Relevant bibliographies by topics / Bladder cancer

Academic literature on the topic 'Bladder cancer'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 June 2024

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Journal articles on the topic "Bladder cancer"

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Bakulesh, Khamar. "Immunotherapy of Bladder Cancer." Cancer Medicine Journal 3, no. 2 (December 31, 2020): 49–62. http://dx.doi.org/10.46619/cmj.2020.3-1020.

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Bladder cancer used to be the only cancer treated by immunotherapy in form of intravesical BCG. Since approval of BCG for Non muscle invasive bladder cancer (NMIBC), there has been significant advancement in our knowledge about immune alteration in cancer and availability of immunotherapeutic agents. Tumor induced cell mediated immunosuppression is identified as a key factor for development and progression of cancer. Immune suppression in bladder cancer is predominantly through Macrophages. Myeloid derived suppressor cell, NK cells, Treg and expression of immune checkpoint receptor inhibitors also contribute to immune suppression. BCG induces innate immune response and its efficacy is limited to NMIBC. Novel immunotherapeutic agents evaluated in bladder cancer are administered locally or systemically to induce innate or adaptive immune response. Systemic administration of antibodies against PD-1/PD-L1 axis are now approved for treatment of locally advanced/metastatic bladder cancer as a first line as well as second line therapy. Pembrolizumab is also approved for BCG unresponsive NMIBC. Since response to immunotherapy are neither uniform nor universal, attempts are made to identify prognostic and predictive biomarkers. Identified biomarkers lack desired specificity and sensitivity. Several immune approaches using innate as well as adaptive mechanism are under evaluation to improve outcome of intravesical BCG or immune check point receptor inhibitors.
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William Arputha Sundar, Sobana. "Nanotechnology in Bladder Cancer." International Journal of Science and Research (IJSR) 13, no. 3 (March 5, 2024): 649–55. http://dx.doi.org/10.21275/sr24308151012.

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Mizutani, Yoichi, and Haruhito Azuma. "Prognostic significance of second mitochondria-derived activator of caspase expression in bladder cancer and target for therapy." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e15000-e15000. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15000.

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e15000 Background: Although the expression of second mitochondria-derived activator of caspase (Smac/DIABLO) has been reported in various cancers, little is known about its clinical significance in bladder cancer. The present study was designed to evaluate the relationship between progression of disease and Smac/DIABLO expression by clinical pathological analysis of patients with bladder cancer. Methods: The level of Smac/DIABLO expression was quantified by western blot analysis using non-fixed fresh frozen tissues derived from patients with bladder cancer. Results: All normal bladders expressed Smac/DIABLO. However, 64/84 ( 76% ) of bladder cancers expressed Smac/DIABLO and 24% were negative. In Ta and T1 superficial bladder cancers, 98% expressed Smac/DIABLO, whereas only 41% expressed Smac/DIABLO in muscle-invasive bladder cancers. Smac/DIABLO expression inversely correlated with the grade of bladder cancer. Patients with Ta and T1 superficial bladder cancer with higher Smac/DIABLO expression had a longer postoperative recurrence-free period than those with lower Smac/DIABLO expression after transurethral resection in the 5-year follow-up. Patients with invasive bladder cancer expressing Smac/DIABLO had a longer postoperative disease-specific survival than those without Smac/DIABLO expression after radical cystectomy in the 5-year follow-up. The cisplatin-resistant T24 bladder cancer line ( T24/CDDP ) and the adriamycin-resistant T24 line ( T24/ADR ) showed lower level of Smac/DIABLO expression, compared with the T24 parental line. Conclusions: The present study demonstrates for the first time that Smac/DIABLO expression was downregulated in bladder cancer, especially in high grade muscle-invasive bladder cancer, and that lower Smac/DIABLO expression in bladder cancer predicted a worse prognosis. In addition, the cisplatin-resistant T24/CDDP line and the adriamycin-resistant T24/ADR line expressed lower level of Smac/DIABLO expression. These results suggest that Smac/DIABLO expression in bladder cancer may be used as a prognostic parameter, and that low Smac/DIABLO expression in bladder cancer may be associated with resistance to chemotherapy.
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O'Donnell, Michael A. "S14 Management of Superficial Bladder Cancer(Keynote Lecture,Symposium 14「Management of Superficial Bladder Cancer」)." Japanese Journal of Urology 97, no. 2 (2006): 176. http://dx.doi.org/10.5980/jpnjurol.97.176.

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Tsushima, Tomoyasu. "S14-3 Intravesical chemotherapy for superficial bladder cancer(Symposium 14「Management of Superficial Bladder Cancer」)." Japanese Journal of Urology 97, no. 2 (2006): 178. http://dx.doi.org/10.5980/jpnjurol.97.178_1.

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Mugiya, Soichi, Hiroshi Furuse, and Seiichiro Ozono. "S14-4 Intravesical BCG for superficial bladder cancer(Symposium 14「Management of Superficial Bladder Cancer」)." Japanese Journal of Urology 97, no. 2 (2006): 178. http://dx.doi.org/10.5980/jpnjurol.97.178_2.

