subject:(Bladder cancer)

1. Zhou, Jiachen. Prospective studies of fluid intake and lower urinary tract symptoms in relation to risk of bladder cancer.

Degree: PhD, Epidemiology, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320597/

► The "urogenous contact" hypothesis states that increase in total fluid intake can decrease risk of bladder cancer by diluting the urine concentration and reducing the… (more)

Subjects/Keywords: bladder cancer

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APA (6^th Edition):

Zhou, J. (2013). Prospective studies of fluid intake and lower urinary tract symptoms in relation to risk of bladder cancer. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320597/

Chicago Manual of Style (16^th Edition):

Zhou, Jiachen. “Prospective studies of fluid intake and lower urinary tract symptoms in relation to risk of bladder cancer.” 2013. Doctoral Dissertation, Brown University. Accessed March 08, 2021. https://repository.library.brown.edu/studio/item/bdr:320597/.

MLA Handbook (7^th Edition):

Zhou, Jiachen. “Prospective studies of fluid intake and lower urinary tract symptoms in relation to risk of bladder cancer.” 2013. Web. 08 Mar 2021.

Vancouver:

Zhou J. Prospective studies of fluid intake and lower urinary tract symptoms in relation to risk of bladder cancer. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2021 Mar 08]. Available from: https://repository.library.brown.edu/studio/item/bdr:320597/.

Council of Science Editors:

Zhou J. Prospective studies of fluid intake and lower urinary tract symptoms in relation to risk of bladder cancer. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320597/

Harvard University

2. Caldwell, Joshua. 5-α Reductase Inhibitors and Risk of Overall and Lethal Bladder Cancer.

Degree: Doctor of Medicine, 2019, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41971516

►

Abstract Purpose: To determine if an association exists between 5-α Reductase Inhibitor (5-ARI) use and the risk of overall bladder cancer or lethal bladder cancer.… (more)

Subjects/Keywords: Bladder Cancer

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APA (6^th Edition):

Caldwell, J. (2019). 5-α Reductase Inhibitors and Risk of Overall and Lethal Bladder Cancer. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:41971516

Chicago Manual of Style (16^th Edition):

Caldwell, Joshua. “5-α Reductase Inhibitors and Risk of Overall and Lethal Bladder Cancer.” 2019. Doctoral Dissertation, Harvard University. Accessed March 08, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:41971516.

MLA Handbook (7^th Edition):

Caldwell, Joshua. “5-α Reductase Inhibitors and Risk of Overall and Lethal Bladder Cancer.” 2019. Web. 08 Mar 2021.

Vancouver:

Caldwell J. 5-α Reductase Inhibitors and Risk of Overall and Lethal Bladder Cancer. [Internet] [Doctoral dissertation]. Harvard University; 2019. [cited 2021 Mar 08]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41971516.

Council of Science Editors:

Caldwell J. 5-α Reductase Inhibitors and Risk of Overall and Lethal Bladder Cancer. [Doctoral Dissertation]. Harvard University; 2019. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41971516

University of Bridgeport

3. Gonzalez, Christian. A Comprehensive Review of Contributory and Potentially Therapeutic factors in Bladder Cancer .

Degree: 2014, University of Bridgeport

URL: https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1411

► This thesis is a comprehensive work of up to date research on the topic of bladder cancer. Until now there have only been published studies… (more)

Subjects/Keywords: Naturopathy; Bladder cancer

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APA (6^th Edition):

Gonzalez, C. (2014). A Comprehensive Review of Contributory and Potentially Therapeutic factors in Bladder Cancer . (Thesis). University of Bridgeport. Retrieved from https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1411

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gonzalez, Christian. “A Comprehensive Review of Contributory and Potentially Therapeutic factors in Bladder Cancer .” 2014. Thesis, University of Bridgeport. Accessed March 08, 2021. https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1411.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gonzalez, Christian. “A Comprehensive Review of Contributory and Potentially Therapeutic factors in Bladder Cancer .” 2014. Web. 08 Mar 2021.

Vancouver:

Gonzalez C. A Comprehensive Review of Contributory and Potentially Therapeutic factors in Bladder Cancer . [Internet] [Thesis]. University of Bridgeport; 2014. [cited 2021 Mar 08]. Available from: https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1411.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gonzalez C. A Comprehensive Review of Contributory and Potentially Therapeutic factors in Bladder Cancer . [Thesis]. University of Bridgeport; 2014. Available from: https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1411

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Zambia

4. Mapulanga, Victor. Pattern of bladder cancer at University Teaching Hopital,lusaka,Zambia in the era of HIV epidemic .

Degree: 2012, University of Zambia

URL: http://hdl.handle.net/123456789/1836

► Background: Human Immunodeficiency Virus (HIV) is endemic to Zambia and is associated with changes in the patterns of both AIDS and non- AIDS defining cancers.… (more)

Subjects/Keywords: Cancer – case studies; Cancre(bladder)

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APA (6^th Edition):

Mapulanga, V. (2012). Pattern of bladder cancer at University Teaching Hopital,lusaka,Zambia in the era of HIV epidemic . (Thesis). University of Zambia. Retrieved from http://hdl.handle.net/123456789/1836

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mapulanga, Victor. “Pattern of bladder cancer at University Teaching Hopital,lusaka,Zambia in the era of HIV epidemic .” 2012. Thesis, University of Zambia. Accessed March 08, 2021. http://hdl.handle.net/123456789/1836.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mapulanga, Victor. “Pattern of bladder cancer at University Teaching Hopital,lusaka,Zambia in the era of HIV epidemic .” 2012. Web. 08 Mar 2021.

Vancouver:

Mapulanga V. Pattern of bladder cancer at University Teaching Hopital,lusaka,Zambia in the era of HIV epidemic . [Internet] [Thesis]. University of Zambia; 2012. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/123456789/1836.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mapulanga V. Pattern of bladder cancer at University Teaching Hopital,lusaka,Zambia in the era of HIV epidemic . [Thesis]. University of Zambia; 2012. Available from: http://hdl.handle.net/123456789/1836

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Colorado State University

5. Nieset, Jessica Rae. Use of cone-beam computed tomography to characterize urinary bladder variations and optimize delivery of radiation therapy for canine bladder cancer.

Degree: PhD, Environmental and Radiological Health Sciences, 2011, Colorado State University

URL: http://hdl.handle.net/10217/46380

► Urinary bladder cancer is the most common cancer of the canine urinary tract, with transitional cell carcinoma (TCC) being the most commonly diagnosed tumor type.… (more)

▼ Urinary bladder cancer is the most common cancer of the canine urinary tract, with transitional cell carcinoma (TCC) being the most commonly diagnosed tumor type. TCC is aggressive, invasive and fatal for most dogs. If left untreated, TCC of the canine bladder has average survival times less than one year. Optimal treatment of this malignancy remains a topic of debate. Different treatment options exist, but many complicating factors make the probability of cure very low, regardless of treatment type, and most care is palliative in nature. Radiation therapy is a possible treatment option, however dailyshape, size, and positional changes (motion) of the bladder and surrounding soft tissue structures often make this modality difficult to incorporate into a curative-intent treatment plan. This study was designed to investigate and quantify the motion characteristics experienced by the canine urinary bladder from day to day. Additionally, this information was then used to examine possible treatment scenarios and determine which of those scenarios would be optimal for canine bladder cancer patients. Retrospective cone beam CT (CBCT) image data from ten dogs were used in this study. Organs of interest were contoured on each daily treatment CBCT data set and the images, along with the contours, were registered (fused) to the original (reference) planning CT. Quantification of bladder motion was determined by making measurements relative to the planning CT. Dosimetric data for the organs of interest were determined using dose volume histograms generated from sample treatment plans. Results indicate a wide range in bladder motion throughout treatment, which partly depends on the methods used for patient positioning (set-up). Of the three patient positioning methods evaluated (dorsal, sternal, and lateral recumbency), the least amount of bladder variability, as well as lowest rectal dose, is seen when dogs are placed in lateral recumbency. Using these motion characteristics, we were able to develop different treatment planning and set-up scenarios that allow for a curative dose to be delivered to the bladder, while simultaneously reducing the dose delivered to the nearby sensitive rectal tissue. All advanced treatment planning techniques produce a better dose distribution than traditional parallel opposed planning, with adaptive radiation therapy (ART) planning techniques showing the most advantageous dose distribution. These results allow for a more informed approach to the treatment of canine bladder cancer, as well as providing possible curative-intent treatment options for canine patients with this malignancy. Advisors/Committee Members: Harmon, Joseph F. (advisor), Bailey, Susan M. (committee member), LaRue, Susan M. (committee member), Worley, Deanna R. (committee member), Johnson, Thomas E. (Thomas Edward), 1964- (committee member).

Subjects/Keywords: canine bladder cancer; radiation therapy

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APA (6^th Edition):

Nieset, J. R. (2011). Use of cone-beam computed tomography to characterize urinary bladder variations and optimize delivery of radiation therapy for canine bladder cancer. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/46380

Chicago Manual of Style (16^th Edition):

Nieset, Jessica Rae. “Use of cone-beam computed tomography to characterize urinary bladder variations and optimize delivery of radiation therapy for canine bladder cancer.” 2011. Doctoral Dissertation, Colorado State University. Accessed March 08, 2021. http://hdl.handle.net/10217/46380.

MLA Handbook (7^th Edition):

Nieset, Jessica Rae. “Use of cone-beam computed tomography to characterize urinary bladder variations and optimize delivery of radiation therapy for canine bladder cancer.” 2011. Web. 08 Mar 2021.

Vancouver:

Nieset JR. Use of cone-beam computed tomography to characterize urinary bladder variations and optimize delivery of radiation therapy for canine bladder cancer. [Internet] [Doctoral dissertation]. Colorado State University; 2011. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/10217/46380.

Council of Science Editors:

Nieset JR. Use of cone-beam computed tomography to characterize urinary bladder variations and optimize delivery of radiation therapy for canine bladder cancer. [Doctoral Dissertation]. Colorado State University; 2011. Available from: http://hdl.handle.net/10217/46380

6. Biggane, Emily Rae. SPARC, A Matricellular Protein, In A Cell Culture Model Of Heavy Metal Cadmium Induced Bladder Urothelial Carcinoma.

