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Genetic epidemiology of prostate cancer statistical analyses of genome-wide association studies of prostate cancerAmin Al Olama, Seyed Ali January 2013 (has links)
No description available.
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Downregulation of RalGTPase-activating protein promotes invasion of prostatic epithelial cells and progression from intraepithelial neoplasia to cancer during prostate carcinogenesis / RalGAPの発現低下は前立腺発癌過程において、前立腺上皮細胞の浸潤能を亢進し上皮内腫瘍から癌への進行を促進する。Uegaki, Masayuki 25 November 2019 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第22115号 / 医博第4528号 / 新制||医||1039(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 松田 道行, 教授 武藤 学, 教授 小川 誠司 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Přírodní léčiva v léčbě a prevenci prostatických onemocnění / Natural drugs in the treatment and prevention of prostate diseasesAlaei Faradonbeh, Danial January 2017 (has links)
Danial Alaei Faradonbeh, Natural drugs in the treatment and prevention of prostate diseases, Charles University in Prague, faculty of pharmacy in Hradec Králové, 2015, 86 pages. "Natural drugs in the treatment and prevention of prostate diseases" deals with prostate diseases which are some of the common ailments affecting men in different parts of the world. The etiology of prostate diseases has been identified but little progress has been witnessed as far as treatment is concerned. Of all prostate diseases identified so far, prostate cancer is the most common and affect me aged 40 and above. Prostate cancer affects the prostate gland and affects the normal function of other genitourinary tissues. Conventional prostate disease therapies have yielded minimal results, leading to increased calls for further research. Successful application of plants in the management of other conditions has attracted the interests of cancer researchers. Focus on a number of plants can provide the much needed reprieve and therapy against prostate cancer. Previous studies have identified a number of plants whose active component can act against cancer cells. Ficus pseudopalma, Nelumbo nuficera, Camptotheca acuminata, Rauvolfa vomitoria and Viscum album are some of the plants which have been identified to act against...
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Efficacy of prostate cancer treatments in African American menReynolds, Janeen 27 February 2021 (has links)
Prostate Cancer is one of the leading causes of male cancer related deaths. African American men who are diagnosed with this disease are over two times more likely to die from it than any other ethnic group. Even with this being a proven fact there are little to know studies that investigate why nor how to remedy the disparity. When a man begins the screening process and all the way until the beginning of treatment, the same guidelines are followed regardless of the patients’ ethnic background. This tactic has led to the developed of the disparity that: African American, even when diagnosed with prostate cancer of similar aggressiveness and receive the same treatments as other non-African American patients, are continuously found to have a less likely chance of survival. Despite all the research and the recurring disparity treatments are continued in the same manner. While the exact reasoning as to why African American males do not respond similarly to treatments as other ethnic groups remains unexplained. It could stem from internal differences, screening process, diagnosing methods, or the treatments themselves. Internal differences, like melanin levels, cannot be changed, but there are ways to circumvent these inevitable differences. Existing studies allow for parallels to be drawn about what effect these inevitable differences may have on the African American response to treatment methods; but clinical trials will need to be completed in order to determine if the parallels drawn hold any merit and if they have the ability to fix the disparity. Once those differences are understood, it will be time to conduct new research to determine if those changes are sufficient enough to eliminate the over two percent chance that African American men are more likely to die from a disease when compared to others.
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Role of extracellular vesicles in development of antiandrogen resistance in prostate cancerJanuary 2018 (has links)
acase@tulane.edu / 1 / Adedoyin Johnson
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Discovery of a Novel Class of Agents that Inhibit EZH2 Activity and Lowers the Expression of Androgen Receptor and their Potential Utility in the Treatment of Castration-Resistant Prostate CancerHan, Zhengyang 15 June 2023 (has links)
No description available.