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Siracusano, Salvatore, Riccardo Rizzetto, and Antonio Benito Porcaro. "Bladder cancer genomics." Urologia Journal 87, no. 2 (January 16, 2020): 49–56. http://dx.doi.org/10.1177/0391560319899011.

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Until recently, the treatment of bladder cancer, for several years, was limited to surgery and to immunotherapy or chemotherapy. Currently, the extensive analysis of molecular alterations has led to novel treatment approaches. The advent of polymerase chain reaction and genomic hybridization techniques has allowed to investigate alterations involved in bladder cancer at DNA level. By this way, bladder cancers can be classified as papillary or non-papillary based on genetic alterations with activation or mutations in FGFR3 papillary tumors and with inactivation or mutations involving TP53 and RB1 in non-papillary tumors. Recently, the patterns of gene expression allow to differentiate basal and luminal subtypes as reported in breast cancer. In particular, basal cancers are composed of squamous and sarcomatoid pathological findings, while luminal cancers are composed of papillary finding features and genetic mutations (FGFR3). In particular, specific investigative studies demonstrated that luminal cancers are associated with secondary muscle invasive cancer while basal tumors are related to advanced disease since they are often metastatic at diagnosis. Moreover, from therapeutic point of view, different researchers showed that mutations of DNA are related to the sensitivity of bladder cancer while performing cisplatin chemotherapy. In this prospective, the bladder cancer molecular subtyping classification might allow identifying the set of patients who can safely avoid neoadjuvant chemotherapy likely because of the low response to systemic chemotherapy (chemoresistant tumors). In this context, the Cancer Genome Atlas (TCGA) project has improved the knowledge of the molecular targets of invasive urothelial cancers allowing the researchers to propose hypothesis suggesting that agents targeting the genomic alterations may be an effective strategy in managing these cancers, which occur in about 68% of muscle invasive cancers. A future goal will be to combine treatment strategies of invasive bladder cancers according to their genetic mutational load defined by molecular pathology.
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Gupta, Meenu, Gopinath Barui, and TusharKanti Das. "Urinary Bladder Cancer : Two Rare Cases." Annals of Pathology and Laboratory Medicine 4, no. 6 (December 10, 2017): C176—C178. http://dx.doi.org/10.21276/apalm.1491.

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Kennelley, Gabrielle E., Jordan J. McDonald, Norbert Sule, Barbara A. Foster, Craig M. Brackett, and Wendy J. Huss. "Abstract 17: Sex disparities in a murine model of BBN-induced bladder cancer." Cancer Research 83, no. 7_Supplement (April 4, 2023): 17. http://dx.doi.org/10.1158/1538-7445.am2023-17.

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Abstract Bladder cancer is one of the most common cancers in the US, with an estimated incidence of 83,730 cases in 2021. Males are four times more likely to develop bladder cancer than females. Ninety percent of cases are diagnosed as urothelial carcinomas, and most cases are not muscle-invasive at the time of diagnosis. Even with treatment, there is a 50-80% chance of bladder cancer recurrence within five years of diagnosis. While non-invasive disease has a five-year survival rate of 77%, if recurrence leads to metastatic disease, the five-year survival rate is only 6%. Therefore, there is a need to predict which patients will recur and progress to metastatic disease. N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) is a cigarette smoke-mimicking carcinogen that can be used in mice to induce urothelial cell proliferation and progression to invasive bladder cancer. This study used a BBN-induced bladder cancer model to evaluate sex differences in urothelial proliferation and bladder pathologies in male and female mice treated with BBN (0.05%) in their drinking water for up to 12 weeks. Mice were then given a 2–20-week period of no treatment following BBN exposure. Bladder specimens were stained with Ki-67 to analyze urothelial proliferation and characterized based on pathology. Male bladder samples characterized as having reactive atypia showed greater proliferation rates than male bladder samples with urothelial dysplasia. Overall, compared to female bladder samples, male bladders showed greater urothelial proliferation in both reactive atypia and dysplasia categories. Additionally, male mice had more tumor initiation and aggressive disease at all examination timepoints, with the most pronounced difference seen at 10-weeks post-BBN exposure. The development of carcinoma in situ (CIS) and invasive disease was seen in 100% of males at 12 weeks post-BBN, while only 40% of female mice had CIS or invasive disease at the same timepoint. Overall, these findings indicate that mouse sex plays a role in bladder tumor progression, with females having delayed tumor initiation and less aggressive disease. This may be due, in part, to varied immune cell profiles in males versus females. A short 2-week exposure to BBN caused a similarly profound neutrophil and macrophage infiltrate in the bladder of both sexes but no changes in immunosuppressive populations such as regulatory T cells (Tregs). In stark contrast, a 12-week exposure to BBN with a 2-week rest period resulted in significantly more macrophages and immunosuppressive PD-L1+ neutrophils and Tregs in the bladders of male mice when compared with females. Chronic exposure to BBN leads to an increase in immunosuppressive immune infiltrates in male bladders and may contribute to sex disparities observed in bladder cancer. Citation Format: Gabrielle E. Kennelley, Jordan J. McDonald, Norbert Sule, Barbara A. Foster, Craig M. Brackett, Wendy J. Huss. Sex disparities in a murine model of BBN-induced bladder cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 17.
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Hinotsu, Shiro, and Hideyuki Akaza. "S14-1 Recurrence hazards of superficial bladder cancer after TURBT(Symposium 14「Management of Superficial Bladder Cancer」)." Japanese Journal of Urology 97, no. 2 (2006): 177. http://dx.doi.org/10.5980/jpnjurol.97.177_1.