Degree: PhD, Biomedical Sciences, 2019, University of North Dakota

URL: https://commons.und.edu/theses/2546

► Bladder cancer, the most common urinary tract malignancy, has environmental toxicant exposure as one of its biggest risk factors. This lab examines potential biomarkers… (more)

▼ Bladder cancer, the most common urinary tract malignancy, has environmental toxicant exposure as one of its biggest risk factors. This lab examines potential biomarkers employing an in vitro model of urothelial carcinoma using a normal bladder cell line and its malignantly transformed cells transformed counterpart, transformed by exposure to long term, low doses of cadmium (Cd2+). Initial microarray analysis determined that Secreted Protein Acidic and Rich in Cysteine (SPARC) was the most repressed gene across all transformed cell lines compared to its normal counterpart (Garrett et al., 2014, Larson et al., 2010). SPARC, an extracellular matrix glycoprotein, functions by regulating cell-matrix interactions. It has both oncogene and tumor suppressor actions depending upon the cancer with its role in bladder carcinoma remaining unclear. Previous lab results identified three key findings regarding the role of SPARC: 1) SPARC was significantly repressed following short term, low dose cadmium exposure; 2) SPARC is expressed at moderate levels in the normal transitional epithelium, however, in urothelial carcinomas, SPARC expression is drastically repressed; and 3) when SPARC was transfected into Cd2+ transformed cells with expression being ‘forced’ via a CMV promoter, heterotransplant tumors again had very little, if any, SPARC expression (Larson et al., 2010; Slusser et al., 2016). The current study is based on 3 overarching hypotheses: 1) SPARC plays a critical role in urothelial cell proliferation, migration, attachment, and spreading; 2) Cadmium transformation significantly decreases SPARC expression by silencing the promoter early in the malignant transformation process; and 3) that in urothelial tumors generated from Cd2+-transformed cell lines, SPARC is prohibitive to tumor initiation. The results of this study advance the understanding of SPARC in transformed cells by showing that SPARC promotes cell spreading which may be inhibitory to tumor initiation, necessitating its repression; preferential transcription factor binding of SOX5 compared to Sp1/Sp3 contributing to SPARC repression; and that in serial heterotransplant tumors, repression of human tumor SPARC continues along with an increase in mouse stromal SPARC. Overall, the conclusion from this research is that SPARC acts as a tumor suppressor in the UROtsa model system requiring repression for malignant transformation and tumor initiation. Advisors/Committee Members: Jane R. Dunlevy.

Subjects/Keywords: Bladder; Cadmium; Cancer; SPARC

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APA (6^th Edition):

Biggane, E. R. (2019). SPARC, A Matricellular Protein, In A Cell Culture Model Of Heavy Metal Cadmium Induced Bladder Urothelial Carcinoma. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/2546

Chicago Manual of Style (16^th Edition):

Biggane, Emily Rae. “SPARC, A Matricellular Protein, In A Cell Culture Model Of Heavy Metal Cadmium Induced Bladder Urothelial Carcinoma.” 2019. Doctoral Dissertation, University of North Dakota. Accessed March 08, 2021. https://commons.und.edu/theses/2546.

MLA Handbook (7^th Edition):

Biggane, Emily Rae. “SPARC, A Matricellular Protein, In A Cell Culture Model Of Heavy Metal Cadmium Induced Bladder Urothelial Carcinoma.” 2019. Web. 08 Mar 2021.

Vancouver:

Biggane ER. SPARC, A Matricellular Protein, In A Cell Culture Model Of Heavy Metal Cadmium Induced Bladder Urothelial Carcinoma. [Internet] [Doctoral dissertation]. University of North Dakota; 2019. [cited 2021 Mar 08]. Available from: https://commons.und.edu/theses/2546.

Council of Science Editors:

Biggane ER. SPARC, A Matricellular Protein, In A Cell Culture Model Of Heavy Metal Cadmium Induced Bladder Urothelial Carcinoma. [Doctoral Dissertation]. University of North Dakota; 2019. Available from: https://commons.und.edu/theses/2546

University of Miami

7. Hoye, Kelly. The Effect of Tobacco Smoke Toxicants on Hyaluronic Acid Family Biomarkers of Urothelial Neoplasms.

Degree: MS, Cancer Biology (Medicine), 2014, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_theses/520

► While cigarette smoking remains the most important risk factor for the development of urothelial neoplasms, the precise mechanisms of urothelial carcinogenesis induced by tobacco… (more)

▼ While cigarette smoking remains the most important risk factor for the development of urothelial neoplasms, the precise mechanisms of urothelial carcinogenesis induced by tobacco smoke toxicants remain obscure. Cigarette smoke is a heterogeneous mix of thousands of compounds, over 60 of which are known human carcinogens. Many of these compounds are electrophilic and form adducts with DNA, leading to mutation in oncogenes and tumor suppressors alike. While this theory remains the primary model of smoke-induced carcinogenesis, recent evidence suggests that cigarette smoke, and the many toxicants contained within, may induce epigenetic and transcriptional changes in smoke-exposed epithelial cells. This thesis aims to elucidate the gene expression modulation of the family of molecules responsible for the synthesis, degradation, and signal transduction of the extracellular glycosaminoglycan, hyaluronic acid. The expression of members of this family of biomolecules is elevated in cases of bladder cancer (BCa) and has been correlated to disease recurrence after resection, progression, and disease-specific mortality. Moreover, several members of this family have been shown in vitro and in vivo to be functionally responsible for BCa growth, angiogenesis, metastasis, and invasion. Despite this knowledge, studies of smoke-induced modulation of this family of biomolecules in the urothelium are yet to be conducted, until now. In this thesis, I have used qPCR and immunoblotting to investigate the transcriptional and translational changes, respectively, in a model of a normal urothelium exposed to whole cigarette smoke, as well as to individual constituents of tobacco smoke. To model the normal urothelium, I have used an SV40 Large T-antigen immortalized normal human urothelial cell line, which maintains similar morphology and stress gene expression to in situ urothelium, but is incapable of soft agar colony formation and does not form tumors upon xenotransplantation into mice. Culturing this cell line, termed UROtsa, in serum-free media results in a multi-layer epithelial sheet, which can be used as a model of a normal transitional urothelium. Using this model, we investigated the transcriptional and translational changes in HA family molecules in confluent UROtsa cultures chronically exposed to a cigarette smoke extract (CSE), generated via bubbling whole smoke through serum-free culture media. After only two weeks of continuous exposure to 0.1% CSE, we found statistically significant elevations in both transcript and protein levels of HA receptor splice variants, CD44v. These elevated levels of CD44v were observed throughout the duration of chronic exposure (up to 6 weeks). This finding is the first evidence of smoke-mediated elevation of these HA receptor variants in urothelial cells. Additionally, we investigated the modulation of the HA family of molecules in response to exposure to two individual constituents of tobacco smoke: BBN and acrolein. After only 1 hour of exposure to these carcinogenic compounds, confluent… Advisors/Committee Members: Vinata B. Lokeshwar, Ralf Landgraf, Robert B. Levy.

Subjects/Keywords: bladder cancer; biomarkers; smoking; toxicants

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APA (6^th Edition):

Hoye, K. (2014). The Effect of Tobacco Smoke Toxicants on Hyaluronic Acid Family Biomarkers of Urothelial Neoplasms. (Thesis). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_theses/520

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hoye, Kelly. “The Effect of Tobacco Smoke Toxicants on Hyaluronic Acid Family Biomarkers of Urothelial Neoplasms.” 2014. Thesis, University of Miami. Accessed March 08, 2021. https://scholarlyrepository.miami.edu/oa_theses/520.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hoye, Kelly. “The Effect of Tobacco Smoke Toxicants on Hyaluronic Acid Family Biomarkers of Urothelial Neoplasms.” 2014. Web. 08 Mar 2021.

Vancouver:

Hoye K. The Effect of Tobacco Smoke Toxicants on Hyaluronic Acid Family Biomarkers of Urothelial Neoplasms. [Internet] [Thesis]. University of Miami; 2014. [cited 2021 Mar 08]. Available from: https://scholarlyrepository.miami.edu/oa_theses/520.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hoye K. The Effect of Tobacco Smoke Toxicants on Hyaluronic Acid Family Biomarkers of Urothelial Neoplasms. [Thesis]. University of Miami; 2014. Available from: https://scholarlyrepository.miami.edu/oa_theses/520

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Manchester

8. Robinson, Richard. Biomarker and treatment target development in muscle invasive bladder cancer.

Degree: Thesis (M.D.), 2015, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/biomarker-and-treatment-target-development-in-muscle-invasive-bladder-cancer(9f7e3dba-9630-4d0d-b7aa-629718d02018).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654813

► Introduction: The outcomes following radical treatment for bladder cancer (BC) remain poor, with 5 year overall survival (OS) rates of approximately 50% and over 5000… (more)

▼ Introduction: The outcomes following radical treatment for bladder cancer (BC) remain poor, with 5 year overall survival (OS) rates of approximately 50% and over 5000 deaths per year in the U.K. There has been paucity of significant therapeutic developments since the introduction of cisplatinum based chemotherapy in the 1970’s. The aim of this study was to identify putative drug targets for the treatment of this aggressive form of cancer. Methods: A tissue microarray (TMA) was constructed from the cystectomy specimens of 497 BC patients and 70 controls, linked to a clinical database with extended follow up. The online database Oncomine® was interrogated to identify putative treatment targets which were subsequently evaluated using in-vitro models of high grade invasive bladder cancer (using the J82 and T24 cell lines). In-vitro modelling was conducted using siRNA target knockdown during proliferation, chemo-sensitivity, migration and Matrigel™ invasion assays. Expression of the putative targets was then correlated with tumour characteristics and patient outcomes, by IHC and automated image analysis of the TMA. Results: The proteins CYR61 and CTGF were selected from Oncomine® and studied in conjunction with the HGF/MET axis, on the basis of known interactions in other cancer types. siRNA knockdown of both proteins abrogated HGF induced Matrigel™ invasion in both cell lines. CYR61 knockdown significantly reduced HGF induced cell migration and foetal calf serum (FCS) induced Matrigel™ invasion in both cell lines. Knockdown of both proteins also significantly increased the sensitivity of both cell lines to cisplatinum. CYR61 expression was significantly increased in BC samples compared to normal controls and an independent predictor of OS at 6 years (HR 1.493, p=0.030). In contrast, loss of CTGF expression was significantly associated with increasing tumour stage and worse OS. MET expression was reduced in BC compared to controls and not predictive of survival following cystectomy. Conclusions: The in-vitro findings for CTGF as a treatment target were encouraging, although these findings were not supported by the TMA data. CYR61 promotes an aggressive bladder cancer phenotype and knockdown reverses features of EMT and increases chemo-sensitivity. Clinical cohort correlation confirms CYR61 to be a promising treatment target in bladder cancer.

Subjects/Keywords: 616.99; Bladder cancer; CYR61; CTGF

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APA (6^th Edition):

Robinson, R. (2015). Biomarker and treatment target development in muscle invasive bladder cancer. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/biomarker-and-treatment-target-development-in-muscle-invasive-bladder-cancer(9f7e3dba-9630-4d0d-b7aa-629718d02018).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654813

Chicago Manual of Style (16^th Edition):

Robinson, Richard. “Biomarker and treatment target development in muscle invasive bladder cancer.” 2015. Doctoral Dissertation, University of Manchester. Accessed March 08, 2021. https://www.research.manchester.ac.uk/portal/en/theses/biomarker-and-treatment-target-development-in-muscle-invasive-bladder-cancer(9f7e3dba-9630-4d0d-b7aa-629718d02018).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654813.

