Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Umeå : Univ., 2007. / Härtill 5 uppsatser.

Jia, Lin. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 124-146). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

by Kwong Joseph. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 142-164). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.iv / Abbreviations --- p.v / Table of contents --- p.vi / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Prostatic Secretory Proteins --- p.1 / Chapter 1.2 --- Rat Prostatic Secretory Proteins --- p.1 / Chapter 1.2.1 --- Prostatic Secretory Proteins in Ventral Prostate --- p.2 / Chapter 1.2.1.1 --- Prostatic Binding Protein (PBP) --- p.2 / Chapter 1.2.1.2 --- Androgen-Suppressed Proteins of Rat Ventral Prostate --- p.6 / Chapter 1.2.1.3 --- The 20-kDa Protein --- p.8 / Chapter 1.2.1.4 --- Spermine-Binding Proteins --- p.9 / Chapter 1.2.1.5 --- Prostatic Acid Phosphatase (PAP) --- p.10 / Chapter 1.2.2 --- Prostatic Secretory Proteins in Dorsal Prostate --- p.12 / Chapter 1.2.2.1 --- Dorsal Proteins I and II (DP I and DPII) --- p.12 / Chapter 1.2.2.2 --- Seminal Vesicle Secretion II (SVSII) --- p.14 / Chapter 1.2.2.3 --- Probasin --- p.16 / Chapter 1.2.3 --- Prostatic Secretory Proteins in Lateral Prostate --- p.18 / Chapter 1.3 --- Human Prostatic Secretion --- p.18 / Chapter 1.4 --- Human Prostatic Secretory Proteins --- p.18 / Chapter 1.4.1 --- Prostatic Acid Phosphatase (PAP) --- p.19 / Chapter 1.4.2 --- Prostate Specific Antigen (PSA) --- p.22 / Chapter 1.4.2.1 --- Molecular Biology of PSA --- p.22 / Chapter 1.4.2.2 --- Synthesis of PSA --- p.23 / Chapter 1.4.2.3 --- Kallikrein Gene Family --- p.23 / Chapter 1.4.2.4 --- Physiological Function of PSA --- p.24 / Chapter 1.4.2.5 --- PSA as an Immunohistochemical Marker --- p.25 / Chapter 1.4.2.6 --- PSA is not a Prostate-Specific Molecule --- p.26 / Chapter 1.4.3 --- Prostatic Secretory Protein of 94 Amino Acids (PSP94) --- p.27 / Chapter 1.4.3.1 --- Nucleotide Sequence of the PSP94 cDNA --- p.28 / Chapter 1.4.3.2 --- Amino Acid sequence of PSP94 --- p.28 / Chapter 1.4.3.3 --- Biological Properties of PSP94 --- p.29 / Chapter 1.4.3.4 --- Physiological Roles of PSP94 --- p.31 / Chapter 1.4.3.5 --- PSP94 and Its mRNA in Other Non-Prostatic Tissue --- p.31 / Chapter 1.4.3.6 --- PSP94 as a Tumor Marker of Prostate Cancer --- p.32 / Chapter 1.4.3.7 --- Homologous Proteins of PSP94 --- p.34 / Chapter 1.5 --- Aim of Study --- p.35 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Origin and Supply of Noble Rat --- p.37 / Chapter 2.2 --- Chemicals --- p.37 / Chapter 2.3 --- Bilateral Ochidectomy of Animals --- p.37 / Chapter 2.4 --- Androgen Replacement --- p.38 / Chapter 2.5 --- Hormonal and Drug Treatments on Castrated Animals --- p.38 / Chapter 2.6 --- Induction of Prostatic Intraepithelial Neoplasia in Noble Rat Prostate Gland by Long-Term Treatment with Steroids --- p.39 / Chapter 2.6.1 --- Preparation of Steroid Hormone-Filled Silastic® Tubings --- p.39 / Chapter 2.6.2 --- Surgical Implantation of Silastic® Tubings --- p.39 / Chapter 2.6.3 --- Protocols of Hormonal Treatments --- p.40 / Chapter 2.7 --- Androgen-Dependent Rat Dunning Prostatic Adenocarcinoma --- p.40 / Chapter 2.8 --- Androgen-Independent Prostatic Carcinoma Line (AIT) of Noble Rat --- p.41 / Chapter 2.9 --- Plasmids --- p.41 / Chapter 2.10 --- Restriction Enzyme Digestions of pLvB10 and cM-403 --- p.42 / Chapter 2.11 --- Amplification of Rat SVSII cDNA Fragment by RT-PCR and Subcloning --- p.42 / Chapter 2.12 --- Purification of DNA Fragment from Agarose Gel --- p.43 / Chapter 2.13 --- Subcloning of DNA into Vector --- p.44 / Chapter 2.14 --- Tissue Preparation for In-situ Hybridization --- p.47 / Chapter 2.15 --- Synthesis of Digoxigenin (DIG)-Labeled RNA Probe --- p.47 / Chapter 2.16 --- In-situ Hybridization --- p.48 / Chapter 2.17 --- Total RNA Extraction --- p.50 / Chapter 2.18 --- Northern Blotting Analysis --- p.51 / Chapter 2.19 --- Primers and Cycling Conditions --- p.53 / Chapter 2.20 --- Reverse Transcription Polymerase Chain Reaction (RT-PCR) --- p.54 / Chapter 2.21 --- Southern Blotting Analysis --- p.56 / Chapter 2.21.1 --- Southern Blotting --- p.56 / Chapter 2.21.2 --- Preparation of DIG-dUTP Labeled Rat PSP94 cDNA Probe --- p.56 / Chapter 2.21.3 --- Hybridization --- p.57 / Chapter 2.22 --- Restriction Mapping --- p.58 / Chapter 2.23 --- Semi-Quantitative RT-PCR --- p.59 / Chapter 2.24 --- Statistical Analysis --- p.59 / Chapter 2.25 --- "Protein Extraction, SDS-PAGE and Western Blotting Analysis" --- p.60 / Chapter 2.26 --- Immunohistochemistry --- p.63 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Subcloning of DNAs into Vector --- p.65 / Chapter 3.1.1 --- Subcloning of 18s Ribosomal RNA cDNA Fragment --- p.65 / Chapter 3.1.2 --- Subcloning of Probasin cDNA Fragment --- p.66 / Chapter 3.1.3 --- Subcloning of SVSII cDNA Fragment --- p.66 / Chapter 3.1.4 --- Restriction Enzyme Mapping for PCR Product of SVSII --- p.67 / Chapter 3.2 --- Detection of mRNA and Protein Expression of PSP94 in Normal Rat Prostates --- p.68 / Chapter 3.2.1 --- In-situ Hybridization --- p.68 / Chapter 3.2.2 --- Northern Blotting --- p.68 / Chapter 3.2.3 --- RT-PCR Amplification --- p.69 / Chapter 3.2.4 --- Immunohistochemistry --- p.69 / Chapter 3.2.5 --- Western Blotting --- p.70 / Chapter 3.3 --- Detection of mRNA Expression of Probasin and SVSII in Normal Rat Prostates --- p.71 / Chapter 3.3.1 --- In-situ Hybridization --- p.71 / Chapter 3.3.2 --- RT-PCR Amplification --- p.71 / Chapter 3.4 --- "Androgen Regulation of PSP94,Probasin and SVSII mRNA Expression" --- p.72 / Chapter 3.4.1 --- In-situ Hybridization --- p.72 / Chapter 3.4.2 --- "Relative Expression Levels of PSP94, Probasin and SVSII mRNA in Normal, Castrated and Androgen Replaced Rat Lateral Prostates as Measured by a Semiquantitative RT-PCR Method" --- p.73 / Chapter 3.4.2.1 --- Determination of Exponential Range of PCR --- p.73 / Chapter 3.4.2.2 --- Semi-Quantitative RT-PCR --- p.74 / Chapter 3.4.3 --- Western Blot Analysis --- p.75 / Chapter 3.5 --- "Effect of Steroid Hormones and Zinc on the PSP94, Probasin and SVSII Expressions in Castrated Rat Prostates" --- p.76 / Chapter 3.5.1 --- Semi-Quantitative RT-PCR --- p.76 / Chapter 3.5.2 --- Western Blot Analysis --- p.77 / Chapter 3.6 --- "Detection of PSP94, Probasin and SVSII mRNA Expression in Dysplastic and Neoplastic Rat Prostates" --- p.78 / Chapter 3.6.1 --- "Detection of PSP94, Probasin and SVSII mRNA Expression in T+E2-Induced Prostatic Intraepithelial Neoplasia (PIN) of the Lateral Prostate of Noble Rats by In-situ Hybridization" --- p.78 / Chapter 3.6.2 --- "Detection of PSP94,Probasin and SVSII mRNA Expression in Dunning Tumor and AIT Prostatic Tumor" --- p.79 / Chapter 3.6.2.1 --- In-situ Hybridization --- p.79 / Chapter 3.6.2.2 --- RT-PCR Amplification --- p.79 / Chapter Chapter 4 --- Discussion / Chapter 4.1 --- Specific Expression of PSP94 in the Lateral Lobe of Rat Prostate --- p.114 / Chapter 4.2 --- Androgen Regulation of PSP94 --- p.118 / Chapter 4.2.1 --- Molecular Mechanism of Androgen Action --- p.118 / Chapter 4.2.2 --- Androgen Regulation of PSP94 in Rat Lateral Prostate --- p.121 / Chapter 4.3 --- "Effect of Steroid Hormones and Zinc on the PSP94, Probasin and SVSII Expressions in Castrated Rat Lateral Prostate" --- p.126 / Chapter 4.4 --- "Detection of PSP94, Probasin, SVSII mRNA Expression in Dysplastic and Neoplastic Rat Prostates" --- p.133 / Chapter 4.5 --- Gene Therapy --- p.139 / Chapter Chapter 5 --- Conclusions --- p.141 / References --- p.142 / Appendixes --- p.165

