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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
31

Identification of potential biomarkers for the detection of aggressive prostate cancer

Whiteland, Helen Louise January 2012 (has links)
No description available.
32

LncRNA PVT1 Associates with c-Myc and Stabilizes Oncogenic Signaling in Prostate Cancer

Jones, Rachel, Jones, Rachel January 2017 (has links)
Understanding the factors that affect c-Myc in prostate cancer is critical to developing an effective means of treatment for aggressive, castration-resistant forms of the disease. Myc is an oncogene known to be overexpressed and stabilized in many types of cancer, prostate included. Recent insights into breast cancer have revealed that Myc protein retains a longer half-life in cancer cells, but the cause for this has yet to be deduced. Due to its close proximity and proven interaction with Myc, I propose that the lncRNA PVT1 is stabilizing Myc and facilitating its activation of target genes in castration-resistant prostate cancer. To explore this hypothesis, metastatic prostate cancer DU145 cells were transfected with both siRNAs and ASOs targeting PVT1. Cells were analyzed for changes in different protein levels, as well as binding partners, through the use of immunoprecipitation and western blot. These results were verified with RT-qPCR data to confirm knockdown levels of PVT1. Proliferation assays were also conducted to explore the proliferative abilities of cells when PVT1 levels were decreased. Transfection of PVT1 with siRNA yielded about a 50% knockdown, while ASO targeting brought PVT1 levels down 80%. PVT1 inhibition had different effects on the level of c-Myc in cells depending on the method of transfection used--while transfection with anti-PVT1 siRNAs slightly decrease the amount of c-Myc protein in the cell, transfection using ASOs significantly increases c-Myc. Most importantly, proliferation of DU145 cells decreased with PVT1 knockdown by ASOs. Removal of this lncRNA, therefore, hinders that oncogenic potential for growth of prostate cancer cells. Since Myc poses a difficult target for cancer therapy, any new method to mitigate its oncogenic signaling would be invaluable. Targeting lncRNA PVT1 may be a successful method of doing just that, but more work needs to be done to explore the effects of different knockdown strategies. It is clear, however, that the relationship between Myc and PVT1 is a convoluted interaction that warrants further research. A breakthrough in this area could lead to huge improvements in the way prostate cancer is diagnosed and treated.
33

The Epidemiology of Prostate Cancer Among Multiethnic Men

Kellier, Nicole 21 October 2011 (has links)
The research goal was to document differences in the epidemiology of prostate cancer among multicultural men [non-Hispanic White (NHW), Hispanic (H), non-Hispanic Black (NHB)], and Black subgroups, particularly among NHB subgroups [US-born (USB) and Caribbean-born (CBB)]. Study findings will be useful in supporting further research into Black subgroups. Aim 1 explored changes over time in reported prostate cancer prevalence, by race/ethnicity and by birthplace (within the Black subgroups). Aim 2 investigated relationships between observed and latent variables. The analytical approaches included confirmatory factor analysis (CFA for measurement models) and structural equation modeling (SEM for regression models). National Center for Health Statistics, National Health Interview Survey (NHIS) data from 1999 – 2008 were used. The study sample included men aged 18 and older, grouped by race/ethnicity. Among the CBB group, survey respondents were limited to the English-speaking Caribbean. Prostate cancer prevalence, by race showed a higher trend among NHB men than NHW men overall, however differences over time were not significant. CBB men reported a higher proportion of prostate cancer among cancers diagnosed than USB men overall. Due to small sample sizes, stable prostate cancer prevalence trends could not be assessed over time nor could trends in the receipt of a PSA exam among NHB men when stratified by birthplace. USB and CBB men differ significantly in their screening behavior. The effect of SES on PSA screening adjusted for risk factors was statistically significant while latent variable lifestyle was not. Among risk factors, family history of cancer exhibited a consistent positive effect on PSA screening for both USB and CBB men. Among the CBB men, the number of years lived in the US did not significantly affect PSA screening behavior. When NHB men are stratified by birthplace, CBB men had a higher overall prevalence of prostate cancer diagnoses than USB men although not statistically significant. USB men were 2 to 3 times more likely to have had a PSA exam compared to CBB men, but among CBB men birthplace did not make a significant difference in screening behavior. Latent variable SES, but not lifestyle, significantly affected the likelihood of a PSA exam.
34

In Vitro Effects of Bisphenol A on Prostate Cells: Searching for Clues of Environmental Carcinogenesis

Sienkiewicz, Marta January 2012 (has links)
Estrogens maintain the appropriate androgen-estrogen balance for normal regulation of the structure and function of the male reproductive tract, including the prostate gland. This research investigated viability of cells and expression of selected genes in prostate carcinoma cells (PC-3) exposed to bisphenol A (BPA), an estrogen-like substance present in a number of plastic materials. PC-3 cells are able to metabolize BPA at concentrations below 100 µM. BPA exposure at concentrations between 1nM and 100 µM does not increase or significantly reduce cell viability of these cells. Although the genes investigated in this study (GSTP1 and MGMT) did not show a significant change in expression following in vitro exposure to BPA, the positive control ethinyl estradiol (EE2) caused an increase in GSTP1 expression at mRNA level. These results indicate that BPA does not affect the viability of prostate cells, and motivate a need for further research to identify other genes that could be affected by BPA.
35