MLA Handbook (7^th Edition):

Robinson, Richard. “Biomarker and treatment target development in muscle invasive bladder cancer.” 2015. Web. 08 Mar 2021.

Vancouver:

Robinson R. Biomarker and treatment target development in muscle invasive bladder cancer. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Mar 08]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/biomarker-and-treatment-target-development-in-muscle-invasive-bladder-cancer(9f7e3dba-9630-4d0d-b7aa-629718d02018).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654813.

Council of Science Editors:

Robinson R. Biomarker and treatment target development in muscle invasive bladder cancer. [Doctoral Dissertation]. University of Manchester; 2015. Available from: https://www.research.manchester.ac.uk/portal/en/theses/biomarker-and-treatment-target-development-in-muscle-invasive-bladder-cancer(9f7e3dba-9630-4d0d-b7aa-629718d02018).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654813

University of Leicester

9. Stanford, Richard Frederick John. Regulation of Fos related antigen-1 (Fra-1) accumulation in human bladder cancer.

Degree: PhD, 2012, University of Leicester

URL: https://figshare.com/articles/Regulation_of_Fos_related_antigen-1_Fra-1_accumulation_in_human_bladder_cancer/10182149 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593653

► Bladder cancer is one of the commoner malignancies in humans and current treatments for invasive disease typically give a five year survival rate of around… (more)

Subjects/Keywords: 616.99462; FRA-1; Bladder Cancer

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APA (6^th Edition):

Stanford, R. F. J. (2012). Regulation of Fos related antigen-1 (Fra-1) accumulation in human bladder cancer. (Doctoral Dissertation). University of Leicester. Retrieved from https://figshare.com/articles/Regulation_of_Fos_related_antigen-1_Fra-1_accumulation_in_human_bladder_cancer/10182149 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593653

Chicago Manual of Style (16^th Edition):

Stanford, Richard Frederick John. “Regulation of Fos related antigen-1 (Fra-1) accumulation in human bladder cancer.” 2012. Doctoral Dissertation, University of Leicester. Accessed March 08, 2021. https://figshare.com/articles/Regulation_of_Fos_related_antigen-1_Fra-1_accumulation_in_human_bladder_cancer/10182149 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593653.

MLA Handbook (7^th Edition):

Stanford, Richard Frederick John. “Regulation of Fos related antigen-1 (Fra-1) accumulation in human bladder cancer.” 2012. Web. 08 Mar 2021.

Vancouver:

Stanford RFJ. Regulation of Fos related antigen-1 (Fra-1) accumulation in human bladder cancer. [Internet] [Doctoral dissertation]. University of Leicester; 2012. [cited 2021 Mar 08]. Available from: https://figshare.com/articles/Regulation_of_Fos_related_antigen-1_Fra-1_accumulation_in_human_bladder_cancer/10182149 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593653.

Council of Science Editors:

Stanford RFJ. Regulation of Fos related antigen-1 (Fra-1) accumulation in human bladder cancer. [Doctoral Dissertation]. University of Leicester; 2012. Available from: https://figshare.com/articles/Regulation_of_Fos_related_antigen-1_Fra-1_accumulation_in_human_bladder_cancer/10182149 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593653

10. Kachrilas, Stefanos. Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως.

Degree: 2018, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/43242

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The purpose of this PhD thesis was to examine the involvement of specific components of the PI3K/AKT pathway in urinary bladder cancer. Samples from sixty-five… (more)

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The purpose of this PhD thesis was to examine the involvement of specific components of the PI3K/AKT pathway in urinary bladder cancer. Samples from sixty-five tumors and thirteen normal bladder tissues were collected. Genomic DNA isolation from snap-frozen and paraffin-embedded laser-microdissected tissues was followed by Sanger sequencing, whereas total RNA was purified for use in RT-PCR analyses. Immunohistochemistry was carried out on sections of paraffin-embedded biopsy material.Three pathogenic mutations (two missense and one frameshift) were identified in exon 20 of PIK3CA {c.3140A>G (p.His1047Arg), c.[3172A>T(;)3174C>T] (p.lle1058Phe), c.3203dupA (p.Asn1068Lysfs*5)} after laser capture microdissection, whereas PTEN mRNA expression was found to be downregulated in bladder cancer tissues compared to normal bladder urothelium. Upregulation of cytoplasmic and nuclear p-AKT expression was detected in low grade tumors, whereas in muscle invasive tumors, p-AKT was shown to be downregulated and confined to the cytoplasm. PTEN expression was weak and mainly cytoplasmic in superficial tumors, but stronger and nuclear in the muscle invasive tumors.In conclusion, PI3K/AKT pathway activation is involved in bladder cancer initiation and progression. In this context, PIK3CA, p-AKT and nuclear PTEN could be used along with other biomarkers for prognostic purposes and for the selection of appropriate therapy in the clinical management of bladder cancer.

Σκοπός αυτής της διδακτορικής διατριβής ήταν να εξετάσει τη πιθανή εμπλοκή του μοριακού μονοπατιού PI3K/AKT στο καρκίνο της ουροδόχου κύστης. Πραγματοποιήθηκε λήψη δειγμάτων από εξήντα πέντε όγκους κύστης και από δεκατρία φυσιολογικούς ιστούς ουροθηλίου της κύστης. Πραγματοποιήθηκε απομόνωση DNA, ακολουθία Sanger, εξέταση RNA, RT-PCR, καθώς και ανοσοιστοχημεία. Διαπιστώθηκαν τρεις παθογενετικές μεταλλάξεις (2 missense, 1 frameshift) στο εξόνιο 20 του PIK3CA {c.3140A>G (p.His1047Arg), c.[3172A>T(;)3174C>T] (p.lle1058Phe), c.3203dupA (p.Asn1068Lysfs*5). Η έκφραση του PTEN mRNA διαπιστώθηκε ότι ήταν μειωμένη στο καρκίνο της κύστης σε σύγκριση με το φυσιολογικό ουροθήλιο της κύστης. Η έκφραση του p-AKT βρέθηκε αυξημένη στο κυτταρόπλασμα και το πυρήνα σε όγκους επιφανειακούς (μη μυοδηιθητικούς) σε αντίθεση με τους μυοδηιθητικούς όγκους όπου η έκφραση του p-AKT βρέθηκε μειωμένη και περιορισμένη κυρίως στο κυτταρόπλασμα. Η έκφραση του PTEN διαπιστώθηκε ότι ήταν ασθενής και κυρίως κυτταροπλασματική στους επιφανειακούς όγκους (μη μυοδηιθητικούς), ενώ στους μυοδιηθητικούς ήταν ισχυρότερη και κυρίως πυρηνική.Συμπερασματικά, το μοριακό μονοπάτι PI3K/AKT εμπλέκεται στην εξέλιξη του καρκίνου της ουροδόχου κύστης και η μέτρηση μορίων του (PIK3CA, p-AKT, PTEN) σε συνδυασμό και με άλλους βιοδείκτες θα μπορύσε να έχει προγνωστικό και θεραπευτικό ρόλο.

Subjects/Keywords: PI3K / Akt signaling pathway; Cancer; Bladder cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kachrilas, S. (2018). Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/43242

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kachrilas, Stefanos. “Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως.” 2018. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 08, 2021. http://hdl.handle.net/10442/hedi/43242.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kachrilas, Stefanos. “Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως.” 2018. Web. 08 Mar 2021.

Vancouver:

Kachrilas S. Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2018. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/10442/hedi/43242.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kachrilas S. Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2018. Available from: http://hdl.handle.net/10442/hedi/43242

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Lund

11. Sjödahl, Gottfrid. Molecular Classification of Bladder Cancer.

Degree: 2013, University of Lund

URL: https://lup.lub.lu.se/record/4173874 ; https://portal.research.lu.se/ws/files/3334190/4173891.pdf

► Decisions in the treatment of bladder cancer today are based on clinical and pathological risk variables such as tumor stage and tumor grade. The importance… (more)

▼ Decisions in the treatment of bladder cancer today are based on clinical and pathological risk variables such as tumor stage and tumor grade. The importance of these conventional risk variables is well documented since more than 10 years, and they are used routinely in the clinics. Over the last ten years, cancer research has seen a gradual transition towards personalized medicine, i.e. the exploitation of specific molecular properties in the treatment of tumors. The starting point for personalized medicine is a taxonomy of the tumor type, where genome, transcriptome, and/or proteome data is used to define molecular subtypes that make sense from biological and clinical viewpoints. The overall aim of the work presented in this thesis is to define the major gene expression subtypes of bladder tumors. The gene expression based subtypes should be viewed as a framework which can be refined either by the integration of genomic, epigenetic, or proteomic data or by the analysis of larger patient cohorts so that the subtypes can be described in greater detail. An exhaustive tumor classification should be based on biological similarity between tumors, and not only group together tumors with similar clinical risk profile. This will increase the probability that the taxonomy is relevant in the evaluation of novel therapies that function by altering pathways or transcriptional programs. In paper 1 we define the two major subtypes of bladder cancer, termed molecular subtype 1 and 2 (MS1 and MS2). In paper 2, MS1 and MS2 are subdivided into five major subtypes named Urobasal A, Urobasal B, Genomically Unstable, SCC-like, and Infiltrated, named after their dominating molecular characteristics. The subtypes were identified in an unsupervised manner and were identified also in external data sets, showing their general applicability. Secondary to the aim of tumor classification is the evaluation of the potential prognostic value of the described subtypes. To allow for clinical comparisons, tumor classification should be possible using immunohistochemistry (IHC) on archived material. In paper 3 we make use of the same set of tumors as in paper 2 and device a simplified classifier based on IHC and histology. This classifier identifies the five subtypes with the exception of Urobasal B which could not be reliably distinguished from the related Urobasal A subtype. The molecular pathological classifier defined in paper 3 thus has room for improvement and will need to evolve as the true molecular subtypes are refined. Up to this point we have shown that the subtypes differ in prognosis, but we could not determine whether this was independent of differences observed in stage and grade. In paper 4 we use an independent population based cohort of T1 tumors to retrospectively estimate the prognostic value of the molecular subtypes. The IHC/histology classifier defined in paper 3 is applied, and the molecular subtypes are compared to a current clinical risk stratification model in multivariate analyses. The results show that the subtypes contain…

Subjects/Keywords: Cancer and Oncology; Bladder cancer; Subtype; Classification

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APA (6^th Edition):

Sjödahl, G. (2013). Molecular Classification of Bladder Cancer. (Doctoral Dissertation). University of Lund. Retrieved from https://lup.lub.lu.se/record/4173874 ; https://portal.research.lu.se/ws/files/3334190/4173891.pdf

Chicago Manual of Style (16^th Edition):

Sjödahl, Gottfrid. “Molecular Classification of Bladder Cancer.” 2013. Doctoral Dissertation, University of Lund. Accessed March 08, 2021. https://lup.lub.lu.se/record/4173874 ; https://portal.research.lu.se/ws/files/3334190/4173891.pdf.

