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1
Holt, Jim. "Prostate Cancer". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6456.
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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.
3
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.
4
Lexander, Helena. "Protein expression in prostate cancer /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-617-4/.
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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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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 advantageDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
7
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.
8
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.
9
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.
10
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.Härtill 5 uppsatser
digitalisering@umu
11
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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Wirth, Manfred P., i Oliver W. Hakenberg. "Brachytherapy for Prostate Cancer". Karger, 1999. https://tud.qucosa.de/id/qucosa%3A27547.
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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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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 BillisDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-09T01:30:27Z (GMT). No. of bitstreams: 1 Quintal_MaisaMomessode_M.pdf: 3825980 bytes, checksum: 7250ae540bacae85643a8842909d79d6 (MD5) Previous issue date: 2007
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
15
Wiklund, Fredrik. "Genetic epidemiology of prostate cancer". Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-281.
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Matar, Corine. "Métabolisme oxydatif et mitochondrial des cellules cancéreuses de prostate". Thesis, Paris Est, 2011. http://www.theses.fr/2011PEST0094.
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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.
18
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 ScienceIt 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.
19
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.
20
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.
21
Harper, Curt E. "Prostate cancer chemoprevention with genistein and resveratrol in models of spontaneously developing prostate cancer". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/harper.pdf.
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Downing, David G. "Cancer-related Masculine Threat, Body Compassion, and Prostate-specific Functioning in Prostate Cancer Patients". Xavier University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=xavier1557162136506447.
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Singh, Rashmi. "Genetic predisposition to prostate cancer". Thesis, Institute of Cancer Research (University Of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416575.
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Mohamed, M. "Epigenetic biomarkers in prostate cancer". Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426926.
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Thorn, Shirley A. "Prostate cancer, the screening conundrum". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0003/MQ32265.pdf.
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Lindmark, Fredrik. "Prostate cancer and inflammatory genes". Doctoral thesis, Umeå : Strålningsvetenskaper, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-667.
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Sorreta, Arianne G. "Docosahexaenoic acid and prostate cancer". abstract and full text PDF (free order & download UNR users only), 2007. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1446441.
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Romanuik, Tammy Lee. "Gene expression in prostate cancer". Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/5313.
Pełny tekst źródłaStreszczenie:
Development and maintenance of the prostate is dependent on androgens and the androgen
receptor. The androgen pathway continues to be important in prostate cancer. Here, we evaluated
the transcriptome of prostate cancer cells in response to androgen using Long Serial Analysis of
Gene Expression (L0ngSAGE) libraries. We identified 35 genes with novel associations to
androgen signalling and validated 24 of these genes using quantitative real time-polymerase
chain reaction (qRT-PCR). These genes were: ARL6IF5, BL VRB, C]9orf48, C]orfJ22,
C6orf66, CAMK2NJ, CCNI, DERA, ERRFI], GLUL, GOLFH3, HMJ3, HSP9OB], MANEA,
NANS, NIPSNAP3A, SLC4JA], SOD], SVIF, TAOK3, TCP], TMEM66, USP33, and
VTAJ. The physiological relevance of these expression trends was evaluated in vivo using the
LNCaP Hollow Fibre model.
There is no cure for castration-recurrent prostate cancer (CRPC), and the mechanisms underlying
the disease are not known. To address this problem, we assayed the transcriptome of LNCaP
human prostate cancer cells as they progress to castration-recurrence in vivo using replicate
L0ngSAGE libraries. We identified 96 novel genes consistently differentially expressed in
CRPC. The expression profiles support a role for the transcriptional activity of the androgen
receptor genes (CCNH, CUEDC2, FLNA, and FSMA 7), steroid synthesis and metabolism genes
(DHCR24, DHRS7, ELOVL5, HSDJ 7B4, and OPRKJ), neuroendocrine cell genes (ENO2,
MAOA, OPRK], SJOOA]O, and TRPM8), and proliferation genes (GAS5, GNB2L], MT-ND3,
NKX3-], PCGEM], PTGFR, STEAFJ, and TMEM3OA) in castration-recurrence.
Screening for prostate cancer using serum levels of prostate-specific antigen has resulted in the
over-treatment of indolent disease. Novel diagnostic and prognostic markers for prostate cancer
are required. To address this need, the levels of 27 transcripts were investigated with qRT-PCR.