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Dissertations / Theses on the topic "Bladder cancer"

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Nicolle, Rémy. "Regulatory networks driving bladder cancer." Thesis, Evry-Val d'Essonne, 2015. http://www.theses.fr/2015EVRY0009/document.

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La carcinogénèse est une conséquence de la continuelle activation de la prolifération cellulaire. Dans les cellules normales, les signaux mitogéniques sont traités par un réseau complexe d’interactions protéiques et de réactions enzymatiques, appelées voies de signalisation. Dans certains cas, le signal peut induire l’activation de nouveaux gènes et ainsi déclencher la mitose. Lors du développement ou de la cicatrisation, cette régulation du phénotype cellulaire contrôle étroitement le nombre et le comportement des cellules contribuant ainsi au maintien d’un tissu fonctionnel sain. A partir de profils génomiques, transcriptomiques et protéomiques de tumeurs de la vessie ainsi que des transcriptomes de cellules urothéliales normales dans différents états de prolifération et de différenciation, j’ai mis au point de nouvelles méthodologies pour caractériser les voies de signalisation et de régulation responsables des cancers de la vessie. Dans un premier temps, j’ai développé des outils pour l’identification et la visualisation des programmes transcriptionnels spécifiques à une tumeur ou à un sous-type tumoral et ce, par l’inférence d’un réseau de co-régulation et la prédiction de l’activité des facteurs de transcription. Ces méthodes sont disponibles dans un package Bioconductor, CoRegNet (bioconductor.org). La mesure de l’activité transcriptionnelle est basée sur l’influence d’un facteur de transcription sur l’expression de ses gènes cibles. Cette mesure a été utilisée pour identifier les régulateurs les plus actifs de chaque sous-type de cancer de la vessie. L’intégration de profils génomiques a mis en avant deux facteurs de transcription génétiquement altérés et ayant des rôles oncogènes dans les tumeurs luminales et basales. L’un d’entre eux a été validé expérimentalement dans ce travail.L’utilisation de CoRegNet a mis en évidence une large utilisation dans les tumeurs,des réseaux normaux de la différenciation et de la prolifération des cellules normales. Un régulateur de la prolifération normale est identifié comme étant activé de fa¸con constitutive par des altérations génétiques dans les tumeurs. Son impact sur la prolifération des cellules tumorales de la vessie a été expérimentalement validé. Par ailleurs, il a été constaté que l’un des régulateurs de la différenciation urothéliale présentant une baisse d’activité dans la quasi-totalité des tumeurs, est fréquemment muté. De plus amples analyses ont mis en avant son rôle majeur dans les tumeurs différenciées. Dans le but de caractériser les voies de signalisation à partir de données protéomiques d’expériences d’immunoprécipitations, j’ai développé un nouvel algorithme visant à construire un réseau dense à partir d’une liste de protéines d’intérêt et d’un ensemble d’interactions protéiques connues. L’algorithme est proposé sous la forme d’une application Cytoscape et s’intitule Pepper: Protein Complex Expansion using Protein-Proteininteraction networks (apps.cytoscape.org) Enfin, en utilisant à la fois le profil protéomique d’une expérience d’immunoprécipitation de FGFR3 ainsi que le profil transcriptomique des gènes qu’il régule en aval, j’ai appliqué Pepper pour caractériser la voie de signalisation de FGFR3 depuis ses partenaires protéiques jusqu’aux facteurs de transcription en aval. Enfin, ce travail a plus particulièrement permis d’identifier un lien de régulation entre FGFR3 et le gène suppresseur de tumeurs TP53
Carcinogenesis is a consequence of the unceasing activation of cell proliferation. In normal cells, mito-genic stimuli are processed by a complex network of protein interactions and enzymatic reactions, often referred to as pathways, which can eventually trigger the activation of new genes to engage the cell into mitosis. During developmental or wound healing processes, this complex regulation of cellular phenotypes results in a tight control of the number and behavior of cells and therefore contributes to the maintenance of a functional and healthy tissue architecture. Based on genomic, transcriptomic and proteomic profiles of bladder tumors and transcriptomes of nor-mal urothelial cells at various states of proliferation and differentiation, I devised novel methodologies to characterize the pathways driving bladder cancer. I first developed a set of tools to identify and visualize sample and subtype-specific transcriptional pro-grams through the inference of a co-regulatory network and the prediction of transcription factor activity. These methods were embedded in a Bioconductor package entitled CoRegNet (bioconductor.org). The measure of transcriptional activity is based on the influence of a transcription factor on the expression of its target genes and was used to characterize the most active regulators of each bladder cancer subtypes. The integration of genomic profiles highlighted two altered transcription factors with driver roles in lumi-nal-like and basal-like bladder cancer, one of which was experimentally validated. The use of CoRegNet to model the contribution of regulatory programs of normal proliferation and diffe-rentiation in bladder cancers underlined a strong preservation of normal networks during tumorigenesis. Furthermore, a regulator of normal proliferation was found to be constitutively activated by genetic al-terations and its influence on bladder cancer cell proliferation was experimentally validated. In addition, a master regulator of urothelial differentiation was found to have a loss of activity in nearly all tumors. This was then associated to the discovery of frequent inactivating mutations and further analysis unco-vered a major role in differentiated tumors. In order to characterize signaling pathways from proteomic pull-down assays, I then designed a novel algorithm to grow a densely connected network from a set of proteins and a repository of protein interac-tions. The proposed algorithm was made available as a Cytoscape application named Pepper for Protein Complex Expansion using Protein- Protein interaction networks (apps.cytoscape.org). Finally, using both a proteomic pull-down assay of the bladder cancer oncogene FGFR3 and a transcrip-tomic profiling of its downstream regulated genes, I applied Pepper to characterize the full FGFR3 signa-ling pathway from its protein partners to the downstream transcriptional regulators. In particular, this uncovered a regulatory link between FGFR3 and the tumor suppressor TP53
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O'Brien, Timothy Stephen. "Angiogenesis in bladder cancer." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388846.