MLA Handbook (7^th Edition):

Sjödahl, Gottfrid. “Molecular Classification of Bladder Cancer.” 2013. Web. 08 Mar 2021.

Vancouver:

Sjödahl G. Molecular Classification of Bladder Cancer. [Internet] [Doctoral dissertation]. University of Lund; 2013. [cited 2021 Mar 08]. Available from: https://lup.lub.lu.se/record/4173874 ; https://portal.research.lu.se/ws/files/3334190/4173891.pdf.

Council of Science Editors:

Sjödahl G. Molecular Classification of Bladder Cancer. [Doctoral Dissertation]. University of Lund; 2013. Available from: https://lup.lub.lu.se/record/4173874 ; https://portal.research.lu.se/ws/files/3334190/4173891.pdf

Freie Universität Berlin

12. Domnitz, Folker. a scientometric analysis.

Degree: 2011, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-10454

► Bladder cancer is still an important disease in industrial countries. Etiologically play consumptional factors as well as exposure to several toxic substances a role. Due… (more)

Subjects/Keywords: bladder cancer; bladder tumor; bladder carcinoma; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Domnitz, F. (2011). a scientometric analysis. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-10454

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Domnitz, Folker. “a scientometric analysis.” 2011. Thesis, Freie Universität Berlin. Accessed March 08, 2021. http://dx.doi.org/10.17169/refubium-10454.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Domnitz, Folker. “a scientometric analysis.” 2011. Web. 08 Mar 2021.

Vancouver:

Domnitz F. a scientometric analysis. [Internet] [Thesis]. Freie Universität Berlin; 2011. [cited 2021 Mar 08]. Available from: http://dx.doi.org/10.17169/refubium-10454.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Domnitz F. a scientometric analysis. [Thesis]. Freie Universität Berlin; 2011. Available from: http://dx.doi.org/10.17169/refubium-10454

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

13. 馬, 良. Dual targeting of heat shock proteins 90 and 70 promotes cell death and enhances the anticancer effect of chemotherapeutic agents in bladder cancer.

Degree: 博士(医学), 2016, Oita University / 大分大学

URL: http://hdl.handle.net/10559/15614

► Heat shock proteins (HSPs), which are molecular chaperones that stabilize numerous vital proteins, may be attractive targets for cancer therapy. The aim of the present… (more)

Subjects/Keywords: HSP90; HSP70; Akt; bladder cancer; chemotherapy

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APA (6^th Edition):

馬, �. (2016). Dual targeting of heat shock proteins 90 and 70 promotes cell death and enhances the anticancer effect of chemotherapeutic agents in bladder cancer. (Thesis). Oita University / 大分大学. Retrieved from http://hdl.handle.net/10559/15614

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

馬, 良. “Dual targeting of heat shock proteins 90 and 70 promotes cell death and enhances the anticancer effect of chemotherapeutic agents in bladder cancer.” 2016. Thesis, Oita University / 大分大学. Accessed March 08, 2021. http://hdl.handle.net/10559/15614.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

馬, 良. “Dual targeting of heat shock proteins 90 and 70 promotes cell death and enhances the anticancer effect of chemotherapeutic agents in bladder cancer.” 2016. Web. 08 Mar 2021.

Vancouver:

馬 �. Dual targeting of heat shock proteins 90 and 70 promotes cell death and enhances the anticancer effect of chemotherapeutic agents in bladder cancer. [Internet] [Thesis]. Oita University / 大分大学; 2016. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/10559/15614.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

馬 �. Dual targeting of heat shock proteins 90 and 70 promotes cell death and enhances the anticancer effect of chemotherapeutic agents in bladder cancer. [Thesis]. Oita University / 大分大学; 2016. Available from: http://hdl.handle.net/10559/15614

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

14. Hsu, Jong-Wei. Androgen Receptor and Vitamin D Signaling in Bladder Cancer.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/19819

► Bladder cancer (BCa) is the fourth most common cancer in American men, and was estimated to be diagnosed in 70,530 people and cause 14,680 deaths… (more)

▼ Bladder cancer (BCa) is the fourth most common cancer in American men, and was estimated to be diagnosed in 70,530 people and cause 14,680 deaths in the USA in 2010. BCa is also the cancer which has the highest cost from diagnosis to death per patient. The cost in BCa is not proportionate to the incidence of BCa, which indicates that the efficacy of follow-up therapies need to be greatly improved. This thesis is focused on investigation of the impacts of androgen receptor (AR) and vitamin D signaling on BCa development and response to therapy, which would lead to the development of novel therapeutic approaches. Men have an approximately 3-fold higher risk of BCa than women in the USA, which indicates that sex hormones may be involved in BCa development. Previous studies suggested that both androgen and AR are involved in BCa development by using the general AR knockout (ARKO) mouse model. However, since 90% of BCa are derived from urothelium, it would be of interest to determine if urothelial AR plays a role in bladder tumorigenesis. To address this question, we generated the urothelial ARKO mouse model and applied two BCa mouse models: chemical N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN)-induced BCa and UPII-SV40T transgenic mouse BCa models. We found that knocking out urothelial AR decreased bladder tumorigenesis and tumor growth in the BBN-induced BCa mice. Consequently, BBN-treated urothelial ARKO mice had a higher survival rate than wildtype BBN-treated mice. Moreover, the mechanisms by which urothelial AR promotes BCa initiation and growth is via inactivation of p53. Therapeutic targeting of AR by AR degrading enhances ASC-J9 to decrease BBNinduced bladder tumorigenesis. In summary, we provide multiple evidences to support pro-cancer roles of AR in BCa development, and targeting urothelial AR might be therapeutically beneficial. Around 80% of BCa patients are first diagnosed with non-muscle invasive tumors, and often treated with the transurethral resection of bladder tumor (TURBT) surgery to remove the tumors, followed by a series of intravesical therapies to eliminate the residual cancer cells and prevent recurrence. Bacillus Calmette-Guérin (BCG) has been the most effective immunotherapy for nonmuscle invasive BCa for decades. However, the responses to BCG treatment vary among patients and the mechanisms of BCG actions in BCa have not been completely understood, which limits the utility of BCG therapy. Vitamin D is associated with both innate and adaptive immune responses and has beneficial effects in BCG therapy in tuberculosis (TB) patients, which provides the rationale that vitamin D may contribute to BCG immunotherapy of BCa. To examine the impact of vitamin D signaling on BCG therapy of BCa, we applied both in vitro and in vivo models. We found that the active form of vitamin D, 1α,25- dihydroxyvitamin D3 (1,25-VD), can synergize with BCG to induce BCa cells to secrete higher level of interleukin-8 (IL-8), which results in recruiting more innate immune cells toward BCa…

Subjects/Keywords: Bladder Cancer; Vitamin D; Androgen Receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hsu, J. (2012). Androgen Receptor and Vitamin D Signaling in Bladder Cancer. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/19819

Chicago Manual of Style (16^th Edition):

Hsu, Jong-Wei. “Androgen Receptor and Vitamin D Signaling in Bladder Cancer.” 2012. Doctoral Dissertation, University of Rochester. Accessed March 08, 2021. http://hdl.handle.net/1802/19819.

MLA Handbook (7^th Edition):

Hsu, Jong-Wei. “Androgen Receptor and Vitamin D Signaling in Bladder Cancer.” 2012. Web. 08 Mar 2021.

Vancouver:

Hsu J. Androgen Receptor and Vitamin D Signaling in Bladder Cancer. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1802/19819.

Council of Science Editors:

Hsu J. Androgen Receptor and Vitamin D Signaling in Bladder Cancer. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/19819

NSYSU

15. Jhung, Jheng-Yan. Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway.

Degree: Master, Institute of Biomedical Sciences, 2017, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806117-173323

► Bladder cancer is derived from urothelial, called urothelial carcinoma. Itâs the most top ten cancer in Taiwan. In addition, the cancer with high mortality rate… (more)

Subjects/Keywords: FOXO3; BCL6; Urothelial; Cell cycle; bladder cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jhung, J. (2017). Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806117-173323

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jhung, Jheng-Yan. “Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway.” 2017. Thesis, NSYSU. Accessed March 08, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806117-173323.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jhung, Jheng-Yan. “Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway.” 2017. Web. 08 Mar 2021.

Vancouver:

Jhung J. Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway. [Internet] [Thesis]. NSYSU; 2017. [cited 2021 Mar 08]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806117-173323.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jhung J. Studies on the oncogene of BCl6 effect in human bladder cancer cell lines through FOXO signaling pathway. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0806117-173323

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Michigan

16. Han, Amy. Regulation of Bladder Cancer Invasion.

Degree: PhD, Molecular & Cellular Pathology, 2016, University of Michigan

URL: http://hdl.handle.net/2027.42/135869

► The most common type of bladder cancer is urothelial carcinoma (UC). Bladder cancers are categorized as either non-muscle invasive (stages Ta-T1) or muscle invasive (stages… (more)

Subjects/Keywords: Bladder Cancer Invasion; Pathology; Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Han, A. (2016). Regulation of Bladder Cancer Invasion. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/135869

Chicago Manual of Style (16^th Edition):

Han, Amy. “Regulation of Bladder Cancer Invasion.” 2016. Doctoral Dissertation, University of Michigan. Accessed March 08, 2021. http://hdl.handle.net/2027.42/135869.

MLA Handbook (7^th Edition):

Han, Amy. “Regulation of Bladder Cancer Invasion.” 2016. Web. 08 Mar 2021.

Vancouver:

Han A. Regulation of Bladder Cancer Invasion. [Internet] [Doctoral dissertation]. University of Michigan; 2016. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/2027.42/135869.

Council of Science Editors:

Han A. Regulation of Bladder Cancer Invasion. [Doctoral Dissertation]. University of Michigan; 2016. Available from: http://hdl.handle.net/2027.42/135869

NSYSU

17. Lee, Ya-Hua. Studies on the roles and mechanisms of the STMN3 gene in human bladder cancer-derived cell lines.

Degree: Master, Institute of Biomedical Sciences, 2018, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0612118-141151

► Our study explored the function and regulatory mechanisms of STMN3 which is the microtubule-destabilizing phosphoprotein in the bladder cancer. Our results showed that stable transfection… (more)

Subjects/Keywords: microtubule; stathmin 3(STMN3); Bladder cancer; oncogene

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lee, Y. (2018). Studies on the roles and mechanisms of the STMN3 gene in human bladder cancer-derived cell lines. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0612118-141151

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lee, Ya-Hua. “Studies on the roles and mechanisms of the STMN3 gene in human bladder cancer-derived cell lines.” 2018. Thesis, NSYSU. Accessed March 08, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0612118-141151.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lee, Ya-Hua. “Studies on the roles and mechanisms of the STMN3 gene in human bladder cancer-derived cell lines.” 2018. Web. 08 Mar 2021.