Expression of POP3 (100 kb from EST CF140309) was prostate-specific, with restricted
expression ofADAM2, POP1 (50 kb from AK000023), POP4 (truncated TMEFF2), POP 10
(intron ofADAM2), ELOVL5, RAMP], and SPON2. ELO VL5, NGFRAP1, POP5 (intron of
NCAM2), POP8 (intron of EFNA5), RAMP], SPON2, and TMEM66 were differentially
expressed between laser microdissected tumour and normal clinical samples of prostatic tissue.
These studies suggest that ADAM2, ELOVL5, POP 1, POP3, POP4, POP 10, RAMP], and SPON2
may be good candidates for biomarkers of prostate cancer.
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Collin, Simon Michael. "Folate metabolism and prostate cancer". Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.541606.
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Mavrou, Athina. "Targeting angiogenesis in prostate cancer". Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654119.
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Angiogenesis, primarily induced by vascular endothelial growth factor (VEGF). has been shown to be required for prostate cancer development and metastasis. Alternatively spliced isoforms associated with cancer progression have been described in all of the hallmarks of cancer, including angiogenesis. VEGF mRNA is alternatively spliced at the terminal exon, to produce two families of isoforms. The pro- angiogenic family, VEGFxxx. has been shown to be up-regulated in several cancer types including prostate cancer, whereas the antiangiogenic family is preferentially expressed in normal non-angiogenic tissues, but down-regulated in prostate cancer. One of the molecules shown to be involved in the regulation of VEGF alternative splicing is SRPK1. This is a protein kinase that phosphorylates the splicing factor SRSF1 and favours the production of the proangiogenic VEGF isoform. I therefore tested the hypothesis that SRPK1 regulates VEGF mRNA splicing in prostate cancer and that down-regulation of this kinase would increase the production of the anti-angiogenic isoform, preventing angiogenesis and tumour growth. I also tested the hypothesis that SRPK1 and SRSF1 are up-regulated in prostate cancer, given the extensive mis-regulation of splicing events in this malignancy. Studies on prostatectomy samples from patients with prostate cancer showed an up -regulation of SRPK1 and SRSF1 in malignant compared to benign tissues. In addition, a panel of prostate cancer cell lines showed increased expression of SRPK1 when compared with primary prostate epithelial cells. Stable SRPK1 knock-down in PC-3 and LnCap prostate cancer cells and inhibition of SRPK1 using small molecule inhibitors caused a reduction in the pro - angiogenic VEGF expression and splice factor phosphorylation . In vivo, inhibition of SRPK1 by lentiviral knockdown and a small molecule inhibitor resulted in a reduction of prostate tumour growth and decreased vascular density. This study identifies a molecular mechanism that regulates angiogenesis in prostate cancer and provides evidence for the potential use of an SRPK1 inhibitor in the treatment of prostate cancer.
31
Wirth, Manfred P., i Oliver W. Hakenberg. "Curative Treatment of Prostate Cancer". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-133890.
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The guidelines for the curative treatment of prostate cancer presented by the German Society of Urology are discussed. They are based on the current knowledge of the outcomes of surgical and radiotherapeutic treatment for prostate cancer. Radical prostatectomy is recommended as the first-line treatment for organ-confined prostate cancer in patients with an individual life expectancy of at least 10 years. Radiotherapy can be considered as an alternative treatment modality, although current knowledge does not allow a definite assessment of the relative value of radiotherapy compared to radical prostatectomy. Locally advanced cT3 prostate cancer is overstaged in about 20% and curative treatment is possible in selected cases. Guidelines represent rules based on the available evidence. This implies that exceptions must be made whenever appropriate and that guidelines have to be reviewed regularly as new information becomes availableDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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Adamson, Andrew Stephen. "Procoagulants, coagulopathy and prostate cancer". Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316445.
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Oxley, Jonathan David. "Prognostic indicators in prostate cancer". Thesis, Queen Mary, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394837.
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Ratan, Hari Lakshmi. "Combinatorial chemoprevention of prostate cancer". Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29474.
