0,1759) não foi estatisticamente significante. Contagens finais maiores na graduação de Gleason na prostatetomia radical se correlacionam com maior extensão tumoral, margens cirúrgicas comprometidas e estádio patológico mais avançado. A maioria dos pacientes mostraram igual ou maior contagem final comparando a contagem final de Gleason na prostatectomia com a biópsia de agulha correspondente. Em nosso estudo, não houve diferença estatisticamente significante em relação à progressão bioquímica quando comparados contagem final <7 vs =7, contagem final 3+4=7 vs 4+3=7 e grau predominante <4 vs =4. predominante 4 ou 5 vs grau predominante menor que 4 (log-rank, p=0,1759) não foi estatisticamente significante
Abstract: There are evidences showing that Gleason grading of prostatic adenocarcinoma is one of the most powerful predictors of biological behavior and one of the most influential factors used to determine treatment for prostate cancer. The aim of the current report was to compare Gleason score on needle biopsy to Gleason score in the correspondent surgical specimen, correlate Gleason score on needle biopsy to tumor extent in surgical specimen, correlate Gleason score in the specimens to several clinicopathologic variables, and compare biochemical (PSA) progression following surgery between patients with Gleason low-grade vs high-grade, Gleason score 3+4 vs 4+3 and Gleason predominant grade <4 or >4. The study population consisted of 200 consecutive patients submitted to radical prostatectomy. Tumor extent was evaluated by a point-count method. Biochemical progression was defined as PSA = 0.5ng/mL. Time to PSA progression was studied using the Kaplan-Meier product-limit analysis. There was exact correspondence in 47.1% of cases, when Gleason score on the biopsy was compared to the correspondent surgical specimen. Gleason score was higher in the specimen in 40.6% of cases and lower in 12.3%. High-grade Gleason score on the biopsy significantly correlated to higher tumor extent (p<0.001). High-grade Gleason score in the surgical specimen significantly correlated to more extensive tumors (p<0.001), positive margins (p<0.001) and extraprostatic extension (pT3a/pT3b) (p<0.001). Time of biochemical (PSA) progression-free survival comparing patients with Gleason score <7 vs =7 (log-rank, p=0.2674), Gleason score 3+4=7 vs 4+3=7 (log-rank, p=0.3207) and Gleason predominant grade <4 vs >4 (log-rank, p=0.1759) was not statistically significant. High-grade Gleason score significantly correlates with more extensive tumors in the surgical specimen, positive margins, and more advanced pathologic staging. Most of the patients show either an exact Gleason score or a higher score in the surgical specimen comparing to the needle biopsy. In our study, time of biochemical (PSA) progression-free survival between patients with Gleason score <7 vs =7, Gleason score 3+4=7 vs 4+3=7 and Gleason predominant grade <4 or >4 was not statistically significant
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas

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42

解文 i Wen Xie. "Morphological and functional studies of the ventral prostate during the development of prostatic intraepithelial neoplasia in the noblerats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241244.

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43

Tayeb, Mohammed Taher. "Genetic risk factors influencing the development of prostate cancer in patients with benign prostatic hyperplasia". Thesis, University of Aberdeen, 2002. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU154536.

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The primary aim of this study is to assess the predictive value of six molecular markers in determining PRCa risk in patients with BPH. These molecular markers are: (A)- Two polymorphic repeats, (CAG)_n and (GGN)_n, in the androgen receptor (AR) gene; (B)- A single nucleotide polymorphism (SNP) in the (-290 A to G) 5' regulatory region of the CYP3A4 gene; (C)- Two SNPs (TaqI and FokI) in vitamin D receptor (VDR) gene; (D)- A SNP (Val655Ile) in the transmembrane domain coding region of HER2 gene. The study evaluated 28 patients who presented with PRCa at least 3 years and up to 15 years after the diagnosis of BPH and 56 matched patients with BPH who did not progress to PRCa over a comparable period. The results of this study showed that CYP3A4 variant genotype identified men with BPH who are at increased risk of developing PRCa (odds ratio 5.2, 95% CI = 1.8-14.3). Similar finding was also seen for VDR TaqI SNP, where TT genotype was associated with a significant 5 fold increase in the risk of developing PRCa in patients previously diagnosed with BPH. Tentative evidence of association between risk of developing PRCa and the variant genotype of HER2 and VDR FokI SNPs was also demonstrated, although the results were not statistically significant. The odds ratio of developing PRCa was 1.88, and 2.33 in BPH patients having HER2 Ile/Ile genotype and VDR FokI FF genotype respectively. This study also showed no evidence for association between the size of AR CAG and GGN repeats and the risk of the development of PRCa in patients with BPH. However, data of this study suggest that BPH patients with AR CAG instability have a 12 fold increase risk in development PRCa. These results provide a potential tool to assist prediction strategies for this important disease.

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44

Klossner, Daniel Patrick. "Improving cryosurgical ablation of advanced state prostate cancer through identification of molecular targets in a prostrate cancer cell model". Diss., Online access via UMI:, 2007.

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45

Xie, Wen. "Morphological and functional studies of the ventral prostate during the development of prostatic intraepithelial neoplasia in the noble rats /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21482664.

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46

Taylor, Michael Dennis. "Prostate cancer clinical practice guidelines clinical and economic outcomes /". [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010098.

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Thesis (Ph.D.)--University of Florida, 2005.
Typescript. Title from title page of source document. Document formatted into pages; contains 99 pages. Includes Vita. Includes bibliographical references.

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47

Storey, Dawn J. "Fatigue and prostate cancer". Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29383.