Vancouver:

Lee Y. Studies on the roles and mechanisms of the STMN3 gene in human bladder cancer-derived cell lines. [Internet] [Thesis]. NSYSU; 2018. [cited 2021 Mar 08]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0612118-141151.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lee Y. Studies on the roles and mechanisms of the STMN3 gene in human bladder cancer-derived cell lines. [Thesis]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0612118-141151

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

18. Perlis, Nathan. Developing the Bladder Utility Symptom Scale: A Multiattribute Health State Classification System for Bladder Cancer.

Degree: 2013, University of Toronto

URL: http://hdl.handle.net/1807/43292

►

Disease-specific (e.g. urinary) and generic problems (e.g. fatigue) impact health-related quality of life (HRQOL) of patients with bladder cancer (BC). A questionnaire addressing both sets… (more)

Subjects/Keywords: Bladder Cancer; Quality of Life; 0564

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APA (6^th Edition):

Perlis, N. (2013). Developing the Bladder Utility Symptom Scale: A Multiattribute Health State Classification System for Bladder Cancer. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/43292

Chicago Manual of Style (16^th Edition):

Perlis, Nathan. “Developing the Bladder Utility Symptom Scale: A Multiattribute Health State Classification System for Bladder Cancer.” 2013. Masters Thesis, University of Toronto. Accessed March 08, 2021. http://hdl.handle.net/1807/43292.

MLA Handbook (7^th Edition):

Perlis, Nathan. “Developing the Bladder Utility Symptom Scale: A Multiattribute Health State Classification System for Bladder Cancer.” 2013. Web. 08 Mar 2021.

Vancouver:

Perlis N. Developing the Bladder Utility Symptom Scale: A Multiattribute Health State Classification System for Bladder Cancer. [Internet] [Masters thesis]. University of Toronto; 2013. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1807/43292.

Council of Science Editors:

Perlis N. Developing the Bladder Utility Symptom Scale: A Multiattribute Health State Classification System for Bladder Cancer. [Masters Thesis]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/43292

19. Sandquist, Elizabeth. N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa.

Degree: PhD, Biomedical Sciences, 2015, University of North Dakota

URL: https://commons.und.edu/theses/1830

► Environmental agents are common causes of bladder cancer. Specifically, arsenic (As3+) and cadmium (Cd2+) are known carcinogens implicated in the development of bladder cancer.… (more)

▼ Environmental agents are common causes of bladder cancer. Specifically, arsenic (As3+) and cadmium (Cd2+) are known carcinogens implicated in the development of bladder cancer. Previous studies from our laboratory have shown that As3+ and Cd2+ can cause malignant transformation of normal immortalized bladder urothelial cells, which can form tumors when injected subcutaneous or intraperitoneal into nude mice. Microarray analysis of repeated metal transformation in parallel revealed that N-cadherin was the most upregulated gene in As3+ transformants, and a top induced gene in Cd2+-transformed cells. The switch from E-cadherin to N-cadherin is a well-known indicator of the epithelial-to-mesenchymal transition occurring in bladder cancer. Further, N-cadherin upregulation is correlated with tumor stage, increased recurrence, and decreased survival in patients. While the factors mediating the decrease in E-cadherin expression are well-established, little is known of the factors regulating the increase in N-cadherin expression. The goal of the present study was to determine how As3+ and Cd2+ regulate N-cadherin expression, whether this expression is maintained in heterotransplant models, and if N-cadherin is promoting the epithelial-to-mesenchymal transition in As3+- and Cd2+-transformed UROtsa cells in vitro. This work has demonstrated that N-cadherin is induced in As3+- and Cd2+-transformed UROtsa cell lines, and that the expression is maintained in intraperitoneal, but not subcutaneous, tumor xenografts. Further, tumor-initiating cells derived from transformed UROtsa cells did not express N-cadherin. This suggests that tumor microenvironment and heterogeneity of cell populations are important factors for the use of animal models in cancer research. The As3+ and Cd2+ UROtsa cell lines represent the initial phases of EMT in bladder cancer, and may demonstrate a unique EMT pathway specific to heavy metal carcinogens. Transcriptional regulation of N-cadherin, which is mostly unknown, may be elucidated by the investigation of the transcription factor Twist and epigenetic regulation, particularly histone acetylation. Advisors/Committee Members: Scott H. Garrett.

Subjects/Keywords: arsenic; bladder cancer; cadmium; N-cadherin; UROtsa

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APA (6^th Edition):

Sandquist, E. (2015). N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/1830

Chicago Manual of Style (16^th Edition):

Sandquist, Elizabeth. “N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa.” 2015. Doctoral Dissertation, University of North Dakota. Accessed March 08, 2021. https://commons.und.edu/theses/1830.

MLA Handbook (7^th Edition):

Sandquist, Elizabeth. “N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa.” 2015. Web. 08 Mar 2021.

Vancouver:

Sandquist E. N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa. [Internet] [Doctoral dissertation]. University of North Dakota; 2015. [cited 2021 Mar 08]. Available from: https://commons.und.edu/theses/1830.

Council of Science Editors:

Sandquist E. N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa. [Doctoral Dissertation]. University of North Dakota; 2015. Available from: https://commons.und.edu/theses/1830

Michigan State University

20. Manis, Melanie Otten. Canine in vivo and in vitro metabolism of bladder carcinogen 4, 4'-Methylenebis (2-chloroaniline).

Degree: PhD, Department of Pharmacology and Toxicology, 1984, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:26720

Subjects/Keywords: Bladder – Cancer; Carcinogens

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APA (6^th Edition):

Manis, M. O. (1984). Canine in vivo and in vitro metabolism of bladder carcinogen 4, 4'-Methylenebis (2-chloroaniline). (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:26720

Chicago Manual of Style (16^th Edition):

Manis, Melanie Otten. “Canine in vivo and in vitro metabolism of bladder carcinogen 4, 4'-Methylenebis (2-chloroaniline).” 1984. Doctoral Dissertation, Michigan State University. Accessed March 08, 2021. http://etd.lib.msu.edu/islandora/object/etd:26720.

MLA Handbook (7^th Edition):

Manis, Melanie Otten. “Canine in vivo and in vitro metabolism of bladder carcinogen 4, 4'-Methylenebis (2-chloroaniline).” 1984. Web. 08 Mar 2021.

Vancouver:

Manis MO. Canine in vivo and in vitro metabolism of bladder carcinogen 4, 4'-Methylenebis (2-chloroaniline). [Internet] [Doctoral dissertation]. Michigan State University; 1984. [cited 2021 Mar 08]. Available from: http://etd.lib.msu.edu/islandora/object/etd:26720.

Council of Science Editors:

Manis MO. Canine in vivo and in vitro metabolism of bladder carcinogen 4, 4'-Methylenebis (2-chloroaniline). [Doctoral Dissertation]. Michigan State University; 1984. Available from: http://etd.lib.msu.edu/islandora/object/etd:26720

Tampere University

21. Seppälä, Ville Juhani. Statins and bladder cancer prognosis in a population-based cohort .

Degree: 2019, Tampere University

URL: https://trepo.tuni.fi/handle/10024/118510

► Statiinit on yhdistetty parempaan ennusteeseen useissa eri syöpätyypeissä. Epidemiologisissa tutkimuksissa virtsarakkosyövän ja statiinien välinen yhteys on kuitenkin ollut ristiriitainen. Tutkimuksen tarkoituksena oli tutkia statiinikäytön yhteyttä… (more)

▼ Statiinit on yhdistetty parempaan ennusteeseen useissa eri syöpätyypeissä. Epidemiologisissa tutkimuksissa virtsarakkosyövän ja statiinien välinen yhteys on kuitenkin ollut ristiriitainen. Tutkimuksen tarkoituksena oli tutkia statiinikäytön yhteyttä virtsarakkosyöpäkuolemiin invasiivisissa syöpätapauksissa sekä virtsarakon höyläyksiin non-invasiivisissa syöpätapauksissa. Aineistona toimi kaikki 14 065 Suomalaiseen syöpärekisteriin kirjattua virtsarakkosyöpädiagnoosia aikaväliltä 1996-2012. Syöpärekisteriin on kirjattu 99% kaikista syöpädiagnooseista Suomessa. Kirjattuna oli diagnoosipäivä, syövän morfologia, kasvaimen levinneisyys, hoitolinja, mahdollinen maastamuuttopäivä Suomesta sekä kuolinsyy ja –päivä. Tapaukset linkitettiin THL:n Hoitoilmoitusjäjestelmään sekä Kansaneläkelaitoksen reseptitietokantaan sosiaaliturvatunnusten perusteella, josta saatiin tiedot komorbiditeeteistä, kirurgisista toimenpiteistä sekä ostetuista lääkkeistä. Kasvaimen levinneisyyttä diagnoosihetkellä analysoitiin pre-diagnostisen statiinikäytön mukaan logistisella regressiomallilla rajattuna henkilöihin, joiden rakkosyöpälevinneisyys tiedettiin ja vakioitiin iän, sukupuolen sekä Charlson komorbiditeetti-indeksin mukaan. Post-diagnostista statiinikäytön ja tehtyjen rakkohöyläystän suhdetta analysoitiin logistisella regressiomallilla rajattuna paikallisiin rakkosyöpätapauksiin. Virtarakkosyöpäkuoleman ja kaikkien kuolemien riskisuhteen arvioimiseen käytettiin Cox regressiota ja Competing risks regressio –analyysia kardiovaskulaarisen kuolleisuuden suhteen suoritettiin arvioimaan ei-syöpäkuolemien yhteyttä statiinikäyttöön ja rakkosyöpäkuoleman riskiin. Pre- ja post-diagnostinen statiinikäyttö assosioitui alentuneeseen syöpäkuolleisuuteen annosriippuvaisesti viitaten mahdolliseen progression inhibitioon invasiivisessa virtsarakkosyövässä. Pre-diagnostinen statiinikäyttö oli käänteisesti verrannollinen rakkohöyläysten lukumäärään diagnoosin jälkeen viitaten mahdolliseen vaikutukseen non-invasiivisissa virtsarakkosyövissä.

Subjects/Keywords: Bladder Cancer; Statins; Survival; Virtsarakkosyöpä; Statiinit; Ennuste

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APA (6^th Edition):

Seppälä, V. J. (2019). Statins and bladder cancer prognosis in a population-based cohort . (Masters Thesis). Tampere University. Retrieved from https://trepo.tuni.fi/handle/10024/118510

Chicago Manual of Style (16^th Edition):

Seppälä, Ville Juhani. “Statins and bladder cancer prognosis in a population-based cohort .” 2019. Masters Thesis, Tampere University. Accessed March 08, 2021. https://trepo.tuni.fi/handle/10024/118510.

MLA Handbook (7^th Edition):

Seppälä, Ville Juhani. “Statins and bladder cancer prognosis in a population-based cohort .” 2019. Web. 08 Mar 2021.

Vancouver:

Seppälä VJ. Statins and bladder cancer prognosis in a population-based cohort . [Internet] [Masters thesis]. Tampere University; 2019. [cited 2021 Mar 08]. Available from: https://trepo.tuni.fi/handle/10024/118510.

