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Journal articles on the topic 'Bladder cancer'

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Author: Grafiati

Published: 4 June 2021

Last updated: 8 June 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Le, Ninh B., Hong Qiu, Emily E. Fink, Surbhi Sona, Angela H. Ting, and Byron H. Lee. "Abstract 4733: Effect of KDM6A mutation in bladder cancer." Cancer Research 83, no. 7_Supplement (April 4, 2023): 4733. http://dx.doi.org/10.1158/1538-7445.am2023-4733.

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Abstract As of 2020, bladder cancer is the tenth most common cancer in the world, with a heavier toll exerted on males. Its higher tumor recurrence and progression rates cause major treatment challenges. One of the most frequent mutations in bladder cancer is in lysine-specific demethylase 6A (KDM6A). This gene encodes for ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX), which catalyzes the demethylation of di- and tri- methylated histones H3 lysine 27 and works as part of “COMPASS-LIKE” protein complexes to coordinate many transcriptional processes. The molecular basis for how KDM6A mutations promote carcinogenesis is still under investigation. In this study, we use single-cell RNA sequencing data from bladder cancers with and without KDM6A mutations in both human and mice to examine the effects of KDM6A mutations on the cellular composition and gene expression of tumor and normal bladders. In mice without tumors, KDM6A mutations seem to correlate with enrichment of macrophages in the bladder tissue microenvironment. The opposite is true, however, in the presence of tumors, as there were not only more macrophages but also more dendritic cells in wildtype mice. This pattern was also observed in human, suggesting differences in immune infiltrates in the tumor microenvironment are part of the phenotype of KDM6A mutation. Lastly, KDM6A mutations may also impact urothelial cell states at baseline, as KDM6A KO mouse bladders contain higher proportions of intermediate cell populations compared with their wildtype counterparts. Together, these observations contribute to a better understanding of the role KDM6A plays in bladder cancer. Citation Format: Ninh B. Le, Hong Qiu, Emily E. Fink, Surbhi Sona, Angela H. Ting, Byron H. Lee. Effect of KDM6A mutation in 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 4733.

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12

Sorbellini, M., A. Giubellino, G. Srivastava, C. Sourbier, E. Jagoda, M. Williams, P. L. Choyke, P. A. Pinto, W. Linehan, and D. P. Bottaro. "Use of a MET-specific photoprobe to identify bladder tumors in an orthotopic xenograft model of bladder cancer." Journal of Clinical Oncology 29, no. 7_suppl (March 1, 2011): 260. http://dx.doi.org/10.1200/jco.2011.29.7_suppl.260.

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260 Background: Met over-expression has been found in bladder cancer (CaB). Stage and grade increases in urothelial carcinoma have been found to correlate with increases in Met expression. To assess whether molecular optical imaging could enhance the detection of bladder tumors, we used a Met-specific soluble photoprobe in an orthotopic xenograft model of bladder transitional cell carcinoma (TCC). Methods: An orthotopic xenograft murine model of CaB was developed with T24-Luciferase-positive bladder cancer cells. Presence of tumor was confirmed by luciferase optical imaging (Xenogen IVIS) of mice, 4 weeks after TCC cell implantation. Mice were euthanized and their bladders removed and bivalved. Bladders were incubated for 30 minutes with unbound fluorophore (Cy5**, Peak emission at 675 nM) and subsequently for another 30 minutes with Cy5** bound to a Met-specific peptide. Fluorescence imaging (Maestro) was performed before and after each incubation period. Following imaging, presence of tumor was confirmed histologically. Results: Cy5**-Met- peptide bound in sufficient density to tumor tissue in bladders for visualization by optical imaging. The tumor to normal bladder imaging ratio ranged from 2:1 to 8:1. Bladder regions with high uptake of Cy5**-Met-peptide corresponded to tumor areas confirmed by histological analysis. Conclusions: Cy5**-Met-peptide successfully targets Met in an orthotopic xenograft model of bladder cancer. Our results suggest that this agent maybe useful for the enhanced visualization of bladder cancer tumors during cystoscopy. No significant financial relationships to disclose.