Temporal Changes in Prostate Biopsy Use in Ontario

Lavallée, Luke Thomas January 2016 (has links)
Abstract 1.1 Introduction The over-diagnosis and over-treatment of prostate cancer is a major public health concern, and in 2012 the United States Preventive Services Taskforce (USPSTF) recommended against prostate cancer screening. Prostate cancer is usually detected by performing a prostate biopsy. Previously, many men received a biopsy at the first sign of an elevated cancer risk identified by screening. Currently, physicians have more tools are their disposal to select men for biopsy who are likely to have clinically significant cancers, including repeat prostate specific antigen (PSA) testing, PSA density, PSA velocity, PSA free/total ratio, and age-specific cutoffs. These tests allow physicians to reduce the number of unnecessary biopsies performed on lower risk patients. One would expect that the use of these tests, in addition to more selective screening, would decrease the incidence of prostate biopsies in the population. I hypothesized that in the last 10 years in Ontario: 1) the incidence of prostate biopsy has decreased, 2) the proportion of biopsies that are malignant has increased, and 3) patients receiving biopsies are healthier. 1.2 Methods I performed a secondary analysis of population-based administrative databases. I validated the prostate biopsy procedure code in the Ontario Health Insurance Plan (OHIP) then used this code to create a cohort of Ontario men who received their first prostate biopsy between 1992 and 2012. Crude and age standardized incidence rates of prostate biopsy were determined for each study year. Era-specific inter-censal population estimates from Statistics Canada were used to establish the number of men at risk of biopsy each year. Changes over time in prostate biopsy incidence were examined using negative binomial regression by comparing the biopsy incidence of each year to a referent year expressed as incident density ratios. Similar analyses were performed to examine changes over time in the proportion of biopsies that are malignant and the health status of patients receiving biopsy. Health status was determined by calculating the Aggregated Diagnosis Group (ADG) score for each patient. 1.3 Results The sensitivity of the OHIP prostate biopsy code improved during the study period and was approximately 90% in recent years. The specificity for identifying the first prostate biopsy a patient received was estimated to exceed 95%. The crude and age standardized incidence of prostate biopsy in Ontario gradually increased between 1992 and 2007 and then dropped sharply in 2008 and 2012. Overall, 39% of biopsies were malignant but this proportion increased during the study period. The health status of patients receiving biopsy, as measured by the ADG score, improved over the study period. 1.4 Conclusions This is the first study to report crude and age standardized prostate biopsy incidence in a population. We found that previously rising biopsy rates decreased significantly in 2008 and 2012 in conjunction with changes to the perceived utility of prostate cancer screening. More years of follow up are required to determine if these changes were transient or the start of broad practice changes.
36

Cytoskeletal Dynamics and cellular differentiation influence tumor progression and metastatic potential in Prostate Adenocarcinoma

Donald, Carlton Dewitt 01 July 1997 (has links)
Cancer cell attachment to and invasion of an extracellular matrix has been associated with metastatic potential. Recently it has become apparent that the extracellular matrix may influence several phenotype properties of metastatic cancer cells. The mechanisms which regulate prostate cancer growth and metastasis may be particularly relevant to the development of clinical strategies for better understanding and ultimate treatment and control of the disease. Cell-matrix interactions of prostate tumor cells were investigated by comparing the invasive ability through and attachment to reconstructed extracellular matrix components. A correlation was found between metastatic potential and adhesive ability. Non-metastatic AT-1 cells possessed a higher adhesive potential to extracellular matrix components than the highly metastatic cells (Mat-Lu, Mat-LyLu and AT-3) which had higher invasive potentials.
37

Characterisation of epidermal growth factor receptor (EGF-R) in the human prostate

Maddy, Samuel Quarcoo January 1988 (has links)
No description available.
38

TINT Tumor Indicating Normal Tissue : new field of diagnostic biomarkers for prostate cancer