Council of Science Editors:

Seppälä VJ. Statins and bladder cancer prognosis in a population-based cohort . [Masters Thesis]. Tampere University; 2019. Available from: https://trepo.tuni.fi/handle/10024/118510

University of Melbourne

22. SAPRE, NIKHIL. Urinary biomarkers and integrated genomics in bladder cancer.

Degree: 2014, University of Melbourne

URL: http://hdl.handle.net/11343/55317

► Much remains to be elucidated regarding the molecular mechanisms driving urothelial carcinoma of the bladder (CaB). While comprehensive molecular analyses of several other cancers such… (more)

▼ Much remains to be elucidated regarding the molecular mechanisms driving urothelial carcinoma of the bladder (CaB). While comprehensive molecular analyses of several other cancers such as melanoma and breast cancer have led to the development of targeted therapies that have fundamentally changed treatment paradigms, there has been little progress in CaB in this arena. As a result, CaB outcomes have not improved in over three decades. Despite extensive efforts, a sensitive and specific non-invasive marker for CaB remains elusive. CaB diagnosis and surveillance are reliant on imaging and invasive procedures such as cystoscopy. Consequently, it is the single most expensive cancer to manage per incident case from diagnosis to death. After reviewing the molecular pathways and the landscape of urinary biomarker profiling in CaB, this thesis highlights the move towards profiling of genomic urinary biomarkers over proteomic and cell-based biomarkers and emphasises the need for a comprehensive and integrated approach to molecular profiling of CaB. It focuses on the role of genomic urinary biomarkers in surveillance of bladder cancer as well as comprehensive genetic and epigenetic profiling of CaB. The establishment of a robust platform for translational research and clinical trials in CaB in the setting of a novel bladder cancer clinical service is presented in these studies. The ability of CaB to recur over a long period of time and the impact of prolonged surveillance protocols on the quality of life of CaB patients further highlights the need for urgent development of clinically useful urinary and tissue biomarkers to predict disease behaviour in what is a very heterogeneous cancer. The integrated CaB service and its use as a platform for fast-tracking such translational studies is highlighted, bridging the gap from bench to bedside. The development and validation of a urinary microRNA signature for the detection of CaB recurrence during surveillance is presented. This thesis presents the outcomes of the first clinical trial of a new commercial mRNA-based urinary test uRNA-2 (Cxbladder) in the surveillance of CaB and highlights the challenges in integrating urinary biomarkers in the clinical management of CaB. Also highlighted are important genes and pathways across the progressive spectrum of CaB, both validating several aspects of current models and drawing attention to novel pathways. The value of a multidimensional analysis is evident when epigenetically driven changes in gene expression are identified and validated. In summary, this thesis reports the establishment of a bladder cancer biorepository with clinically annotated tissues and the subsequent use of this platform for development and validation of urinary biomarkers in CaB and a comprehensive molecular analysis of CaB. These studies represent an important step towards use of urinary and tissue biomarkers to predict bladder cancer behaviour and their use in a clinical setting.

Subjects/Keywords: bladder cancer; surveillance; urinary biomarkers; genomics

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APA (6^th Edition):

SAPRE, N. (2014). Urinary biomarkers and integrated genomics in bladder cancer. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/55317

Chicago Manual of Style (16^th Edition):

SAPRE, NIKHIL. “Urinary biomarkers and integrated genomics in bladder cancer.” 2014. Doctoral Dissertation, University of Melbourne. Accessed March 08, 2021. http://hdl.handle.net/11343/55317.

MLA Handbook (7^th Edition):

SAPRE, NIKHIL. “Urinary biomarkers and integrated genomics in bladder cancer.” 2014. Web. 08 Mar 2021.

Vancouver:

SAPRE N. Urinary biomarkers and integrated genomics in bladder cancer. [Internet] [Doctoral dissertation]. University of Melbourne; 2014. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/11343/55317.

Council of Science Editors:

SAPRE N. Urinary biomarkers and integrated genomics in bladder cancer. [Doctoral Dissertation]. University of Melbourne; 2014. Available from: http://hdl.handle.net/11343/55317

23. R. Kandimalla (Raju). Genome-Wide DNA methylation profiling in Bladder cancer and identification of diagnostic and prognostic markers.

Degree: 2012, Erasmus University Rotterdam

URL: http://hdl.handle.net/1765/38061

Subjects/Keywords: bladder cancer

…under the curve BC Bladder cancer BS-SNaPshot Bisulfite specific single nucleotide primer… …bladder cancer NMIBC Non-muscle invasive bladder cancer NPV Negative predictive value PCA… …Chapter 1 Introduction and scope of the thesis 1.1 Bladder cancer: clinical characteristics… …Bladder cancer (BC) is the fifth most common cancer in the western world after… …environmental factors. Smoking is the most important risk factor associated with bladder cancer […

12 more images…

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APA (6^th Edition):

(Raju), R. K. (2012). Genome-Wide DNA methylation profiling in Bladder cancer and identification of diagnostic and prognostic markers. (Thesis). Erasmus University Rotterdam. Retrieved from http://hdl.handle.net/1765/38061

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

(Raju), R. Kandimalla. “Genome-Wide DNA methylation profiling in Bladder cancer and identification of diagnostic and prognostic markers.” 2012. Thesis, Erasmus University Rotterdam. Accessed March 08, 2021. http://hdl.handle.net/1765/38061.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

(Raju), R. Kandimalla. “Genome-Wide DNA methylation profiling in Bladder cancer and identification of diagnostic and prognostic markers.” 2012. Web. 08 Mar 2021.

Vancouver:

(Raju) RK. Genome-Wide DNA methylation profiling in Bladder cancer and identification of diagnostic and prognostic markers. [Internet] [Thesis]. Erasmus University Rotterdam; 2012. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1765/38061.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

(Raju) RK. Genome-Wide DNA methylation profiling in Bladder cancer and identification of diagnostic and prognostic markers. [Thesis]. Erasmus University Rotterdam; 2012. Available from: http://hdl.handle.net/1765/38061

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Miami

24. Yates, Travis J. Biomarkers and Targeted Therapies for Genitourinary Malignancies.

Degree: PhD, Cancer Biology (Medicine), 2013, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/1095

► Molecular determinants of genitourinary metastasis can potentially serve as accurate diagnostic and prognostic markers, and can also be targeted for therapy. Prostate cancer (PCa) is… (more)

▼ Molecular determinants of genitourinary metastasis can potentially serve as accurate diagnostic and prognostic markers, and can also be targeted for therapy. Prostate cancer (PCa) is one of the leading cancers in men in the United States. Approximately 30% of the men with PCa eventually experience hormone refractory disease, which is the main cause of morbidity and mortality associated with PCa. Bladder cancer (BCa) is a common cancer of the urinary tract. Due to frequent recurrence, multi-focality and heterogeneity in tumor progression the clinical management of bladder cancer is the costliest among all cancer patients. When renal cell carcinoma (RCC) is initially diagnosed, ~25% of patients will present with metastatic disease, further, nearly a third of those treated with nephrectomy will eventually experience recurrence. Metastatic-RCC is insidious, as despite several FDA-approved treatments, the five-year survival of patients is less than 10%. Hyaluronic acid (HA) family members are associated with bladder, prostate and kidney cancer progression. HA, a non-sulfated glycosaminoglycan that is synthesized by HA-synthases: HAS1, HAS2 and HAS3 (Hyaluronidase (HAase) degrades HA into small angiogenic fragments. HYAL-1 is the major tumor-derived HAase. Both HA and angiogenic HA fragments induce intracellular signaling by binding to HA receptors, CD44 and RHAMM. Using genitourinary cancer cells as model systems our laboratory has established that the tumor-associated HA-HYAL-1 system promotes tumor growth, angiogenesis, and progression. Prior work from our laboratory has demonstrated that when HA or angiogenic HA fragments generated by degradation of tumor-associated HA by HYAL-1, bind to HA receptors CD44 or RHAMM, it induces HA signaling that ultimately stimulates tumor cell growth, invasion, motility and angiogenesis. Therefore, we hypothesized that targeting the HA-HAase system with HA & HAase inhibitors would inhibit tumor formation, growth and metastasis. In our laboratory we have established sulfated hyaluronic acid (sHA) as a specific inhibitor of HYAL-1 and 4-methylumbelliferone is known to be an inhibitor of HA synthesis. In my first project, I demonstrated that sHA inhibited proliferation, motility, and invasion of PCa cells that expressed HYAL-1 Furthermore, sHA inhibited Akt signaling and showed potent antitumor activity in xenografts, without significant toxicity. Addition of angiogenic HA fragments, as well as, overexpression of a constitutively active form of Akt (myr-Akt) inhibited sHA effects. Contrarily, downregulation of HA receptors, mimicked the effects of sHA. Therefore, the mechanism of the potent antitumor activity of sHA involves the inhibition of the generation of angiogenic HA fragments and subsequently inhibition of HA signaling. My second project was built on prior published results from the laboratory, which showed that 4-MU has potent anti-tumor activity in PCa models. To determine whether 4-MU has chemo-preventive, anti-metastatic properties, and the mechanism of such activities, I… Advisors/Committee Members: Vinata B. Lokeshwar, Priyamvada Rai, Murugesan Manoharan, Enrique A. Mesri, Xiangxi Xu.

Subjects/Keywords: Prostate Cancer; Bladder Cancer; Kidney Cancer; TRAMP; Hyaluronic Acid; 4-MU

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APA (6^th Edition):

Yates, T. J. (2013). Biomarkers and Targeted Therapies for Genitourinary Malignancies. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1095

Chicago Manual of Style (16^th Edition):

Yates, Travis J. “Biomarkers and Targeted Therapies for Genitourinary Malignancies.” 2013. Doctoral Dissertation, University of Miami. Accessed March 08, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/1095.

MLA Handbook (7^th Edition):

Yates, Travis J. “Biomarkers and Targeted Therapies for Genitourinary Malignancies.” 2013. Web. 08 Mar 2021.

Vancouver:

Yates TJ. Biomarkers and Targeted Therapies for Genitourinary Malignancies. [Internet] [Doctoral dissertation]. University of Miami; 2013. [cited 2021 Mar 08]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1095.