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13

Geramizadeh, Bita, and Ali Kashkooe. "Incidental Gall Bladder Adenocarcinoma in Cholecystectomy Specimens; A Single Center Experience and Review of the Literature." Middle East Journal of Digestive Diseases 10, no. 4 (September 15, 2018): 249–53. http://dx.doi.org/10.15171/mejdd.2018.118.

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BACKGROUND Gallbladder adenocarcinoma is the most common malignant tumor of the biliary tract. Most of gall bladder cancers are detected incidentally only after pathological examination of the surgical specimens. In this study we investigated the characteristics of incidental gallbladder cancers in our center and also reviewed the current literature regarding the diagnosis and treatment of such incidentally detected tumors in the gall bladder. METHODS We retrospectively reviewed all of the cholecystectomy specimens in the archives of Pathology Department in the hospitals affiliated to Shiraz University of Medical Sciences in the study period (2010-2016). Clinicopathological characteristics were extracted from the patients’ clinical charts, which included symptoms, radiological findings, laboratory data, and surgical procedures as well as outcome. RESULTS During these 7 years we identified 18 cases of incidental gall bladder cancer, consisted of 13 women and 5 men with the age range of 32 to 85 (62.5 ± 14.2) years detected after pathological study of the resected gall bladders among more than 4800 resected gall bladders. During the period, only two patients were operated on with the impression of gall bladder adenocarcinoma, which was not included in the study. Ten cases were T1 and eight were T2 at the time of surgery. They have been followed up for 1-7 years, during which, six cases of T2 died. All of the T1 cases are alive and symptom free. CONCLUSION By increasing laparoscopic cholecystectomies in our center we observed 0.37% incidental cases of gall bladder adenocarcinoma. Preoperative diagnosis of this cancer in early stages is very difficult and needs high degree of suspicion. The most important predictor of prognosis is the stage of the cancer at the time of surgery. To the best of our knowledge, this is the first report of incidental gall bladder cancer from Iran.

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Hayashi, Takuji, Kazutoshi Fujita, Yujiro Hayashi, Koji Hatano, Atsunari Kawashima, David J. McConkey, and Norio Nonomura. "Mutational Landscape and Environmental Effects in Bladder Cancer." International Journal of Molecular Sciences 21, no. 17 (August 23, 2020): 6072. http://dx.doi.org/10.3390/ijms21176072.

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Bladder cancer is the most common cancer of the urinary tract. Although nonmuscle-invasive bladder cancers have a good prognosis, muscle-invasive bladder cancers promote metastases and have a poor prognosis. Comprehensive analyses using RNA sequence of clinical tumor samples in bladder cancer have been reported. These reports implicated the candidate genes and pathways that play important roles in carcinogenesis and/or progression of bladder cancer. Further investigations for the function of each mutation are warranted. There is suggestive evidence for several environmental factors as risk factors of bladder cancer. Environmental factors such as cigarette smoking, exposure to chemicals and gases, bladder inflammation due to microbial and parasitic infections, diet, and nutrition could induce several genetic mutations and alter the tumor microenvironment, such as immune cells and fibroblasts. The detailed mechanism of how these environmental factors induce carcinogenesis and/or progression of bladder cancer remains unclear. To identify the relationship between the mutations and the lifestyle could be useful for prevention and treatment of bladder cancer.

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Noone, Anne-Michelle, Clara J. K. Lam, Angela B. Smith, Matthew E. Nielsen, Eric Boyd, Angela B. Mariotto, and Mousumi Banerjee. "Machine Learning Methods to Identify Missed Cases of Bladder Cancer in Population-Based Registries." JCO Clinical Cancer Informatics, no. 5 (June 2021): 641–53. http://dx.doi.org/10.1200/cci.20.00170.

