Orientador: Wilter Ricardo Russiano Vicente / Banca: Aracélle Elisane Alves / Banca: Fabiana Ferreira de Souza / Banca: Maria Denise Lopes / Banca: Maricy Apparicio Ferreira / Resumo: A hiperplasia prostática benigna (HPB) tem início no animal com um a dois anos de idade, no entanto, sua fisiopatologia não está totalmente compreendida. O objetivo principal do tratamento da HPB é controlar o crescimento do órgão, prevenir complicações e efeitos colaterais. Desta maneira, o efeito da toxina botulínica tem sido investigado, mostrando bons resultados no homem. Com base nisso, este estudo objetivou fornecer informações acerca dos efeitos da finasterida e da TB-A no tratamento da HPB canina. Para tanto, 24 cães adultos foram divididos aleatoriamente em quatro grupos e submetidos à administração de solução fisiológica 0,9%, 5 mg de finasterida, 500 U de TB-A ou 500 U de TB-A associada a finasterida, e avaliados durante 16 semanas. Complicações locais ou alterações sistêmicas não foram observadas nos animais pertencentes aos grupos experimentais. Após 16 semanas da administração de 5 mg de finasterida o volume prostático reduziu 45,3% e ocorreu um aumento de 5 vezes nas taxa de morte celular. Comparando-se os valores do volume prostático após 16 semanas da aplicação de 500 U de TB-A ou 500 U de TB-A associada a finasterida com os valores basais, observamos uma redução de 30,9 e 51,3%, respectivamente. Neste mesmo período, ocorreu um aumento de seis e oito vezes da taxa de apoptose nos animais do grupo III e IV. Os resultados sugerem que os três protocolos terapêuticos promovem significativa redução do volume prostático e esta se deve a apoptose celular ao invés de necrose. Desta forma, o presente ensaio contribui de forma singular e inovadora para o conhecimento dos efeitos desta nova modalidade de tratamento na HPB canina / Abstract: Benign prostatic hyperplasia (BPH) starts the development in animals aging about 1 - 2 years, however, its pathophysiology is not fully elucidated. The main goal of BPH is to control the growth of the prostate, to prevent complications, and to minimize the adverse effects. Thus, the effect of botulinum toxin A (BT-A) has been investigated in humans with good results. Based on that, this study aimed to provide information about the effects of finasteride and BT-A in the treatment of BPH in dogs. For that, 24 adults dogs were randomly divided in four groups and submitted to administration of saline solution, 5 mg of finasteride, 500 of BT-A or 500 U of BT-A associated with finasteride, and evaluated along 16 weeks. Local complications and systemic effects were not observed. After 16 weeks of the application of 5 mg of finasteride the prostatic volume decreased 45,3% and occurred a 5-fold increased in the rate of cell death. Comparing the values of the prostatic volume after 16 weeks of administration of 500 U of BT-A or 500 U BT-A associated with finasteride with the baseline, a decrease of 30,9 and 51,3% were observed, respectively. In the same period, a increase of 6 and 8 times occurred in the rate of apoptosis in the animals of group III and IV. The results suggest that all 3 treatments protocols further significant reduction in the prostate volume have shown to significantly reduce the volume of prostate, and this reduction is due apoptosis instead necrosis. This way, the present study is an innovative and singular contribution for the knowledge of the effects of BT-A on canine prostate / Doutor

Mutation of the p53 gene is the most common genetic alteration in human cancers. The mutant p53 protein is more stable than the wild type and can be detected by immunohistology. The objective of the current study was to evaluate the immunohistological detection of p53 protein in prostate cancer and its utility as a prognostic indicator. We used a monoclonal anti-p53 antibody and immunostained primary prostate adenocarcinomas (stages Al to Dl) from 109 patients with a mean follow-up of 3.8 years (range, 1.3 to 9.3 years). Immunoreactivity for p53 was seen in 23 cancers (21%). There were 12 instances of progression (14%) among the p53-negative cancers versus seven (30%) among the p53-positive group. Survival analysis using three univariate statistical tests showed that p53 reactivity (P < .03), Gleason score (P < .01), and stage (P < .05) had significant effects on time to progression of prostate cancer. Multivariate analyses showed that Gleason score was significant with all three tests; p53 reactivity was significant with the Wilcoxon test but only approached significance by the log rank and Cox tests. When the analyses included only patients with Gleason scores 2 to 7 (N = 94), univariate analyses showed that p53 reactivity was strongly related to progression of prostate cancer (P < .007). Stage also was significant (P < 0.04), but Gleason score was not. Multivariate analyses showed only p53 reactivity to be significant (P < .007). In conclusion, mutation of the p53 gene may be involved in prostate cancer carcinogenesis. p53 reactivity marks an aggressive subset of prostate cancer and appears to be an independent prognostic indicator that is particularly valuable among the low to intermediate grade cancers.