Council of Science Editors:

Yates TJ. Biomarkers and Targeted Therapies for Genitourinary Malignancies. [Doctoral Dissertation]. University of Miami; 2013. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1095

Loyola University Chicago

25. Davidson, Valerie. Emetine as an Anti-Cancer Therapeutic in Bladder Cancer.

Degree: MS, Molecular Biology, 2015, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_theses/3129

► Bladder cancer is a serious health concern among the older population, as it is responsible for thousands of deaths annually in the United States.… (more)

▼ Bladder cancer is a serious health concern among the older population, as it is responsible for thousands of deaths annually in the United States. Patients that are diagnosed with muscle-invasive disease have a 5-year survival rate of only 20 percent. Additionally, muscle-invasive disease has a high metastatic potential; half of all patients develop metastatic disease within 3 years. Patients with muscle-invasive disease are presented with few treatment options aside from surgery. The current standard of care is a chemotherapeutic combination therapy of cisplatin and gemcitabine. This therapy is highly toxic, and due to the high instance of co-morbidities in these patients, approximately half are unfit for therapy. An alternative combination of carboplatin plus gemcitabine allows for the inclusion of more patients, but is an inferior therapy. Development of an alternative treatment option is necessary. Previous studies in the Foreman lab have shown a synergistic decrease in bladder cancer cell proliferation when the natural alkaloid emetine is combined with cisplatin in vitro. Here, we expanded these studies to demonstrate that the addition of emetine to both the cisplatin-gemcitabine as well as carboplatin-gemcitabine standard of care regimens resulted in an additive decrease in bladder cancer cell proliferation. Moreover, the addition of low dose emetine allows for up to a 10-fold decrease in effective dose of cisplatin or carboplatin. Treatment with this triple therapy appears to be inducing growth arrest in the cancer cells. Hypoxia Inducible Factors (HIFs) are upregulated in response to low oxygen conditions, and regulate a wide range of genes responsible for giving tumor cells a selective advantage. HIF-α overexpression in bladder cancer corresponds to a poorer prognosis. This, as well as the concise regulation of HIFs, makes them an attractive target for anti-cancer therapy. HIF-1α and HIF-2α are aberrantly upregulated under normoxia conditions in the invasive bladder cancer cell lines UMUC3, HT1376, and T24. Emetine is a know protein synthesis inhibitor at the micromolar level, but less is known about its actions at lower concentrations. We demonstrate here that low, nanomolar concentrations of emetine act to preferentially downregulate levels of HIF-1α and HIF-2α. Emetine appears to be acting via decreased HIF-1α protein synthesis. We hypothesize that emetine is acting in a similar manner on HIF-2α, but further work is necessary to confirm. This regulation of hypoxia signaling may act to decrease the cell’s selective advantage and proliferative potential.

Subjects/Keywords: Bladder Cancer; Cancer Biology; Cancer Therapeutics; Molecular Biology; Molecular Biology

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APA (6^th Edition):

Davidson, V. (2015). Emetine as an Anti-Cancer Therapeutic in Bladder Cancer. (Thesis). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_theses/3129

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Davidson, Valerie. “Emetine as an Anti-Cancer Therapeutic in Bladder Cancer.” 2015. Thesis, Loyola University Chicago. Accessed March 08, 2021. https://ecommons.luc.edu/luc_theses/3129.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Davidson, Valerie. “Emetine as an Anti-Cancer Therapeutic in Bladder Cancer.” 2015. Web. 08 Mar 2021.

Vancouver:

Davidson V. Emetine as an Anti-Cancer Therapeutic in Bladder Cancer. [Internet] [Thesis]. Loyola University Chicago; 2015. [cited 2021 Mar 08]. Available from: https://ecommons.luc.edu/luc_theses/3129.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Davidson V. Emetine as an Anti-Cancer Therapeutic in Bladder Cancer. [Thesis]. Loyola University Chicago; 2015. Available from: https://ecommons.luc.edu/luc_theses/3129

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

26. Rebel, Annemarie. Tumour cell expansion in bladder epithelium.

Degree: 1995, Erasmus University Medical Center

URL: http://hdl.handle.net/1765/21508

► textabstractBladder cancer is common in western society. The major problem of patients with superficial bladder cancer is the high recurrence rate and multifocality of these… (more)

Subjects/Keywords: bladder cancer; bladder epithelium; recurrence; urology

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APA (6^th Edition):

Rebel, A. (1995). Tumour cell expansion in bladder epithelium. (Doctoral Dissertation). Erasmus University Medical Center. Retrieved from http://hdl.handle.net/1765/21508

Chicago Manual of Style (16^th Edition):

Rebel, Annemarie. “Tumour cell expansion in bladder epithelium.” 1995. Doctoral Dissertation, Erasmus University Medical Center. Accessed March 08, 2021. http://hdl.handle.net/1765/21508.

MLA Handbook (7^th Edition):

Rebel, Annemarie. “Tumour cell expansion in bladder epithelium.” 1995. Web. 08 Mar 2021.

Vancouver:

Rebel A. Tumour cell expansion in bladder epithelium. [Internet] [Doctoral dissertation]. Erasmus University Medical Center; 1995. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1765/21508.

Council of Science Editors:

Rebel A. Tumour cell expansion in bladder epithelium. [Doctoral Dissertation]. Erasmus University Medical Center; 1995. Available from: http://hdl.handle.net/1765/21508

Vanderbilt University

27. Hebron, Katie Elizabeth. ALCAM Dynamically Regulates Tumor Cell Adhesion Through Differential Proteolysis and a Novel Binding Partner, Tetraspanin CD151.

Degree: PhD, Cancer Biology, 2018, Vanderbilt University

URL: http://hdl.handle.net/1803/11464

► Metastasis persists as a significant unsolved hurdle in cancer treatment, with greater than 90% of cancer-related deaths attributed to metastasis. In order for cells to… (more)

▼ Metastasis persists as a significant unsolved hurdle in cancer treatment, with greater than 90% of cancer-related deaths attributed to metastasis. In order for cells to successfully metastasize, they must dynamically regulate cell adhesion. However, cell adhesion molecules are rarely mutated or deleted genetically in cancer, indicating that tumor cells are able to co-opt intrinsic regulatory mechanisms of adhesion to drive metastasis. We previously identified Activated Leukocyte Cell Adhesion Molecule (ALCAM) as a clinically relevant driver of metastasis and hypothesized that tunable regulation of its function contributes to tumor cell adhesion and metastasis. We tested this hypothesis through two channels. We identified ALCAM as a novel binding partner of tetraspanin CD151, a known regulator of cell adhesion and motility. We previously demonstrated that clustering of integrin-free CD151 (CD151free) increased cell adhesion, decreased cell motility, and inhibited metastasis. Here, we identified ALCAM as a novel CD151 partner required for CD151free to control adhesion. Biochemical analyses revealed that CD151free is coupled to ALCAM by the scaffolding protein syntenin-1. Additionally, we show that the intracellular domain of ALCAM (ALCAM-ICD) is susceptible to ɣ-secretase cleavage, which releases a PDZ-binding peptide capable of disrupting the CD151/syntenin-1/ALCAM complex. Disruption of this complex impedes CD151free-mediated regulation of tumor cell adhesion and metastasis, demonstrating that CD151free controls tumor cell migration through a trimeric complex of CD151/syntenin-1/ALCAM. Further evaluate of ALCAM revealed a potential alternative splicing which we predicted to control proteolytic shedding of its extracellular domain. We demonstrate that the loss of the membrane-proximal exon13 generates an ALCAM splice variant (ALCAM-Iso2) that enhances metastasis four-fold. Mechanistic studies identified a novel MMP14-dependent, membrane distal cleavage site in ALCAM-Iso2, which increases shedding ten-fold, thereby decreasing cellular cohesion and promoting motility. ALCAM-Iso2-expression was greatly increased in bladder cancer, further emphasizing that ALCAM alternative splicing can contribute to clinical disease progression. The requirement for both the loss of exon 13 and the gain of metalloprotease activity suggests that ALCAM shedding and concomitant regulation of dissemination is a locally tunable process. In summary, this dissertation presents two mechanisms by which tumor cells are able to dynamically regulate cell adhesion to modulate migration and metastasis. Advisors/Committee Members: Simon Hayward (committee member), Deborah Lannigan (committee member), Andries Zijlstra (committee member), Barbara Fingleton (Committee Chair).

Subjects/Keywords: cancer; metastasis; bladder cancer; protein processing; alternative splicing

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APA (6^th Edition):

Hebron, K. E. (2018). ALCAM Dynamically Regulates Tumor Cell Adhesion Through Differential Proteolysis and a Novel Binding Partner, Tetraspanin CD151. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11464

Chicago Manual of Style (16^th Edition):

Hebron, Katie Elizabeth. “ALCAM Dynamically Regulates Tumor Cell Adhesion Through Differential Proteolysis and a Novel Binding Partner, Tetraspanin CD151.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 08, 2021. http://hdl.handle.net/1803/11464.

MLA Handbook (7^th Edition):

Hebron, Katie Elizabeth. “ALCAM Dynamically Regulates Tumor Cell Adhesion Through Differential Proteolysis and a Novel Binding Partner, Tetraspanin CD151.” 2018. Web. 08 Mar 2021.

Vancouver:

Hebron KE. ALCAM Dynamically Regulates Tumor Cell Adhesion Through Differential Proteolysis and a Novel Binding Partner, Tetraspanin CD151. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 08]. Available from: http://hdl.handle.net/1803/11464.

Council of Science Editors:

Hebron KE. ALCAM Dynamically Regulates Tumor Cell Adhesion Through Differential Proteolysis and a Novel Binding Partner, Tetraspanin CD151. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/11464

28. Van Gieson, Jamie Lynn. The Impact Of Anterior Gradient 2 (AGR2) Expression In Models Of Arsenite And Cadmium Induced Breast And Bladder Cancers.

Degree: PhD, Biomedical Sciences, 2016, University of North Dakota

URL: https://commons.und.edu/theses/2079

► Bladder cancer constitutes one of the most prevalent cancers and is among the leading causes of cancer-related deaths in the United States. This work… (more)

▼ Bladder cancer constitutes one of the most prevalent cancers and is among the leading causes of cancer-related deaths in the United States. This work sought to better characterize and understand the role of the proto-oncogene anterior gradient 2 (AGR2) in bladder cancers. Immunohistochemical analysis of AGR2 expression in a range of bladder cancer specimens indicated that the expression of AGR2 decreases with an increase in the stage and grade of bladder cancers. The environmental carcinogens arsenic and cadmium (Cd2+) have been implicated in various cancers. This laboratory has demonstrated that arsenite (As3+) and Cd2+ can malignantly transform the bladder epithelium cell line UROtsa. This study therefore sought to determine AGR2 expression in six As3+ and seven Cd2+-transformed UROtsa cell lines in which real-time PCR and western blotting data indicated that AGR2 expression was increased in several of the transformed cell lines. Next AGR2 expression was evaluated in mouse heterotransplant tumors arising from the injection of the previously transformed UROtsa cell lines in athymic nude (Foxn1nu) mice. Results from real-time PCR analysis and immunohistochemistry on tumor samples demonstrated that AGR2 expression remained increased in most of the Cd2+ heterotransplants but was significantly increased in only a couple of the As3+ heterotransplants. UROtsa cells were further exposed to 2, 4, or 6 μM As3+ or to 1, 2, or 4 μM Cd2+ for up to 72 hours and real-time PCR analysis was performed to evaluate AGR2 expression. While AGR2 exhibited increased expression in response to 48 hours As3+ exposure, expression was not induced to the same extent in Cd2+ exposed UROtsa cells. Spheroids containing cancer initiating cells (CICs) were generated from the transformed and the parent UROtsa cells and the expression of AGR2 was determined. The results obtained suggested that there was an increase in the expression of AGR2 in all of the spheroids isolated from the As3+-transformed cells whereas some of the spheroids isolated from the Cd2+-transformed cells expressed high levels of AGR2 when compared to the spheroids isolated from the parent UROtsa cells. This laboratory has also shown that As3+ and Cd2+ can cause malignant transformation of a breast epithelial cell line, MCF-10A. Previous studies have shown that the expression of AGR2 promotes breast tumorigenesis in mice. This gene is known to play a role in promoting cellular transformation, tumor growth, and metastasis in various cancers. This study was interested in determining the expression level of AGR2 in As3+ and Cd2+-transformed MCF-10A cells. Real-time PCR and Western analysis indicated that the expression of AGR2 was significantly increased in the MCF-10A cells transformed with As3+ when compared to the Cd2+-transformed cells. Exposure of the parent MCF-10A cells to 4, 8, and 16 μM As3+ for 48 hours resulted in a significant increase in the expression of AGR2 whereas exposure to Cd2+ did not increase the expression of AGR2, suggesting… Advisors/Committee Members: Seema Somji.