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PEDERZOLI, FILIPPO. "Microbiome and bladder cancer." Doctoral thesis, Università Vita-Salute San Raffaele, 2021. http://hdl.handle.net/20.500.11768/121778.

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The microbiome has gained increasing momentum in cancer research, as it has become clear that microorganisms residing within our body are involved in mediating the cellular and tissue metabolism in health and disease. In bladder cancer research, there are different microbial communities that may mediate cancer pathobiology and response to therapy: the gut microbiome, the urinary microbiome, the urothelium-bound microbiome. These bacterial communities may mediate the processes of carcinogenesis or recurrence, modify the response to local intravesical therapies or influence the activity of systemic anticancer protocols. Based on these premises, my research project aimed to unveil the urinary and urothelium-bound microbiome in therapy-naïve bladder cancer patients, describing the differently enriched bacterial communities using a sex-based stratification. Compared to healthy controls, I found that the urine of men affected by bladder cancer were enriched in the order Opitutales and subordinate family Opitutaceae, together with the isolated class Acidobacteria-6, while in female patients I found enriched the genus Klebsiella. Notably, the bladder cancer tissue was enriched in the genus Burkholderia in both men and women, when compared to non-neoplastic, paired urothelium biopsies. Then, I also characterized the gut microbiome of bladder cancer patients undergoing neoadjuvant pembrolizumab to understand if the intestinal bacteria may influence the immune-mediated anticancer activity. In this set, I have reported that antibiotic therapy has a negative effect on immunotherapy efficacy. Second, the gut microbiome of patients not responding to neoadjuvant pembrolizumab was characterized by a higher abundance of Ruminococcus bromii, while patients who showed a response were enriched in the genus Sutterella. Lastly, I started the implementation of in vivo and in vitro systems to test the mechanistic role of the bacteria identified in human samples. This thesis work reported innovative data on the role of different microbial communities (urinary/urothelium-bound/fecal) in bladder cancer and bladder cancer therapy, and provided novel in vivo and in vitro models to validate those finding and uncover the complex microbiome-host cells crosstalk in bladder cancer patients.
The microbiome has gained increasing momentum in cancer research, as it has become clear that microorganisms residing within our body are involved in mediating the cellular and tissue metabolism in health and disease. In bladder cancer research, there are different microbial communities that may mediate cancer pathobiology and response to therapy: the gut microbiome, the urinary microbiome, the urothelium-bound microbiome. These bacterial communities may mediate the processes of carcinogenesis or recurrence, modify the response to local intravesical therapies or influence the activity of systemic anticancer protocols. Based on these premises, my research project aimed to unveil the urinary and urothelium-bound microbiome in therapy-naïve bladder cancer patients, describing the differently enriched bacterial communities using a sex-based stratification. Compared to healthy controls, I found that the urine of men affected by bladder cancer were enriched in the order Opitutales and subordinate family Opitutaceae, together with the isolated class Acidobacteria-6, while in female patients I found enriched the genus Klebsiella. Notably, the bladder cancer tissue was enriched in the genus Burkholderia in both men and women, when compared to non-neoplastic, paired urothelium biopsies. Then, I also characterized the gut microbiome of bladder cancer patients undergoing neoadjuvant pembrolizumab to understand if the intestinal bacteria may influence the immune-mediated anticancer activity. In this set, I have reported that antibiotic therapy has a negative effect on immunotherapy efficacy. Second, the gut microbiome of patients not responding to neoadjuvant pembrolizumab was characterized by a higher abundance of Ruminococcus bromii, while patients who showed a response were enriched in the genus Sutterella. Lastly, I started the implementation of in vivo and in vitro systems to test the mechanistic role of the bacteria identified in human samples. This thesis work reported innovative data on the role of different microbial communities (urinary/urothelium-bound/fecal) in bladder cancer and bladder cancer therapy, and provided novel in vivo and in vitro models to validate those finding and uncover the complex microbiome-host cells crosstalk in bladder cancer patients.
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Hung, Tzong Tyng Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Studies of bladder cancer progression." Awarded by:University of New South Wales, 2009. http://handle.unsw.edu.au/1959.4/39786.