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Improved understanding of the molecular biology of prostate cancer has lead to the identification and development of a number of agents which may be well suited to the task of chemoprevention. In the work described here, two novel agents, resveratrol and gefitinib, have been evaluated for their anticancer effects using in vitro and in vivo models of prostate cancer. Specifically, the hypothesis that these two agents can act synergistically to achieve a greater antineoplastic effect has been tested. Resveratrol is a diet-derived naturally-occurring polyphenol which displays anti-oxidant and anti-inflammatory properties. Gefitinib (ZD1839. "Iressa", AstraZeneca Pharmaceuticals) is a small molecule inhibitor of the epidermal growth factor (EGFR) tyrosine kinase. EGFR is increasingly implicated in prostatic carcinogenesis. The results presented here demonstrate that both resveratrol and gefitinib inhibit the proliferation of hormone-sensitive and hormone-resistant cells in vitro, although there was no synergy between these two compounds. Both compounds modulate cell cycle kinetics causing arrest in various phases of the cycle. Gefitinib was shown to effectively abrogate EGFR phosphorylation in prostate cancer cell lines. No effect of resveratrol on oxidative DNA damage in prostate cancer cells was observed and its effects on COX-2 expression could not be evaluated. Gefitinib potently inhibited the development of DU145 xenografts in a nude mouse model of prostate cancer. No significant effect of resveratrol could be seen in the same mouse model. These results suggest that gefitinib may well have a role to play in the chemotherapy and chemoprevention of prostate cancer. Despite its potent in vitro antiproliferative effects, further in vivo evaluation of resveratrol is required prior to its use alone or in combination with other agents can be recommended in prostate cancer.
35
Wirth, Manfred P., i Oliver W. Hakenberg. "Curative Treatment of Prostate Cancer". Karger, 1999. https://tud.qucosa.de/id/qucosa%3A27546.
Pełny tekst źródłaStreszczenie:
The guidelines for the curative treatment of prostate cancer presented by the German Society of Urology are discussed. They are based on the current knowledge of the outcomes of surgical and radiotherapeutic treatment for prostate cancer. Radical prostatectomy is recommended as the first-line treatment for organ-confined prostate cancer in patients with an individual life expectancy of at least 10 years. Radiotherapy can be considered as an alternative treatment modality, although current knowledge does not allow a definite assessment of the relative value of radiotherapy compared to radical prostatectomy. Locally advanced cT3 prostate cancer is overstaged in about 20% and curative treatment is possible in selected cases. Guidelines represent rules based on the available evidence. This implies that exceptions must be made whenever appropriate and that guidelines have to be reviewed regularly as new information becomes available.Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
36
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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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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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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Amin, Al Olama Seyed Ali. "Genetic epidemiology of prostate cancer statistical analyses of genome-wide association studies of prostate cancer". Thesis, University of Cambridge, 2013. https://www.repository.cam.ac.uk/handle/1810/252290.
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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.
Pełny tekst źródłaStreszczenie:
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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Li, Xing. "Novel brachytherapy techniques for cervical cancer and prostate cancer". Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1682.
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Intensity-modulated brachytherapy techniques, compensator-based intensity modulated brachytherapy (CBT) and interstitial rotating shield brachytherapy (I-RSBT), are two novel conceptual radiation therapies for treating cervical and prostate cancer, respectively. Compared to conventional brachytherapy techniques for treating cervical cancer, CBT can potentially improve the dose conformity to the high-risk clinical target volume (CTV) of the cervix in a less invasive approach. I-RSBT can reduce the dose delivered to the prostate organ at risks (OARs) with the same radiation dose delivered to the prostate CTV. In this work, concepts and prototypes for CBT and I-RSBT were introduced and developed. Preliminary dosimetric measurements were performed for CBT and I-RSBT, respectively.
A CBT prototype system was constructed and experimentally validated. A prototype cylindrical compensator with eight octants, each with different thicknesses, was designed. Direct metal laser sintering (DMLS) was used to construct CoCr and Ti compensator prototypes, and a 4-D milling technique was used to construct a Ti compensator prototype. Gafchromic EBT2 films, held by an acrylic quality assurance (QA) phantom, were irradiated to approximately 125 cGy with an electronic brachytherapy (eBT) source for both shielded and unshielded cases. The dose at each point on the films were calculated using a TG-43 calculation model that was modified to account for the presence of a compensator prototype by ray-tracing.
With I-RSBT, a multi-pass dose delivery mechanism with prototypes was developed. Dosimetric measurements for a Gd-153 radioisotope was performed to demonstrate that using multiple partially shielded Gd-153 sources for I-RSBT is feasible. A treatment planning model was developed for applying I-RSBT clinically. A custom-built, stainless steel encapsulated 150 mCi Gd-153 capsule with an outer length of 12.8 mm, outer diameter of 2.10 mm, active length of 9.98 mm, and active diameter of 1.53 mm was used. A partially shielded catheter was constructed with a 500 micron platinum shield and a 500 micron aluminum emission window, both with 180° azimuthal coverage. An acrylic phantom was constructed to measure the dose distributions from the shielded catheter in the transverse plane using Gafchromic EBT3 films. Film calibration curves were generated from 50, 70, and 100 kVp x-ray beams with NIST-traceable air kerma values to account for energy variation.