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PURPOSE Population-based cancer incidence rates of bladder cancer may be underestimated. Accurate estimates are needed for understanding the burden of bladder cancer in the United States. We developed and evaluated the feasibility of a machine learning–based classifier to identify bladder cancer cases missed by cancer registries, and estimated the rate of bladder cancer cases potentially missed. METHODS Data were from population-based cohort of 37,940 bladder cancer cases 65 years of age and older in the SEER cancer registries linked with Medicare claims (2007-2013). Cases with other urologic cancers, abdominal cancers, and unrelated cancers were included as control groups. A cohort of cancer-free controls was also selected using the Medicare 5% random sample. We used five supervised machine learning methods: classification and regression trees, random forest, logic regression, support vector machines, and logistic regression, for predicting bladder cancer. RESULTS Registry linkages yielded 37,940 bladder cancer cases and 766,303 cancer-free controls. Using health insurance claims, classification and regression trees distinguished bladder cancer cases from noncancer controls with very high accuracy (95%). Bacille Calmette-Guerin, cystectomy, and mitomycin were the most important predictors for identifying bladder cancer. From 2007 to 2013, we estimated that up to 3,300 bladder cancer cases in the United States may have been missed by the SEER registries. This would result in an average of 3.5% increase in the reported incidence rate. CONCLUSION SEER cancer registries may potentially miss bladder cancer cases during routine reporting. These missed cases can be identified leveraging Medicare claims and data analytics, leading to more accurate estimates of bladder cancer incidence.

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Taylor, Jacob, Adam B. Weiner, Binhuan Wang, Arjun V. Balar, Gary D. Steinberg, and Richard S. Matulewicz. "Lung Metastases Versus Second Primary Lung Cancers in Patients with Primary Urothelial Carcinoma of the Bladder: A National Population-Based Assessment." Bladder Cancer 7, no. 3 (August 31, 2021): 347–54. http://dx.doi.org/10.3233/blc-210008.

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BACKGROUND: The work-up and diagnosis of indeterminate lung nodules at time of bladder cancer diagnosis may delay or change treatment. OBJECTIVE: To quantify the incidence of synchronous and metachronous lung cancers in adults with bladder cancer and compare these rates to the incidence of bladder cancer metastases in the lung. METHODS: We retrospectively analyzed all adults diagnosed with bladder cancer in the Surveillance, Epidemiology and End Results (SEER) registry (2010– 2015) and identified second primary lung cancers defined as being either synchronous (diagnosed within 6 months of bladder cancer diagnosis) or metachronous (more than 6 months following index bladder cancer diagnosis). The risk of second primary lung cancers were reported as a standardized incidence ratio (SIR) reflecting observed and expected case ratios. RESULTS: A total of 88,335 patients diagnosed with bladder cancer were included. Among adults with NMIBC (n = 66,071) and MIBC (n = 18,879), 0.3% and 3.9% had bladder cancer metastatic to the lungs at diagnosis. Synchronous second primary lung cancers were diagnosed in 0.4% and 0.7% of patients with NMIBC and MIBC, respectively. Compared to the general population, the SIR for synchronous lung cancers among adults with NMIBC was 2.5 (95% CI 2.3– 2.9) and was 4.7 (95% CI 4.0– 5.6) for adults with MIBC. CONCLUSIONS: Bladder cancer metastatic to the lung is more common in adults with MIBC compared to NMIBC. There are similar frequencies of synchronous second primary lung cancers regardless of initial bladder cancer stage.

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Rousseau, Matthieu, Conan J. O. O’Brien, Eduardo Antequera, Hana Zdimerova, Dilay Cansever, Tracy Canton, Anna Zychlinsky Scharff, and Molly A. Ingersoll. "Identification of Sex Differences in Tumor-Specific T Cell Infiltration in Bladder Tumor-Bearing Mice Treated with BCG Immunotherapy." Bladder Cancer 6, no. 4 (December 14, 2020): 507–24. http://dx.doi.org/10.3233/blc-200384.

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BACKGROUND: Bladder cancer is the fourth most common cancer for men. However, women are often diagnosed with later stage disease and have poorer outcomes. Whether immune-based sex differences contribute to this discrepancy is unclear. In addition, models to investigate tumor-specific immunity in bladder cancer, in the context of tumor development or response to therapy, are lacking. OBJECTIVE: To address this specific unmet need, we incorporated a commonly used model antigen, ovalbumin, into two well-established models of bladder cancer; the orthotopic MB49 cell line model and the carcinogenic BBN bladder cancer model. METHOD: We tested the utility of these models to investigate tumor-specific immunity in the context of immunotherapy in both sexes. RESULTS: We found that BCG vaccination, prior to weekly BCG instillation does not impart an immune-specific benefit to tumor-bearing mice in the context of multiple BCG instillations. Furthermore, tumors developed in the testes in male mice, precluding the use of the MB49 model to directly investigate sex-based immune differences. In the BBN model, we observed that more tumor antigen-specific CD8+ T cells infiltrated male bladders compared to female bladders in the context of BCG immunotherapy whereas regulatory T cells had higher levels of the exhaustion marker PD-1 in female mice. CONCLUSIONS: We propose our modified BBN model will contribute to our understanding of how tumor-specific immunity arises in bladder cancer. Additionally, the BBN bladder cancer model may help to uncover sex differences in tumor-specific immunity, which would provide valuable information for the development of new treatments or combination therapies for bladder cancer in women and men.