Chan Chi-keung. / Thesis (M.Sc.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 93-107). / Abstracts in English and Chinese. / List of Tables --- p.ix / List of Figures --- p.x / Chapter 1. --- Literature Review --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.2 --- Oncogenic anatomy of the prostate gland --- p.1 / Chapter 1.3 --- Characteristics of prostate cancer --- p.7 / Chapter 1.4 --- Incidences of prostate cancer --- p.8 / Chapter 1.5 --- Risk factors for prostate cancer --- p.14 / Chapter 1.5.1 --- Endogenous risk factors --- p.14 / Chapter (A) --- Age --- p.14 / Chapter (B) --- Race --- p.16 / Chapter (C) --- Family history --- p.21 / Chapter (D) --- Hormonal factors --- p.24 / Chapter (I) --- Androgen --- p.24 / Chapter (II) --- Vitamin D --- p.32 / Chapter 1.5.2 --- Exogenous risk factors --- p.41 / Chapter (A) --- Dietary factors --- p.41 / Chapter (B) --- Body Mass Index & physical condition --- p.44 / Chapter (C) --- Occupation --- p.46 / Chapter (D) --- Vasectomy --- p.47 / Chapter (E) --- Others --- p.48 / Chapter 2. --- Introduction to the project --- p.49 / Chapter 3. --- Objectives --- p.50 / Chapter 4. --- Materials and Methods --- p.51 / Chapter 4.1 --- Prostate cancer cases --- p.51 / Chapter 4.2 --- Controls --- p.52 / Chapter (A) --- Benign prostatic hyperplasia --- p.52 / Chapter (B) --- Population control --- p.52 / Chapter 4.3 --- DNA extraction --- p.53 / Chapter 4.4 --- Amplification of target DNA --- p.54 / Chapter 4.5 --- Allele typing --- p.55 / Chapter 4.6 --- Statistical analysis --- p.55 / Chapter 5. --- Results --- p.60 / Chapter 5.1 --- Optimization of DNA extraction --- p.60 / Chapter 5.2 --- Optimization of PCR condition --- p.61 / Chapter 5.3 --- Allele typing --- p.65 / Chapter 5.4 --- Characteristics of subjects samples --- p.68 / Chapter 5.4.1 --- Age of subjects and tumor grading --- p.68 / Chapter 5.4.2 --- Genotype typing --- p.69 / Chapter (A) --- Bsm genotype --- p.69 / Chapter (B) --- Fok genotype --- p.69 / Chapter 6. --- Discussions --- p.73 / Chapter 6.1 --- Technical issues --- p.73 / Chapter (A) --- DNA extraction --- p.73 / Chapter (B) --- Primer design --- p.76 / Chapter (C) --- Determination of the optimal PCR condition --- p.77 / Chapter (D) --- Restriction enzyme digestion --- p.82 / Chapter 6.2 --- Age distribution of prostate cancer patients --- p.83 / Chapter 6.3 --- Genotype frequency --- p.84 / Chapter 6.4 --- Histopathological samples of case and control --- p.87 / Chapter 6.5 --- Vitamin D receptor genotypes and prostate cancer --- p.89 / Chapter 7. --- Conclusions --- p.92 / Chapter 8. --- References --- p.93

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.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2007. / Härtill 4 uppsatser.

No description available.