Subjects/Keywords: Anterior Gradient 2; Arsenic; Bladder Cancer; Breast Cancer; Cadmium

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Van Gieson, J. L. (2016). The Impact Of Anterior Gradient 2 (AGR2) Expression In Models Of Arsenite And Cadmium Induced Breast And Bladder Cancers. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/2079

Chicago Manual of Style (16^th Edition):

Van Gieson, Jamie Lynn. “The Impact Of Anterior Gradient 2 (AGR2) Expression In Models Of Arsenite And Cadmium Induced Breast And Bladder Cancers.” 2016. Doctoral Dissertation, University of North Dakota. Accessed March 08, 2021. https://commons.und.edu/theses/2079.

MLA Handbook (7^th Edition):

Van Gieson, Jamie Lynn. “The Impact Of Anterior Gradient 2 (AGR2) Expression In Models Of Arsenite And Cadmium Induced Breast And Bladder Cancers.” 2016. Web. 08 Mar 2021.

Vancouver:

Van Gieson JL. The Impact Of Anterior Gradient 2 (AGR2) Expression In Models Of Arsenite And Cadmium Induced Breast And Bladder Cancers. [Internet] [Doctoral dissertation]. University of North Dakota; 2016. [cited 2021 Mar 08]. Available from: https://commons.und.edu/theses/2079.

Council of Science Editors:

Van Gieson JL. The Impact Of Anterior Gradient 2 (AGR2) Expression In Models Of Arsenite And Cadmium Induced Breast And Bladder Cancers. [Doctoral Dissertation]. University of North Dakota; 2016. Available from: https://commons.und.edu/theses/2079

Texas Medical Center

29. Tran, Mai. THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS.

Degree: PhD, 2013, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/335

► p63, a p53 family member, is a transcription factor that has complex roles in cancer. This study focuses on the role of the ∆Np63α… (more)

▼ p63, a p53 family member, is a transcription factor that has complex roles in cancer. This study focuses on the role of the ∆Np63α isoform in bladder cancer (BC). Epithelial – mesenchymal transition (EMT) is a physiological process that plays an important part in metastasis and drug resistance. At the molecular level, EMT is characterized by the loss of the epithelial marker E-cadherin, and the acquisition of the transcriptional repressors of E-cadherin (ZEB1, ZEB2, TWIST, SNAI1 and SNAI2). Recent publications highlight the role of microRNAs belonging to the miR-200 family and miR-205 in preventing EMT through suppression of ZEB1 and ZEB2. p53, the homologue of p63, is implicated in regulating EMT by modulating the expression of miR-200c; however, the mechanisms underlying miR-205 control remain unclear. Here we show that ∆Np63α regulates the transcription of miR-205 and controls EMT in human BC cells. We observed a strong correlation between the expression of ∆Np63α, miR-205 and E-cadherin in a panel of BC cell lines (n=28) and also in bladder primary tumors from a cohort of patients (n=98). A remarkably inverse correlation is observed between ∆Np63α and ZEB1/2 in cell lines. Stable knockdown (KD) ∆Np63α in UC6, an “epithelial” BC cell line, decreased the expression of miR-205 and induced ZEB1/2 expression, the effects that were reversed by expression of exogenous miR-205. Moreover, overexpressing ∆Np63α in UC3, a “messenchymal” BC cell line, brought about opposite results, an increase in miR-205 expression and a reduction in ZEB1/2 expression. Modulation of ∆Np63α expression resulted in a parallel change in the expression of miR-205 and miR-205 “host” gene (miR-205HG). Nuclear run-on and chromatin immunoprecipitation experiments demonstrated that ∆Np63α regulates the transcription of miR-205 through controlling the recruitment of RNA Polymerase II to the promoter of miR-205HG. Interestingly, high miR-205 expression correlated with poor clinical outcome in BC patients, consistent with our recent publication highlighting the enrichment of ∆Np63 in a lethal subset of muscle invasive BC. In summary, our data present the important roles of ∆Np63α in preventing EMT mediated by miR-205. Our study also identifies miR-205 as a potential molecular marker to predict clinical outcome in BC patients. Advisors/Committee Members: David J. McConkey, Michelle C. Barton, Sendurai Mani.

Subjects/Keywords: p63; EMT; miR-205; transcription; bladder cancer; Cancer Biology; Cell Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tran, M. (2013). THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/335

Chicago Manual of Style (16^th Edition):

Tran, Mai. “THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS.” 2013. Doctoral Dissertation, Texas Medical Center. Accessed March 08, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/335.

MLA Handbook (7^th Edition):

Tran, Mai. “THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS.” 2013. Web. 08 Mar 2021.

Vancouver:

Tran M. THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS. [Internet] [Doctoral dissertation]. Texas Medical Center; 2013. [cited 2021 Mar 08]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/335.

Council of Science Editors:

Tran M. THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS. [Doctoral Dissertation]. Texas Medical Center; 2013. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/335

University of Miami

30. Escudero, Diogo O. Hyaluronic Acid Family of Molecules: Biomarkers and Functional Studies in Bladder Cancer.

Degree: PhD, Molecular Cell and Developmental Biology (Medicine), 2013, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/1019

► Profound changes in the extracellular matrix (ECM) in the vicinity of tumor cells occur as the tumor establishes its own microenvironment. Among these changes, elevated… (more)

▼ Profound changes in the extracellular matrix (ECM) in the vicinity of tumor cells occur as the tumor establishes its own microenvironment. Among these changes, elevated deposition of hyaluronic acid (HA), as well as abnormal expression and activity of the HA-family of molecules HAS1, HAS2, HAS3, HYAL-1, CD44, RHAMM are observed in a variety of tumors (Simpson and Lokeshwar 2008). In this study we evaluated whether the members of the HA-family of molecules, either alone or in combination with one another, are accurate diagnostic and prognostic markers for patients with bladder cancer (BCa). Additionally, we investigated whether HYAL-4 expression, a novel mammalian chondroitinase, is predictive of tumor outcome. Moreover, this study analyzed potential underlying molecular mechanisms through which HYAL-4 expression may be a modulator of tumor growth and progression. Using RT-qPCR, we found that the mRNA transcript levels of all 3 HA-synthases, HYAL-1, CD44v, and RHAMM were elevated by 4-16 fold in bladder cancer tissues, in comparison with normal bladder tissue (p<0.001). Furthermore, the expression of HAS1 and HYAL-1 were predictive of metastasis, while HYAL-1 expression was also predictive of disease-specific mortality. Subsequently, in exfoliated urothelial cells, the transcript levels of all three HA synthases and HYAL-1 were significantly elevated in specimens from BCa patients, while the combination HAS2-HYAL-1 was a sensitive biomarker, detecting BCa with 85.4% sensitivity, 79.5% specificity, and 81.7% accuracy. Using commercially available qPCR tissue array plates, we found that HYAL-4 transcript levels are elevated in a number of tumors including bladder, kidney, stomach and breast. Furthermore, we successfully cloned and isolated HYAL-4, identifying in the process 2 novel and unpublished alternative splicing variants for this gene, namely HYAL-4 V1, and HYAL-4 V2. Interestingly, when analyzing the gene expression levels of these HYAL-4 isoforms in BCa tissue and exfoliated urothelial cells, we found that the levels of HYAL-4 V1 were elevated by 26-fold in bladder tissue and 2 to 6-fold in exfoliated cells from BCa patients. As a biomarker, HYAL-4 V1 showed 90% sensitivity and 83.3% specificity to detect BCa in bladder tissue specimens. However, in exfoliated urothelial cells, HYAL-4 V1 displayed excellent sensitivity (81.8%), but inadequate specificity (60%). Additionally, we successfully generated stable over-expression transfectants using 2 BCa cell lines (253J-Lung and T24) and a normal urothelial cell line (UROsta). Using antibodies specific for chondroitin sulfate 4 and chondroitin sulfate 6, we showed by immunoblotting that both HYAL-4 wt and V1 appear to have chondroitinase activity in 253J-Lung cells; HYAL-4 V1 showed chondroitinase activity in all cell lines tested. Analysis of versican expression, a chondroitin sulfate proteoglycan overexpressed in a number of solid tumors, suggested that HYAL-4 V1 may be a regulator of versican degradation and activity, possibly through hydrolysis of… Advisors/Committee Members: Vinata B. Lokeshwar, Mary Lou King, Bal Lokeshwar, Diana Lopez, Richard K. Lee.

Subjects/Keywords: Hyaluronic Acid Family; Bladder Cancer; Cancer Biomarkers; Chemoresistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Escudero, D. O. (2013). Hyaluronic Acid Family of Molecules: Biomarkers and Functional Studies in Bladder Cancer. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1019

Chicago Manual of Style (16^th Edition):

Escudero, Diogo O. “Hyaluronic Acid Family of Molecules: Biomarkers and Functional Studies in Bladder Cancer.” 2013. Doctoral Dissertation, University of Miami. Accessed March 08, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/1019.

MLA Handbook (7^th Edition):

Escudero, Diogo O. “Hyaluronic Acid Family of Molecules: Biomarkers and Functional Studies in Bladder Cancer.” 2013. Web. 08 Mar 2021.

Vancouver:

Escudero DO. Hyaluronic Acid Family of Molecules: Biomarkers and Functional Studies in Bladder Cancer. [Internet] [Doctoral dissertation]. University of Miami; 2013. [cited 2021 Mar 08]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1019.

Council of Science Editors:

Escudero DO. Hyaluronic Acid Family of Molecules: Biomarkers and Functional Studies in Bladder Cancer. [Doctoral Dissertation]. University of Miami; 2013. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1019

Open Access Theses and Dissertations