Adamo, Hanibal Hani January 2016 (has links)
Background: Prostate cancer is the most common cancer in Sweden. Due its highly variable behavior, multifocal nature, and insufficient diagnostic methods, prostate cancer is difficult to diagnose and prognosticate. Some patients have an aggressive lethal disease, but the majority of prostate cancer patients have slow-growing, non-lethal disease with long expected survival without treatment. Current diagnostic methods―serum levels of prostate-specific antigen (PSA) and histological grading of biopsied prostate tissue―often do not give the information required to be able to safely differentiate indolent tumors from potentially lethal ones. Many prostate cancers are difficult to detect by imaging, so tissue biopsy cannot be safely guided towards the tumor, and particularly not towards the most aggressive forms. To overcome this problem, multiple needle biopsies are taken from the organ, but biopsies are small and they sample less than 1% of the whole prostate. In this thesis, we explore the non-malignant prostate tissue adjacent to tumors, which is always sampled in biopsies, and we study adaptive changes in this tissue, which may provide new diagnostic and prognostic markers for prostate cancer. We have therefore proposed that this type of tissue should be termed TINT (Tumor Instructed/indicating Normal Tissue).  Methods: In our studies, we used orthotopic rat prostate cancer models with tumors of different aggressiveness. We also used clinical materials from patients diagnosed with prostate cancer at transurethral resection (1975‒1990); the majority of these men were followed with watchful waiting. Analyses were performed with whole-genome expression array, quantitative real-time PCR, immunohistochemistry, and western blotting.  Results: Using the animal model, we found that the presence of a tumor induces changes in gene expression in the surrounding tumor-bearing organ (TINT). The gene signature of TINT was linked to processes such as extracellular matrix organization, immune responses, and inflammation. We also showed that some of these adaptive TINT changes appear to be related to the aggressiveness and metastatic potential of the growing tumor, such as increases in macrophages, in mast cells, in vascular densities, and in vascular cell-proliferation. Some of these findings were confirmed by our observations in patient samples. We found that high staining of the extracellular matrix component hyaluronan in the stroma of the non-malignant prostate tissue was prognostic for short cancer-specific survival. We also found that an elevated proportion of C/EBP-beta positive epithelial cells in non-malignant (TINT) prostate tissue was associated with a good prognosis.  Conclusions: Using animal experiments and patient samples, we showed that the presence of prostate cancer induces changes in the tumor-bearing organ, alterations associated with tumor aggressiveness, and that grading of these changes in TINT can be used to predict outcome in prostate cancer patients.
39

Measurement of individualised quality of life in patients with prostatic adenocarcinoma

Pearcy, Richard Malcolm January 2003 (has links)
No description available.
40

THE ROLE OF POU5F1B IN PROSTATE CANCER

Jiang, Hongmei 01 August 2014 (has links)
Accounting for 14% of all new cancer diagnosis in the United States, prostate cancer is the most commonly diagnosed cancer and the second leading cause of cancer related death in the United States. Prognosis for patients diagnosed with metastatic disease is especially poor, since no effective treatments have been developed (1). In this study, we examined the expression and function of POU5F1B, a protein-encoding pseudogene of the homeodomain transcription factor Oct4, in prostate cancer. POU5F1B is located at 8q24, a "gene desert" containing numerous alleles associated with prostate cancer risk. A recent study has indicated that a number of these risk alleles are correlated with POU5F1B expression and prostate cancer susceptibility. The role of POU5F1B in prostate cancer carcinogenesis and progression, however, is not known. In our study, we found that POU5F1B expression is upregulated in prostate cancers and highly overexpressed by high grade (Gleason ≥8) and metastatic prostate cancers. We cloned POU5F1B from prostate cancer cell lines, which contains prostate cancer risk associated SNPs, including a missense mutation inside the homeobox DNA binding domain, to study the functional effects of POU5F1B overexpression in prostate cancers. Here, we report that POU5F1B from prostate tumor encodes functional proteins that exhibit gene transactivation activity comparable to its parent gene, Oct4. Further, we report that POU5F1B overexpression in prostate cancer cell lines increases prostate cancer cell proliferation, migration, anchorage independent growth, and drug resistance in vitro and tumor xenograft growth in vivo. Conversely, shRNA mediated knockdown of endogenous POU5F1B expression in prostate cancer cells inhibit cell proliferation in vitro and tumor growth in vivo, as well as prolong tumor free survival in animal models. The data provide compelling evidence that POU5F1B is an important mediator of prostate cancer progression. We further examined the molecular mechanism behind POU5F1B driven prostate cancer progression. Our studies found that POU5F1B overexpression suppresses E-Cadherin expression at both mRNA and protein levels. Our studies further found POU5F1B overexpression in prostate cancer cells increases Wnt1, TCF1, and TCF4 expression, as well as increased Wnt/β-Catenin signaling - indicating the induction of epithelial-to-mesenchymal transition (EMT) in POU5F1B overexpressing cells(2). Consistently, qPCR analysis found that POU5F1B overexpression significantly increased the expressions of numerous EMT related genes and prostate cancer stem cell markers. Functional studies further confirmed that the transactivation activity of Nanog, another stem cell related transcription factor, is dramatically increased in POU5F1B overexpressing cells. Taken together, our data strongly suggests that POU5F1B overexpression drives prostate cancer progression through the induction of EMT and conferment of stem-cell properties to tumor cells. In summary, our data demonstrated that POU5F1B is overexpressed in prostate tumors, especially high-grade and metastatic tumors, and is a functional driver of prostate cancer progression by inducing EMT in prostate cancer cells. Our study also showed that POU5F1B can potentially be targeted to treat prostate cancer. Based on our findings, depletion of POU5F1B may reduce the risk of metastatic disease or tumor recurrence when used with concurrent therapies in early state tumors and may attenuate treatment resistance in diseases at advanced stages.

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