In conclusion, CBT, which is a non-invasive alternative to supplementary interstitial brachytherapy, is expected to improve dose conformity to bulky cervical tumors relative to conventional intracavitary brachytherapy. However, at the current stage, it would be time-consuming to construct a patient-specific compensator using DMLS, and the quality assurance of the compensator would be difficult. I-RSBT is a promising approach to reducing radiation dose delivered to prostate OARs. The next step in making Gd-153 based I-RSBT feasible in clinic is developing a Gd-153 source that is small enough such that the source, shield, and catheter all fit within a 16 guage needle, which has a 1.65 mm diameter.
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Walker, Sandra. "Prostate cancer support groups an evaluation /". Australasian Digital Thesis Program, 2005. http://adt.lib.swin.edu.au/public/adt-VSWT20060905.085536.
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Thesis (DPysch) - Dept. of Psychology, Swinburne University of Technology, 2005.Submitted in fulfilment of the requirements for the degree of Professional Doctorate Health Psychology, Department of Psychology, Swinburne University of Technology - 2005. Typescript. Includes bibliographical references (p. 151-159).
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Sridhar, Gayathri. "Meta-analysis: Racial Disparities in Prostate Cancer Survival and Case-Control Study: Association between Family History of Cancers, Obesity and Prostate Cancer". VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1758.
Pełny tekst źródłaStreszczenie:
This is a compilation of 3 abstracts for the three manuscripts included in this dissertation. I. Meta-Analysis: Racial Disparities in Prostate Cancer Survival: Prostate cancer is the second leading cause of cancer-related mortality in men. Previous studies have drawn inconsistent conclusions on racial differences in prostate cancer survival. This meta-analysis was conducted to investigate the relationship between race and survival from prostate cancer. A systematic review of published articles from 1968 to 2007 assessing survival from prostate cancer among African American and White men was conducted. The search yielded 20 eligible published manuscripts. Analysis of unadjusted studies showed African American men have an increased risk of all-cause mortality (Hazard ratio (HR) = 1.47, 95% confidence interval (CI): 1.31, 1.65, P < 0.001). However, examination of adjusted studies showed no difference (HR = 1.07, 95% CI: 0.94, 1.22, P = 0.308). No statistically significant difference was observed in prostate cancer-specific survival in both analyses using unadjusted (HR = 1.11, 95% CI: 0.94, 1.31, P = 0.209) and adjusted studies (HR = 1.15, 95% CI: 0.95, 1.41, P = 0.157). There was evidence of heterogeneity that was unexplained by factors analyzed in overall survival but explained by stage in prostate cancer-specific survival. This meta-analysis concludes that there are no racial differences in the overall and prostate cancer-specific survival between African American and White men. II. Case-Control study: Association between Family History of Cancers and Prostate Cancer: Family history of prostate cancer is an established risk factor for prostate cancer. However, the relationship between family history of cancers other than prostate cancer and prostate cancer risk is inconclusive. This study sought to examine the association between family history of cancers and prostate cancer. A case-control study was conducted in which cases and controls were randomly selected from a large urology clinic in Central Virginia. Cases were 600 histologically confirmed prostate cancer patients who were diagnosed between January 2000 and December 2005, and controls were 686 patients who visited the clinic during the same period and diagnosed with urological illnesses other than cancers and prostate-related problems. Data on family history of cancers, lifestyle and demographic factors were collected. Unconditional logistic regression analysis was used to estimate the odds ratios and the corresponding 95% confidence intervals after adjustment for potential confounding factors. Multiple comparisons adjustments were made using Bonferroni adjustment. Men with family history of any cancer in first-degree relatives including parents (OR=2.42, 95% CI: 1.53, 3.84) and parents only (OR=1.90, 95% CI: 1.23, 2.94) were at increased risk of developing prostate cancer compared to men with no such family history of cancer. Significant increased risk was also observed with family history of prostate cancer in first-degree relatives (OR=2.68, 95% CI: 1.53, 4.69) and parents only (OR=3.26, 95% CI: 1.71, 6.24) compared to men with no family history of prostate cancer. Even after adjustments for multiple comparisons, the significance persisted both in first-degree relatives (OR=2.68, 95% CI: 1.16, 6.21) and parents alone (OR=3.26, 95% CI: 1.24, 8.63). No association was found with family history of other cancers including breast, colon, lung, skin, digestive tract, stomach, liver, pancreas, female cancers, urogenital, urinary bladder, brain, blood and lymph node and other cancers and risk of prostate cancer. This study demonstrated an increased prostate cancer risk for men with a family history of any cancer or prostate cancer in first-degree relatives including parents and parents alone. Health care providers need to be aware of the potential risk of family history of cancers on prostate cancer. III. Case-Control