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Methods: Four studies were conducted: Study A, was a pilot study which examined fatigue over 3 months after different treatments for localised prostate cancer (radiotherapy, brachytherapy and androgen deprivation, n=45). Study B focussed on fatigue over 12 months after brachytherapy (n=51). Two cross sectional postal surveys explored fatigue in recurrence free prostate cancer survivors (Study C, n=443) and hormone controlled prostate cancer (Study D, n=198). Throughout, fatigue was assessed using the Brief Fatigue Inventory and a case definition of clinically significant fatigue (CSF) was also constructed and applied in Studies A and B. Results: Study A found CSF increased after treatment but returned to baseline 3 months after radiotherapy, whereas it appeared to be prolonged after brachytherapy. CSF was not associated with C reactive protein or interleukin-6. Study B found CSF increased between baseline and 1 month after brachytherapy (6 vs.29%, p=0.001) and was higher than the non-cancer comparison group (29 vs. 4% p=0.001). CSF returned towards baseline levels of 6 months. There were no baseline predictors of developing CSF. Study C found 29% of recurrence free prostate cancer survivors had fatigue after radiotherapy or radical prostatectomy (33 vs. 22% p=0.024) but it was not independently associated with treatment received after controlling for other factors 43% of men with hormone controlled prostate cancer had fatigue in Study D. Conclusions: Fatigue is an important symptom in men treated for prostate cancer but resolves within months of brachytherapy. Almost one third of recurrence free survivors have fatigue but it does not appear to be related to the type of treatment received. Fatigue is most prevalent in men with hormone controlled prostate cancer.

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48

Hendrickx, Wouter R. L. "Selenium and prostate cancer". Thesis, University of East Anglia, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588614.

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Prostate cancer is the second most common diagnosed cancer and the third most common cause of death related to cancer among men in developed countries. Several epidemiological studies, prospective cohort studies and animal tumour models state an inverse relationship between selenium status and cancer incidence. Se- methylselenocysteine (SeMSC), present in garlic, onions, leeks and broccoli, has been shown to be the most effective anti-carcinogenic selenium form in animal models. The aim of the work presented in this thesis was to investigate the influence of selenium compounds (Se-methylselenocysteine and selenomethionine) on prostate cancer progression and metastasis using various human cell lines (LNCaP, OU145 and PC3). Standard 20 gel and SILAC (stable isotope labelling with amino acids in cell culture) proteomics were used, in combination with mass spectrometry, to identify selenium- responsive proteins. IMPOH2, GPI, EZR and RGS10 were validated by western blot, while POIA3 and 00X5 showed a selenium response under serum depleted conditions. Some proteins require more scrutinizing (galectin-1, XRCC5, TAGLN2, 00X5 and FLT) as conflicting results were obtained during validation. Preliminary analysis using 20 gel proteomics revealed galectin-1 to be selenium-responsive in PNT1A cells, although this could not be confirmed by Western blot or an in-house ELlSA. Previously, it has been shown that SeMSC decreased the expression of collagen I and increased that of collagen IV and collagen VI. A LNCaP 3D gel suspension model was developed to allow further investigation of extracellular matrix components using fluorescence microscopy. In addition, the effect of selenium exposure on the migration and invasion of PC3 cells was investigated using a transwell kinetic assay and revealed a dose response increase, especially under low baseline selenium concentrations. In order to optimize future selenium in vitro projects the dynamics of several selenium biomarkers were investigated using different conditions, enabling better comparison between cell lines and/or selenium compounds.

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49

Grönberg, Henrik. "Prostate cancer : epidemiological studies". Doctoral thesis, Umeå universitet, Onkologi, 1995. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96894.

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Prostate cancer is a large and increasing medical problem both in Sweden and in the rest of the developed world, with about 300.000 new cases diagnosed world wide annually. Despite the high incidence of this disease, little is known about the aetiology of prostate cancer. The aim of this study was to try to understand more about the natural history and to find possible a etiological risk factors for this tumour. In a population based study of prostate cancer cases in northern Sweden it was found that the large increase in prostate cancer during the last two decades was mainly caused by well (Gl) and moderately (G2) differentiated tumours. However, the incidence of poorly differentiated (G3) tumours remained unchanged. The introduction of new diagnostic methods is the most plausible explanation for the increase of these low grade tumours. The relative survival in prostate cancer was found to be independent of patient age at diagnosis, indicating that tumour proliferation and the aggressiveness of this disease is equal in all ages. However, due to the increasing occurrence of concurrent diseases with growing age the number of lost years caused by prostate cancer decreases dramatically in older age groups. The overall cause specific mortality for prostate cancer was found to be around 50%. In accordance with most other cancer tumours, the annual mortality rate decreased with longer survival also for prostate cancer patients. In a study from the Swedish Twin Register it was found that the proband concordance rates for prostate cancer were 4,5 time greater among monozygotic compared to dizygotic twins. In a large nation-wide cohort study of men who had a father with prostate cancer, the overall standardised incidence ratio (SIR) was 1.70 for prostate cancer. Younger age at diagnosis among the fathers were associated with an increased risk among sons. This cohort study and the twin study indicates that both inherited and familial factors are of importance in a subgroup of prostate cancer patients. In a prospective case-control study, both a high body mass index (BMI) and a high food intake were found to be independent risk factors for prostate cancer. Both BMI and a high food intake might be indicators of a high fat diet, which so far is the most consistent exogenous risk factor for prostate cancer. The use of tobacco or alcoholic beverages were not associated with prostate cancer risk.

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50

Wirth, Manfred P., i Oliver W. Hakenberg. "Brachytherapy for Prostate Cancer". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-133901.

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