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Bladder cancer (BlCa) is the second most common genitourinary cancer, affecting both men and women. Most (70%) cases present at the superficial stage; 20% of these recur with muscle-invasive disease. Major genetic alterations associated with BlCa include: loss/gain in expression or mutations in Retinoblastoma (RB) gene, human epidermal growth factor receptors (HERs), H-ras, p53 and FGFR3. Only p53 mutations are well correlated with invasive BlCa; other changes show variable correlations with disease status. To understand the progression of BlCa, a model of nine human BlCa cell sublines derived from a single parent but differing in in vivo characteristics, has been developed previously. These cells represent a heterogenous population from a single tumour and a model of different stages of BlCa progression, from non-tumourigenic to invasive. Two sublines were selected for further investigation: C3 (non-tumourigenic) and B8 (invasive). These were transfected with green (C3-GSP-2) and red fluorescent reporters (B8-RSP-gck) respectively to investigate the effects of their co-injection in vivo, specifically, promotion of C3 tumour growth by B8 cells. Surprisingly, B8 tumour growth was inhibited by C3 cells in vivo at different cell numbers and proportions of cells injected. Microarray analysis of C3 and B8 cells revealed differential expression of 1367 genes with dramatic differences in the transforming growth factor-?? and integrin-mediated pathways. Gene expression of BMP2, INHBB, FST, NOG, ID4 and TGF- ??1, in the TGF- ?? pathway was further analysed with qRT-PCR in all nine sublines. Expression of BMP2 was significantly related to tumourigenic potential (p=0.0238, Mann-Whitney) and INHBB to invasive ability (p=0.0476, Mann-Whitney). The BlCa model did not include a metastatic component. To broaden the model, cell lines were established from an invaded lymph-node (B8-RSP-LN) and a bone-metastasis (B8-RSP-BN) after subcutaneous and intra-cardiac injection of B8-RSP-gck cells. No significant differences were observed in the migratory capability and anchorage-independent colony formation of these metastatic cells compared with B8 cells. Evaluation of expression of the panel of TGF-beta genes (BMP2, INHBB, FST, NOG, ID4 and TGF- ??1) and metastasis-related genes (MMP9, MMP2 and KAI1) indicated that expression of BMP2, FST, ID4 and MMP9 was decreased or lost in the metastatic sublines.
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Hung, Tzong-Tyng Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Studies of bladder cancer progression." Awarded by:University of New South Wales. Clinical School - Prince of Wales Hospital, 2007. http://handle.unsw.edu.au/1959.4/40450.

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Bladder cancer (BICa) is the second most common genitourinary cancer, affecting both men and women. Most (70%) cases present at the superficial stage; 20% of these recur with muscle-invasive disease. Major genetic alterations associated with BICa include: loss/gain in expression or mutations in Retinoblastoma (RB) gene, human epidermal growth factor receptors (HERs), H-ras, p53 and FGFR3. Only p53 mutations are well correlated with invasive BICa; other changes show variable correlations with disease status. To understand the progression of BICa, a model of nine human BICa cell sublines derived from a single parent but differing in in vivo characteristics, has been developed previously. These cells represent a heterogenous population from a single tumour and a model of different stages of BICa progression, from non-tumourigenic to invasive. Two sublines were selected for further investigation: C3 (non-tumourigenic) and B8 (invasive). These were transfected with green (C3-GSP-2) and red fluorescent reporters (B8-RSP-gck) respectively to investigate the effects of their co-injection in vivo, specifically, promotion of C3 tumour growth by B8 cells. Surprisingly, B8 tumour growth was inhibited by C3 cells in vivo at different cell numbers and proportions of cells injected. Microarray analysis of C3 and B8 cells revealed differential expression of 1367 genes with dramatic differences in the transforming growth factor- ?? and integrin-mediated pathways. Gene expression of BMP2,INHBB, FST, NOG, ID4 and TGF- ??1, in the TGF- ?? pathway was further analysed with qRT-PCR in all nine sublines. Expression of BMP2 was significantly related to tumourigenic potential (p=0.0238, Mann-Whitney) and INHBB to invasive ability (p=0.0476, Mann-Whitney). The BICa model did not include a metastatic component. To broaden the model, cell lines were established from an invaded lymph-node (B8-RSP-LN) and a bonemetastasis (B8-RSP-BN) after subcutaneous and intra-cardiac injection of B8- RSP-gck cells. No significant differences were observed in the migratory capability and anchorage-independent colony formation of these metastatic cells compared with B8 cells. Evaluation of expression of the panel of TGF-beta genes (BMP2, INHBB, FST, NOG, /04 and TGF- (31) and metastasis-related genes (MMP9, MMP2 and KAI1) indicated that expression of BMP2, FST, /04 and MMP9 was decreased or lost in the metastatic sublines.
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Yong, Sze Ming. "Mucin expression in bladder cancer." Thesis, University of Aberdeen, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440597.