study: Association between Obesity and Prostate Cancer: Obesity is a major public health problem in the United States. Several studies have investigated the association between obesity and prostate cancer risk. However the impact of early-adult obesity on prostate cancer is not well studied. This study proposes to investigate the relationship between prostate cancer and early-onset obesity and current obesity. A case-control study was conducted to investigate the relationship between obesity and prostate cancer in a large urology clinic population in Central Virginia. Cases included histologically confirmed prostate cancer patients of all stages and grades diagnosed from January 2000 to December 2005. Controls were patients who were diagnosed with urological illness other than cancers and prostate-related problems. Self-reported data was collected on anthropometric, lifestyle and demographic factors through a mail survey. Unconditional logistic regression analysis was conducted to investigate the association between prostate cancer and early-onset obesity (BMI at age 18) and current obesity. Odds ratios and corresponding 95% confidence intervals were calculated after accounting for significant interaction terms and adjusting for potential confounding variables. This study showed statistically significant association between BMI at age 18 and prostate cancer risk in the multivariate analysis when BMI was evaluated as a continuous variable. There was a 7% decrease in the odds of prostate cancer risk for every 1 kg/m(2) increment in BMI at age 18 (OR=0.93, 95% CI: 0.87, 0.98). Analysis of BMI at age 18 as a categorical variable also showed reduced risk though statistically non-significant. Obese men (OR=0.62, 95% CI: 0.12, 3.08) and overweight men (OR=0.60, 95% CI: 0.35, 1.05) had a non-significant decreased risk of developing prostate cancer compared to normal weight men at age 18. Examination of current BMI showed a non-statistically significant decreased risk of prostate cancer when examined as a continuous variable. However, there was significant interaction between current BMI treated categorically and age. This study concludes that there is decreased prostate cancer risk associated with increasing BMI at age 18. Future large prospective studies are needed to better understand the association between early-onset obesity and risk of prostate cancer and explore the biological factors associated especially in the early ages. This document was created in Microsoft Word 2003.
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Bouffard, Elise. "Synthèse de glyconanovecteurs pour la thérapie photodynamique des cancers de la prostate". Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20231.
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Le récepteur du mannose 6-phosphate cation indépendant (RM6P-CI) permet l'endocytose puis le transfert de molécules porteuses du marqueur mannose 6-phosphate (M6P) vers les lysosomes. Le RM6P-CI, qui est surexprimé par les cellules de cancer de la prostate, est une cible de choix pour augmenter la délivrance de principes actifs dans ces cellules. Cependant le M6P est dégradé par les phosphatases présentes dans le sérum. Dans le but d'augmenter à la fois la stabilité et l'affinité pour le RM6P-CI, nous avons entrepris la synthèse d'analogues isostères du mannose 6-phosphate. Ces analogues sont fonctionnalisés en position anomère afin de permettre leur greffage sur des nanoparticules de silice mésoporeuse incorporant un photosensibilisateur. L'évaluation biologique a montré un gain d'affinité des nouveaux analogues synthétisés pour le RM6P-CI ainsi qu'une forte augmentation de l'efficacité des nanoparticules fonctionnalisées avec les analogues pour la thérapie photodynamique, in vitro, de cellules de cancer de la prostateThe cation independant mannose 6-phosphate receptor (CI-M6PR) allows the endocytosis and the transport of mannose 6-phosphate (M6P) bearing molecules toward the lysosomes. The CI-M6PR, which is overexpressed by prostate cancer cells, is a target of interest to increase drug delivery in these cells. However, M6P is sensitive to degradation by phosphatases in the serum. To increase both the stability and the affinity for the CI-M6PR, we synthesized new M6P isosteric analogs. These analogs are functionnalized at the anomeric position to permit their grafting on mesoporous silica nanoparticles incorporating a photosensitizer. The biological evaluation demonstrated an affinity gain of the new analogs for the CI-M6PR as well as an increase of the efficacy of the nanoparticles functionnalized with these analogs for the in vitro photodynamic therapy of cancer prostate cells
45
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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Lawson, Deborah A. "Prostate cancer screening practices of Missouri physicians /". free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901254.
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Powolny, Anna Aleksandra. "Diet, nutrition and prostate cancer angiogenesis". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148992965.
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Rodgers, Lisa. "The phosphagen system in prostate cancer". Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8520/.
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Young, James Graham. "Gene & immunotherapy of prostate cancer". Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289297.
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