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PROGNOSTIC GENE SIGNATURE FOR INTERMEDIATE RISK PROSTATE CANCERLi, Brian January 2016 (has links)
The Gleason Score (GS) is a powerful predictor of outcome among prostate cancer patients. Patients with tumours graded with a GS of 2 to 6 have a much greater chance of survival compared to those with a GS of 8 to 10. A significant proportion (~40%) of men present with early stage GS 7 tumours (indicating intermediate risk) for whom prognosis is highly variable. Three gene signatures were derived from publicly available gene expression profiles of prostate cancers from the Swedish Watchful Waiting cohort: 1) The Genomic Grade Index consisted of the top 24 genes discriminating between high (8, 9 & 10) and low (≤ 6) GS tumours, 2) The Lethal Gene Score consisted of the top 24 genes discriminating between lethal and indolent disease within GS 7 tumours only, and 3) The network-based gene signature consisted of 88 genes. When these gene signatures were tested in silico on the gene expression profiles of GS 7 patients in both the SWW and the Mayo cohort, patients were stratified into high and low risk for recurrence. These results demonstrate that gene signatures are capable of differentiating low risk and high risk patients within GS 7 tumours. The prognostic capacity of our gene signature will be tested prospectively in a retrospective collection of archived prostate cancer tissue blocks from a phase 3 clinical trial, and it is hypothesized that the patients can be stratified into good and poor outcome groups. NanoString Technology will be used to quantify mRNA values for the signature genes on selected paraffin blocks. Expression values of candidate genes will be correlated with patients’ long-term follow-up information to derive a clinically meaningful signature. Outcome will be defined as biochemical recurrence or metastatic event. The goal of this study is to identify multiple genes whose expression could be formulated into a clinically applicable assay, the implementation of which could serve to better stratify intermediate risk prostate cancer patients for appropriate treatment. / Thesis / Master of Science (MSc) / The over-treatment of prostate cancer patients is a significant concern, as recent clinical trials has shown that it can lead to significant patient morbidity. Although the Gleason Scoring system is a powerful predictor of lethal or indolent disease, a significant proportion of men who present with early stage Gleason Score 7 tumours experience poorer prognosis than expected. The goal of this study is to develop and optimize a gene signature that can be utilized on Gleason Score 7, intermediate risk prostate cancer patients to differentiate them into good and poor outcome groups. We hypothesize that this signature will be able to accurately predict outcome in a separate retrospective cohort of prostate cancer patients. In short, our study hopes to provide proof-of-principle that through the use of gene signatures, it is possible to better differentiate prostate cancer patients into different outcome groups so that they may receive more appropriate treatment specific to their disease type.
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The Diabetes Drug Canagliflozin Enhances the Response of Prostate Cancer to RadiotherapyMekhaeil, Bassem January 2020 (has links)
Canagliflozin (CANA) is a sodium-glucose co-transporter 2 (SGLT2) inhibitor used for the treatment of type II diabetes. There is recent evidence suggesting that Canagliflozin has antiproliferative effects against malignant tumours. Canagliflozin is able to inhibit cell growth and cancer progression by inhibiting mitochondrial complex I leading to a reduction in cellular ATP levels. This alteration in the energy status of the cell leads to AMP-activated kinase (AMPK) activation, which in turn downregulates protein synthesis, lipogenesis and induces cell cycle arrest. The aim of this thesis is to explore whether Canagliflozin can be combined with radiation to enhance the outcome of radiation therapy in the treatment of prostate cancer and to further our knowledge on the cellular pathways impacted by Canagliflozin. Proliferation and clonogenic survival assays were used to establish the antiproliferative effect of Canagliflozin in vitro alone and when combined with radiation. Prostate cancer cell lines with different mutation profiles were used to assess the effectiveness of the drug under different radiation doses. A xenograft model was then used to test Canagliflozin’s effects in vivo. PC-3 cells were injected in the flank of balb/c nude mice. Mice were treated with Canagliflozin, radiation or a combined treatment and tumour growth was monitored. Furthermore, a western blot analysis of cells treated with Canagliflozin and radiation was performed to deepen our understanding of the cellular pathways affected by Canagliflozin. Our results show that Canagliflozin has an additive effect when combined with radiation. Canagliflozin was able to effectively downregulate the mTOR pathway, blocking mitosis and leading to cell cycle arrest. These findings provide evidence that Canagliflozin could be used as an adjunct to radiation therapy in clinical settings. / Thesis / Master of Science in Medical Sciences (MSMS) / Radiation therapy is a key therapy for prostate cancer. Although it is very effective at treating early stages of prostate cancer, prostate cancer cells develop resistance to radiation therapy rendering it less effective. One way to overcome this obstacle is by delivering higher doses of radiotherapy. However, this leads to increased side effects caused by radiation on normal tissues surrounding the prostate. An additional potential solution to this problem is administering a drug that can make cancer cells more sensitive to radiotherapy. This way we can deliver lower doses of radiation to avoid side effects while treating the disease. This study focuses on using a drug called Canagliflozin in combination with radiation in order to improve the outcomes of radiotherapy in prostate cancer.
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Targeting HOX transcription factors in prostate cancerMorgan, Richard, Boxall, A., Harrington, K.J., Simpson, G.R., Michael, A., Pandha, H.S. 02 May 2014 (has links)
Yes / Background: The HOX genes are a family of transcription factors that help to determine cell and tissue identity
during early development, and which are also over-expressed in a number of malignancies where they have been
shown to promote cell proliferation and survival. The purpose of this study was to evaluate the expression of HOX
genes in prostate cancer and to establish whether prostate cancer cells are sensitive to killing by HXR9, an inhibitor
of HOX function.
Methods: HOX function was inhibited using the HXR9 peptide. HOX gene expression was assessed by RNA
extraction from cells or tissues followed by quantitative PCR, and siRNA was used to block the expression of the
HOX target gene, cFos. In vivo modelling involved a mouse flank tumour induced by inoculation with LNCaP cells.