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Certain membrane bound mucins such as MUC1, MUC4, and MUC12 were expressed in normal bladder urothelium.  MUC1 expression was the highest in normal bladder urothelium and was present in almost all samples. In superficial bladder cancer, MUC1 demonstrated a pattern of expression that increased in proportion to the increase in tumour grade from Grade 1 to Grade 3 and carcinoma in situ.  Utilising TMAs, membrane-bound mucins such as MUC1, MUC3, MUC4, MUC12 and MUC 16 were shown to have increased incidence of expression with tumour stage progression  to muscle-invasive bladder cancer (stage T2 and above).  Secretory mucins showed a more varied pattern of expression.  MUC2 mRNA was up-regulated in progressive muscle-invasive bladder cancer.   MUC5AC and MUC5B displayed a low incidence of expression in superficial tumours and muscle invasive bladder cancer. MUC7 mRNA expression, however, was limited to only muscle-invasive disease similar to the membrane-bound mucins described above. In a small proportion of patients in the recurrent progressive TMA, expression of MUC4, MUC5AC and MUC5B in penultimate superficial tumours prior to tumour progression allowed prediction of impending disease progression to muscle invasive disease.  MUC5B, MUC12 and MUC13 were expressed at higher incidence in the single non-recurrent TMA, compared with the incidence of expression in the recurrent non-progressive TMA. The expression of these mucins in newly diagnosed superficial bladder tumours may thus favour better prognosis, with a subsequent reduced risk of tumour recurrence.
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Sherwood, Benedict T. "Radiosensitivity in bladder cancer cells." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29874.

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Potentially curative treatment options for patients with organ-confined transitional cell carcinoma (TCC) of the bladder (T1-4a/N0/M0) are radical cystectomy or radiotherapy (RT)-based 'bladder-preserving' regimens. A substantial number of patients who receive RT fail to respond (approximately 50%). Consequently, a greater understanding of the mechanisms of radioresistence is required, together with predictive information regarding the response of tumours to RT. Hypoxia and intrinsic cellular Radiosensitivity (IRS) are examined here, a factors that may influence the outcome of RT.;An immunohistochemical assay using hypoxia-related carbonic anhydrase IX (CA IX) was undertaken to determine the prognostic significance of hypoxia in bladder tumours treated with RT. A modified version of the alkaline comet assay (ACA) was used to examine differences in IRS between cells derived from TCC specimens. Nuclear factors that influence comet formation (and therefore radiosensitivity) were also examined, such as DNA double strand break (DSB) rates and differences in nuclear matrix protein (NMP) composition.;CA IX immunostaining did not provide prognostic information with respect to response to radical RT. ACA analysis indicated a wide range of responses between tumours. In TCC cell lines, DSB rates are not demonstrably different in cells of differentiated radiosensitivity, however, comparative analysis of nuclear proteins identified differences in their constitutive NMPs and repair enzymes.;These results do not provide evidence that hypoxia influences outcome after RT, but support the contention that ICR is important in dictating the response of bladder tumours to RT. Furthermore, in bladder cancer cell lines of differing radiosensitivity, differences in NMP and repair enzymes are identified. Further work is required to determine whether these are of prognostic importance.
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Hemelt, Marjolein. "Risk factors for bladder cancer : The South and East China case-control study on bladder cancer." Thesis, University of Birmingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.532307.

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Marsh, Howard Piers. "Genetic polymorphisms in bladder cancer angiogenesis." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428513.

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Beatty, John David. "Characterisation of Bladder Cancer Dentritic Cells." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487987.

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Bacillus Calmette-Guerin (BCG) is the most effective intravesical therapy for superficial bladder cancer. It is hypothesised that BCG therapy has a local and systemic effect on antigen-presenting dendritic cells (DC) and that characteristics and variations in DC may reflect those of DC in cancer tissue. Blood, urine and tissue samples were taken from patients with bladder cancer before and during treatment with intravesical BCG. In blood the percentages and numbers of DC expressing maturation, co-stimulatory and intracellular cytokine markers were measured using flow cytometry. Immune responses in bladder cancer were monitored by the identification and characterisation of DC from the urine and tissue of patients with bladder cancer using flow cytometry, immunohistochemistry and electron microscopy. Significantly increased numbers of blood plasmacytoid DC in patients with T1 G3 bladder cancer decreased during BCG therapy so that after 6 treatments there were no differences in the number of blood DC in patients with stages of superficial bladder cancer. DC numbers expressing CD40 increased in the blood of patients treated with BCG. Numbers of DC expressing T helper 1 (Th1) cytokine increased in patients who did not develop an early recurrence of bladder cancer. Immature DC were identified in tissue and urine from patients with superficial bladder cancer and confirmed in samples of urine by immunohistochemistry and electron microscopy. BCG therapy decreased the percentage of DC in the urine of patients who subsequently had recurrent bladder cancer. The therapeutic effect of BCG may be mediated by normalising circulating numbers of plasmacytoid DC and by increasing numbers of DC expressing the costimulatory molecule CD40. In response to BCG therapy increased numbers of circulating Th1 cytokine (IL-12) expressing DC and increased percentages of urine DC may be crucial in preventing recurrent bladder cancer.
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Books on the topic "Bladder cancer"

1

Droller, Michael J. Bladder Cancer. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592590977.