by Kin-mang Lau. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 148-167). / Chapter I --- ABSTRACT --- p.1 / Chapter II --- INTRODUCTION --- p.3 / Chapter II. 1 --- Epidemiology of prostate cancer --- p.3 / Chapter II.2 --- Anatomy of the human prostate --- p.13 / Chapter II.3 --- Pathology of prostate diseases --- p.14 / Chapter II.3.1 --- Prostatic Hyperplasia / Chapter II.3.2 --- Atypical Hyperplasia / Chapter II.3.3 --- Prostatic Carcinoma / Chapter II.4 --- Tumour Suppressor Gene - Human p53 --- p.19 / Chapter II.4.1 --- General aspects / Chapter II.4.2 --- Human p53 gene - Historical perspectives / Chapter II.4.3 --- Human p53 gene - Structure / Chapter II.4.4 --- Human p53 protein - Structure / Chapter II.4.5 --- Wild-type p53 protein - Biochemical functions / Chapter II.4.6 --- Wild-type p53 protein - Biological function / Chapter II.4.7 --- Regulation of p53 function / Chapter II.4.8 --- p53 mutations in Human cancers / Chapter II.4.9 --- Properties of mutant p53 protein / Chapter II.5 --- Human Papillomavirus (HPV) --- p.38 / Chapter II.5.1. --- Virion Structure / Chapter II.5.2 --- Classification / Chapter II.5.3. --- Papillomaviruses in Human Cancers / Chapter II.5.4. --- Relationship between p53 alteration and HPV infection / Chapter II.6 --- p53 alteration and Prostate cancers --- p.42 / Chapter II.6.1. --- Cytogenetic studies / Chapter II.6.2. --- Hybridization analysis / Chapter II.6.3. --- p53 alterations and Prostatic cell lines / Chapter III. --- OBJECTIVES OF STUDY --- p.46 / Chapter IV --- MATERIALS & METHODS --- p.47 / Chapter IV.1 --- Patients and Materials --- p.47 / Chapter IV.2 --- Histological Grading --- p.47 / Chapter IV.2.1 --- Gleason grading / Chapter IV.2.2 --- W.H.O. grading (Mostofi) / Chapter IV.3 --- Staging of Prostatic carcinoma --- p.48 / Chapter IV.4 --- Collection of Blood and Tissue samples --- p.49 / Chapter IV.5 --- Immunohistochemical studies of Prostatic lesions --- p.50 / Chapter IV.5.1 --- Antibodies used / Chapter IV.5.2 --- Methods in frozen sections / Chapter IV.5.3 --- Methods in paraffin sections / Chapter IV.5.4 --- Controls / Chapter IV.5.5 --- Immunohistochemical evaluation / Chapter IV.6 --- Extraction of DNA from tissues and blood samples --- p.52 / Chapter IV.6.1 --- Extraction of genomic DNA from blood / Chapter IV.6.2 --- Extraction of genomic DNA from tissue / Chapter IV.7 --- Hybridization analysis --- p.54 / Chapter IV.7.1 --- Preparation of Cloned Probe DNA / Chapter IV.7.2 --- Transformation of CaCl2-treated competent cell / Chapter IV.7.3 --- Cultures of Transformants / Chapter IV.7.4 --- Isolationof plasmid DNA from transformant cultures / Chapter IV.7.5 --- Purification of DNA Probe by electroelution / Chapter IV.7.6 --- Radioactive labelling of DNA Probes / Chapter IV.7.7 --- Purification of radioactive labelled DNA Probes / Chapter IV.7.8 --- Southern Blotting Technique / Chapter IV.7.9 --- Hybridization of DNA Blots with labelled DNA Probe / Chapter IV.8 --- Polymerase Chain Reaction - Single Stranded Conformational Polymorphism (PCR-SSCP) --- p.63 / Chapter IV.8.1 --- 5'-radioactive labelling of primer / Chapter IV.8.2 --- Amplification of target sequence by PCR / Chapter IV.8.3 --- Nondenaturing Polyacrylamide Gel Electrophoresis / Chapter IV.8.4 --- Direct DNA sequencing of PCR products with p53 mutation / Chapter IV.8.5 --- Controls / Chapter IV.9 --- PCR method for detection of Human Papillomavirus (HPV) --- p.71 / Chapter IV.9.1 --- PCR-Amplification / Chapter IV.9.2 --- DNA alkali Blotting Technique / Chapter IV.9.3 --- Preparation of Radioactive