Results: In this study we show that the expression of HOX genes in prostate tumours is greatly increased with
respect to normal prostate tissue. Targeting the interaction between HOX proteins and their PBX cofactor induces
apoptosis in the prostate cancer derived cell lines PC3, DU145 and LNCaP, through a mechanism that involves a
rapid increase in the expression of cFos, an oncogenic transcription factor. Furthermore, disrupting HOX/PBX
binding using the HXR9 antagonist blocks the growth of LNCaP tumours in a xenograft model over an extended
period.
Conclusion: Many HOX genes are highly over-expressed in prostate cancer, and prostate cancer cells are sensitive
to killing by HXR9 both in vitro and in vivo. The HOX genes are therefore a potential therapeutic target in prostate
cancer. / The authors gratefully acknowledge the support of the Prostate Project charity (UK).
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Étude de l'enzyme UGT2B28 et son rôle dans le cancer de la prostateBelledant, Anaïs 24 April 2018 (has links)
Contexte: L’inactivation des androgènes est majoritairement régulée par des enzymes du métabolisme de la famille des UDP-glucuronosyltransferase (UGT). Ce procédé métabolique permet de contrôler la biodisponibilité des hormones stéroïdiennes systémiques et locales. Objectif : L’objectif était d’étudier la relation entre l’expression de l’enzyme UDP-glucuronosyltransferase 2B polypeptide 28 (UGT2B28), impliquée dans la biotransformation des hormones, avec les niveaux hormonaux circulants, et les caractéristiques clinico-pathologiques dans le cancer de la prostate (CaP). Conception et participants : Nous avons utilisé dans cette étude la technique d’immunohostochimie à grande échelle (tissue microarray) sur les tissus de 239 patients ayant un CaP localisé. L’étude des 51 patients additionnels ne possédant pas l’enzyme UGT2B28 dans leur génome, a été effectuée pour confirmer l’importance de cette enzyme sur les niveaux hormonaux circulants. Résultats : La surexpression de l’enzyme UGT2B28 a été associée à des niveaux d’antigène prostatique spécifique (APS) au diagnostic plus faibles, à un score de Gleason plus élevé, à des marges et statuts nodaux positifs, et fut associée de façon indépendante au risque de progression. La surexpression de l’enzyme fut également associée à des niveaux circulants de testostérone (T) et dihydrotestostérone (DHT) plus élevés. Les patients n’exprimant pas le gène UGT2B28 avaient des niveaux plus bas de T (19%), de DHT (17%), de métabolites glucuronidés (18-38%), et des niveaux plus élevés du précurseur surrénalien androsténédione (36%). Conclusion : L’enzyme UGT2B28 modifie les niveaux circulants de T et DHT, et sa surexpression est associée avec un CaP à plus haut grade. Notre étude a permis de découvrir un nouveau rôle d’UGT2B28, celui de régulateur de la stéroïdogenèse, et a souligné l’interconnexion entre les capacités de biotransformation hormonale des cellules cancéreuses, des niveaux hormonaux, des caractéristiques clinicopathologiques et du risque de progression. / Background : Androgen inactivation occurs mainly through the glucuronidation conjugative reaction mediated by UDP-glucuronosyltransferases (UGTs). This metabolic process is involved in the control of systemic and local androgen bioavailability. Objective : To examine the relationship among expression of the androgen-inactivating UGT2B28 enzyme, circulating steroid hormone levels, and clinical phenotype in prostate cancer (PCa). Design, setting, and participants : We conducted an analysis of a high-density prostate tumor tissue microarray consisting of 239 localized PCa cases. The study of 51 additional PCa patients with no copies of UDP glucuronosyltransferase 2B subfamily, polypeptide B28 (UGT2B28) in their genomes was performed to confirm the importance of the enzyme on circulating hormone levels. Outcome measurements and statistical analysis : Steroid hormones were measured by mass spectrometry. Multivariate Cox proportional hazard models assessed the influence of UGT2B28 on progression, and general linear model regression evaluated variations in hormone levels. Results and limitations : Tumor overexpression of UGT2B28 was associated with lower prostate-specific antigen levels at diagnosis, higher Gleason scores, margin and nodal invasion status, and it was shown to be an independent prognostic factor associated with progression. Enzyme overexpression correlated with 30% higher circulating levels of testosterone (T) and dihydrotestosterone (DHT). Patients with no copies of UGT2B28 in their genomes have lower levels of T (19%), DHT (17%), its glucuronide metabolites (18–38%), and enhanced levels of the adrenal precursor androstenedione (36%). Conclusions : The UGT2B28 steroid-inactivating pathway modifies circulating T and DHT levels, and UGT2B28 overexpression is associated with high-grade PCa. Our work has uncovered the role of UGT2B28 as a regulator of steroidogenesis and underscores the interconnectivity among the steroid-inactivation capacity of cancer cells, hormone levels, disease characteristics, and the risk of cancer progression.
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