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Kamat, Ashish M., and Peter C. Black, eds. Bladder Cancer. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70646-3.

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Lee, Cheryl T., and David P. Wood, eds. Bladder Cancer. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-417-9.

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Zingg, E. J., and D. M. A. Wallace, eds. Bladder Cancer. London: Springer London, 1985. http://dx.doi.org/10.1007/978-1-4471-1362-1.

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Lerner, Seth P., Mark P. Schoenberg, and Cora N. Sternberg, eds. Bladder cancer. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118674826.

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J, Zingg Ernst, and Wallace, D. M. A. 1946-, eds. Bladder cancer. Berlin: Springer-Verlag, 1985.

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1948-, Bailey Michael, ed. Bladder cancer. 2nd ed. Abingdon: Health, 2006.

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W, Kantoff Philip, and Scher Howard I, eds. Bladder cancer. Philadelphia: Saunders, 1992.

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D, Oliver R. T., and Coptcoat Malcolm J, eds. Bladder cancer. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1998.

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Campaign, Cancer Research. Bladder cancer - UK. [London]: Cancer Research Campaign, 1997.

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Book chapters on the topic "Bladder cancer"

1

Strope, Seth A., and John L. Gore. "Bladder cancer." In Bladder cancer, 395–401. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118674826.ch35.

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Garcia, Michael A., and Albert J. Chang. "Bladder Cancer." In Handbook of Evidence-Based Radiation Oncology, 545–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_25.

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Jiang, Ping, and Juergen Dunst. "Bladder Cancer." In Target Volume Definition in Radiation Oncology, 323–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45934-8_16.

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Calvo, Felipe A., Oscar Abuchaibe, Javier Aristu, Javier Zudiare, and José María Berián. "Bladder Cancer." In Intraoperative Radiotherapy, 73–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84183-5_10.

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Heinz-Peer, G., and C. Kratzik. "Bladder Cancer." In Urogenital Imaging, 235–55. Chichester, UK: John Wiley & Sons, Ltd, 2009. http://dx.doi.org/10.1002/9780470741108.ch11.

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Goltz, Heather Honoré, Marc A. Kowalkouski, Stacey L. Hart, and David Latini. "Cancer, Bladder." In Encyclopedia of Behavioral Medicine, 346–49. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1330.

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Goltz, Heather Honoré, Marc A. Kowalkouski, Stacey L. Hart, and David Latini. "Cancer, Bladder." In Encyclopedia of Behavioral Medicine, 305–9. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1330.

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Mose, Stephan, Stephan Mose, Brandon J. Fisher, Iris Rusu, Charlie Ma, Lu Wang, Larry C. Daugherty, et al. "Bladder Cancer." In Encyclopedia of Radiation Oncology, 40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_329.

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Gomella, L. G., and W. M. Linehan. "Bladder Cancer." In New Directions in Cancer Treatment, 496–500. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83405-9_33.

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Shu, Jia He. "Bladder Cancer." In Alternative and Complementary Therapies for Cancer, 319–50. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-0020-3_13.

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Conference papers on the topic "Bladder cancer"

1

"Bladder Cancer Translational Research Meeting." In Bladder Cancer Translational Research Meeting. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-670-3.

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"Bladder Cancer Translational Research Meeting 2020." In Bladder Cancer Translational Research Meeting 2020. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-590-0.

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Van Hemelrijck, Mieke. "4th Bladder Cancer Translational Research Meeting." In 4th Bladder Cancer Translational Research Meeting, edited by Rick Bryan. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88971-017-1.

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Weilguni, Michael, Walter Smetana, Michael Edetsberger, and Gottfried Kohler. "Bladder cancer cell imaging system." In 2009 32nd International Spring Seminar on Electronics Technology (ISSE). IEEE, 2009. http://dx.doi.org/10.1109/isse.2009.5206970.

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Demos, Stavros G., Regina Gandour-Edwards, Rajen Ramsamooj, and Ralph de Vere White. "Spectroscopic imaging of bladder cancer." In Biomedical Optics 2003, edited by Lawrence S. Bass, Nikiforos Kollias, Reza S. Malek, Abraham Katzir, Udayan K. Shah, Brian J. F. Wong, Eugene A. Trowers, et al. SPIE, 2003. http://dx.doi.org/10.1117/12.476382.

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Johansson, A., H. Stepp, W. Beyer, T. Pongratz, R. Sroka, M. Bader, M. Kriegmair, et al. "Photodynamic management of bladder cancer." In 12th World Congress of the International Photodynamic Association, edited by David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.828315.

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Hoffman, Vanessa. "Abstract ADV09: Bladder cancer basics." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-adv09.