labelled Oligoprobes / Chapter IV.9.4 --- Hybridization of DNA Blots with radioactive labelled Oligoprobes / Chapter IV.9.5 --- Controls / Chapter IV.9.6 --- Sensitivity of HPV 18 detection by PCR / Chapter V --- RESULTS --- p.76 / Chapter V.1 --- Grading and Staging of patients with prostatic carcinoma --- p.76 / Chapter V.2 --- Immunohistochemistry in prostatic lesions --- p.80 / Chapter V.3 --- Results of hybridization analysis --- p.81 / Chapter V.4 --- PCR-SSCP findings in prostatic hyperplasia and carcinoma --- p.97 / Chapter V.5 --- PCR detection of HPV in human prostate --- p.110 / Chapter VI --- DISCUSSION --- p.125 / Chapter VII --- CONCLUSION --- p.146 / Chapter VIII --- REFERENCES --- p.148 / Chapter IX --- APPENDIX --- p.168 / Chapter X --- ACKNOWLEDGEMENT --- p.172

by Kwan Yiu Wing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 167-187). / Abstracts in English and Chinese. / ACKNOWLEDGMENTS --- p.IV / ABSTRACT --- p.1 / Chapter CHAPTER 1. --- INTRODUCTION --- p.5 / Chapter I. --- Epidemiology of Prostate Cancer --- p.5 / Chapter II. --- The Normal Prostate - Prostatic Anatomy --- p.9 / Chapter III. --- Pathology of Prostatic Cancers --- p.12 / Chapter CHAPTER 2. --- PROSTATIC INTRAEPITHELIAL NEOPLASIA --- p.16 / Chapter I. --- Introduction --- p.16 / Chapter II. --- "Definition, Characteristics and Grading" --- p.16 / Chapter III. --- Incidence and Prevalence of PIN --- p.26 / Chapter IV. --- Evidence Linking PIN with Prostatic Carcinoma --- p.27 / Chapter V. --- Conclusion --- p.37 / Chapter CHAPTER 3. --- HISTOLOGIC BIOMARKERS --- p.39 / Chapter I. --- p53 Protein --- p.39 / Chapter II. --- Proliferating Cell Nuclear Antigen (PCNA) --- p.44 / Chapter III. --- Ki-67 Antigen --- p.48 / Chapter IV. --- Epidermal Growth Factor Receptor --- p.49 / Chapter V. --- E-Cadherin --- p.51 / Chapter VI. --- CD44 --- p.54 / Chapter VII. --- nm23 --- p.58 / Chapter CHAPTER 4. --- OBJECTIVES OF STUDY --- p.62 / Chapter CHAPTER 5. --- MATERIALS AND METHODS --- p.63 / Chapter I. --- Materials --- p.63 / Chapter II. --- Methods --- p.71 / Chapter III. --- Interpretation of Immunostaining Results --- p.78 / Chapter IV. --- Statistical Analysis --- p.82 / Chapter CHAPTER 6. --- RESULTS --- p.83 / Chapter I. --- Immunohistochemical Results for p53 Protein --- p.83 / Chapter II. --- Results of Immunostaining of PCNA --- p.90 / Chapter III. --- Immunostaining and Quantitation of Ki-67 Expression --- p.97 / Chapter IV. --- Immunohistochemical Expression of EGFr --- p.105 / Chapter V. --- E-Cadherin --- p.110 / Chapter VI. --- CD44 --- p.115 / Chapter VII. --- Expression of nm23 in Prostatic Lesions --- p.122 / Chapter VIII. --- Correlation and Association of Expressions of All Biomarkers in Prostatic Lesions --- p.128 / Chapter CHAPTER 7. --- DISCUSSION --- p.132 / Chapter I. --- p53 Protein --- p.135 / Chapter II. --- PCNA --- p.137 / Chapter III. --- Ki-67 --- p.140 / Chapter IV. --- EGFr --- p.143 / Chapter V. --- E-Cadherin --- p.146 / Chapter VI. --- CD44 --- p.148 / Chapter VII. --- nm23 --- p.151 / Chapter VIII. --- Association between Biomarkers and Prostate lesions --- p.154 / Chapter CHAPTER 8. --- SUMMARY AND CONCLUSION --- p.157 / APPENDICES --- p.164 / Chapter I. --- Table of incidence and mortality rates of prostate cancer in the United States from 1973 to 1995 by race --- p.164 / Chapter II. --- Table of leading cancer deaths in Hong Kong from 1971 to 1996 --- p.165 / Chapter III. --- Table of incidence and mortality rate caused by prostate cancer in Hong Kong --- p.166 / Chapter IV. --- Reagents --- p.167 / REFERENCES --- p.169