Xu, Dandan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 209-231). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Background: The relative treatment effectiveness of surgery versus radiotherapy for early-stage prostate cancer is uncertain and randomized clinical trials are unlikely to be performed. This study describes the difference in cause-specific survival between patients treated with radiotherapy versus surgery, using a number of design and analytic steps to mitigate confounding by indication within an observational study. Methods: We conducted a population-based case-cohort study, sampling patients from the Ontario Cancer Registry who were treated or were candidates for cure by radiotherapy or surgery. Cases were those who died of prostate cancer within 10 years. Cause-specific survival was analyzed using Cox-proportional hazard regression, with variance adjustment for the case-cohort sampling. Analysis using intent to treat was compared to that using treatment received. Propensity scores were also calculated and Cox-proportional hazard regression was conducted within each propensity score quintile. We formed instrumental variable groups based on radiotherapy rates in Cancer Care Ontario Regions (CCORs) using the study population sampling frame and checked the instrumental variable assumption of equal distribution of covariates by comparing those covariates across these groups using data from the subcohort. Results: The adjusted hazard ratios for risk of prostate cancer death for radiotherapy compared to surgery were 1.44 (95% CI 0.86-2.40) and 1.84 (1.06-3.17) using intent to treat and treatment received respectively. Stratified hazard ratios comparing radiotherapy to surgery for death from prostate cancer from the lowest propensity quintile to the highest propensity quintile were 0.30 (0.04-2.28), 1.54 (0.35-6.77), 0.90 (0.29-2.82), 2.71 (1.01-7.31) and 1.08 (0.41-2.81). Differences among these hazard ratios were not statistically significant (p=0.13). The distributions of all prognostic indicators were statistically significantly different between instrumental variable groups. Conclusion: Analysis by intent to treat produced a hazard ratio closer to the null than analysis by treatment received, indicating that uncontrolled confounding toward more serious cases getting radiotherapy was present in the analysis by treatment received. Future studies should focus on obtaining enough numbers for subgroup analysis such as the stratification by risk groups. Caution should be used when using the instrumental variable approach in this population, as prognostic indicators were not as equally distributed as expected. / Thesis (Master, Community Health & Epidemiology) -- Queen's University, 2009-09-24 17:54:09.955

Background: Life expectancy (LE) estimation is an important part of both screening and treatment decision-making for potentially curable prostate cancer. Clinicians’ estimation of patient life expectancy is typically made using population-based life tables and intuition and it is often inaccurate. This study explores methods to improve LE prediction by formally considering patient co-morbid illness status, in addition to age, in the development of a LE prediction tool. Methods: We conducted a population-based retrospective cohort study of patients from the Ontario Cancer Registry who were curative treatment candidates, identified between 1990-1998. We analyzed data on three sub-populations of this cohort, and we used LE estimates from the Ontario Life Tables. Each model utilized Cox proportional hazards analysis, and/or the declining exponential approximation of LE, to estimate the survival experience of potential curative treatment candidates, including the impact due to both age and co-morbid illness status. We developed five separate models, tested them using a random subset of the cohort study sample, and compared their predictive accuracy by measuring both discriminative ability and calibration to determine the ‘best’ model. We also conducted a supplementary analysis using logistic regression to develop a model to predict the probability of 10-year survival. Results: The ‘best’ of our models demonstrated a c-index of 0.65 and very good calibration. Further analysis revealed that our ‘best’ model violated the Cox PH assumption for age and it’s predictions consistently over-estimated observed LE. Supplementary analysis of the logistic regression prediction model demonstrated a c-index of 0.70. Conclusions: Our exploration of methods to predict LE resulted in modest predictive accuracy. However, based on the results of the logistic regression model, we conclude that the results of our LE prediction models are reasonable, and obtaining a high level of predictive accuracy may not be possible given just age and co-morbidities as predictors. Further studies should continue to explore these and other methods for LE prediction. External validation of the ‘best’ model from the current study is required before the model and its accompanying LE reference tables can be recommended for use in a clinical setting for screening or treatment decision-making. / Thesis (Master, Community Health & Epidemiology) -- Queen's University, 2011-04-07 19:11:34.216

Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 4 uppsatser.

Written for the Medical Physics Unit. Title from title page of PDF (viewed 2009/06/19). Includes bibliographical references.

Thesis (M.S.)--University of Michigan, 1990.