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Przygoda, Maria, and David Aebisher. "Bladder Cancer and Fluorescence Cystoscopy." In IECN 2022. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/iecn2022-12402.

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Fu, Yi-Ping, Indu Kohaar, Lee Moore, Petra Lenz, Jonine D. Figueroa, Wei Tang, Patricia Porter-Gill, et al. "Abstract 944: Translational implications of the 19q12 bladder cancer GWAS signal for aggressive bladder cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-944.

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Nseyo, Unyime O., Donald L. Lamm, and Cindy Carpenter. "Safety of sequential whole bladder photodynamic therapy (WBPT) in bladder cancer." In BiOS 2001 The International Symposium on Biomedical Optics, edited by R. Rox Anderson, Kenneth E. Bartels, Lawrence S. Bass, C. Gaelyn Garrett, Kenton W. Gregory, Abraham Katzir, Nikiforos Kollias, et al. SPIE, 2001. http://dx.doi.org/10.1117/12.427814.

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Reports on the topic "Bladder cancer"

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Williamson, Sean. Pathology of bladder cancer. BJUI Knowledge, November 2019. http://dx.doi.org/10.18591/bjuik.0135.

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Paul, Satashree. Level of DNA Damage from Smoking in Bladder Cancer. Science Repository OÜ, May 2021. http://dx.doi.org/10.31487/sr.blog.36.

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Smoking is the most common and important risk factor for bladder cancer. The reason lying behind the fact is that – the smoke toxins accelerate other DNA damaging events and attention being focused on a family of enzymes called “APOBEC.
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Narayan, Vikram, and Badrinath Konety. Managing the primary in muscle-invasive bladder cancer. BJUI Knowledge, December 2021. http://dx.doi.org/10.18591/bjuik.0138.v2.

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Dong, Liang, Alexandre R. Zlotta, Cynthia Kuk, and Annette Erlich. Non-muscle-invasive bladder cancer - understanding and managing risk. BJUI Knowledge, December 2021. http://dx.doi.org/10.18591/bjuik.0136.v2.

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Tan, Melissa, and Robert Huddart. The evidence for neoadjuvant chemotherapy in muscle invasive bladder cancer. BJUI Knowledge, November 2020. http://dx.doi.org/10.18591/bjuik.0139.

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Tan, Melissa, and Robert Huddart. The evidence for neoadjuvant chemotherapy in muscle invasive bladder cancer. BJUI Knowledge, November 2020. http://dx.doi.org/10.18591/bjuik.0139.v2.

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Gupta, Arti, and Pankaj Kumar Gupta. HISTOPATHOLOGICAL DISTRIBUTION OF MALIGNANT CASES IN A TERTIARY CARE CENTRE. World Wide Journals, February 2023. http://dx.doi.org/10.36106/ijar/1007787.

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Introduction- Malignancy/cancer is a dreadful condition affecting not only physical but also mental wellbeing of a person. Surgeries associated with its treatment are also leads to morbidity. So apart from treatment we need to nd out the factors which are precipitating for any cancer.I tried to study the distribution of malignant cases received in histopathology lab of a tertiary care centre in two and a half month period with respect to its frequency, site,age gender and important histological types. In this study, we Resultshave seen 118 cases of malignancy in histopathology section in 2 and half months period. Ratio of malignancy in male and female is 0.9 that is malignancy rate is slightly more in females. The reason is increasing incidence of malignancy of uterine cervix and breast.Out of 62 cases of malignancy in females ,24 is in cervix only and 11 is in breast, which together constitute more than half of all cases in females. Among males most common malignancy was oral cavity squamous cell carcinoma, it constitute nearly half of all malignant cases in males, which is 27 out of 56 cases. Two cases of laryngeal carcinoma, and 4 cases of urinary bladder carcinoma are seen exclusively in males, Probably because all the three cancers i.e. oral cavity, larynx and urinary bladder are associated with smoking and tobacco chewing .Hence If a campaign is started to Prohibit smoking and tobacco chewing and more important if there production and selling can be banned by government, the incidence of malignancy can become nearly half in males. This study provides a framework for assessing the s Conclusion - tatus and trends of cancer in India. It shall guide for action to strengthen efforts to improve cancer prevention and control to reduce morbidity and mortality
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He, Silei, Jiawen Xu, Minlin Chen, Jiajin Li, and Shiqian Li. A meta-analysis of UCA1 accuracy in the detection of bladder cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2023. http://dx.doi.org/10.37766/inplasy2023.9.0042.

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Jian, Zhongyu, Yucheng Ma, Hong Li, and Kunjie Wang. The Association Between Hepatitis C Virus Infection and Renal Cell Cancer, Prostate Cancer, and Bladder Cancer: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0086.

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Robison, Katina, Kyle Wohlrab, Vivian Sung, Melissa Clark, Christine Luis, Christina Raker, Chanelle Howe, et al. Comparing Surgeries for Women Who Have Both Cancer of the Uterus and Bladder Problems. Patient-Centered Outcomes Research Institute (PCORI), November 2020. http://dx.doi.org/10.25302/11.2020.cer.140922034.

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