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Tse, Ryan Tsz-Hei, Hongda Zhao, Christine Yim-Ping Wong, Carol Ka-Lo Cheng, Angel Wing-Yan Kong, Qiang Peng, Peter Ka-Fung Chiu, Chi-Fai Ng, and Jeremy Yuen-Chun Teoh. "Urinary Cell-Free DNA in Bladder Cancer Detection." Diagnostics 11, no. 2 (February 14, 2021): 306. http://dx.doi.org/10.3390/diagnostics11020306.

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Urinary bladder cancer is a common urological cancer. Although flexible cystoscopy is widely employed in bladder cancer detection, it is expensive, invasive, and uncomfortable to the patients. Recently, urinary cell-free DNA (ucfDNA) isolated from urine supernatant has been shown to have great potential in bladder cancer detection and surveillance. Molecular features, such as integrity and concentration of ucfDNA, have been shown to be useful for differentiating bladder cancer patients from healthy controls. Besides, bladder cancer also exhibits unique genetic features that can be identified from sequencing and expression of ucfDNA. Apart from bladder cancer detection, ucfDNA is also useful for molecular classification. For example, ucfDNA exhibits significant differences, both molecularly and genetically, in non-muscle-invasive and muscle-invasive bladder cancers. There is no doubt that ucfDNA is a very promising tool for future applications in the field of bladder cancer.

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Wang, Jiaqi, Ruizhe Fang, Lu Wang, Guang Chen, Hongzhi Wang, Zhichao Wang, Danfeng Zhao, et al. "Identification of Carbonic Anhydrase IX as a Novel Target for Endoscopic Molecular Imaging of Human Bladder Cancer." Cellular Physiology and Biochemistry 47, no. 4 (2018): 1565–77. http://dx.doi.org/10.1159/000490875.

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Background/Aims: Emerging novel optical imaging techniques with cancer-specific molecular imaging agents offer a powerful and promising platform for cancer detection and resection. White-light cystoscopy and random bladder biopsies remain the most appropriate but nonetheless suboptimal diagnostic technique for bladder cancer, which is associated with high morbidity and recurrence. However, white-light cystoscopy has intrinsic shortcomings. Although current optical imaging technologies hold great potential for improved diagnostic accuracy, there are few imaging agents for specific molecular targeting. Carbonic anhydrase IX (CAIX) plays a pivotal role in tumorigenesis and tumor progression with potential value as an imaging target. Here, we investigated the feasibility of CAIX as a target and validated the diagnostic performance and significance of CAIX as an imaging agent. Methods: We first analyzed the data from The Cancer Genome Atlas (TCGA). Pairs of samples comprising bladder cancer and adjacent normal tissue were collected. All tissue samples were used for real-time PCR and immunohistochemistry to compare CAIX expression in normal and cancer tissue. Using blue-light cystoscopy, we observed the optical distribution of fluorescently labeled CAIX antibody in freshly excised human bladders and obtained random bladder biopsies to assess sensitivity and specificity. Results: The TCGA data revealed that CAIX expression was significantly higher in bladder cancer specimens than in normal tissue. The outcome was similar in quantitative real-time PCR analysis. In immunohistochemical analysis, bladder cancer specimens classified in four pathological subtypes presented a variety of positive staining intensities, whereas no benign specimens showed CAIX staining. Using blue-light cystoscopy, we distinguished bladder cancers that were mainly papillary, some variants of urothelial carcinoma, and less carcinoma in situ, from benign tissue, despite the presence of suspicious-appearing mucosa. The sensitivity and specificity for CAIX-targeted imaging were 88.00% and 93.75%, respectively. Conclusions: CAIX-targeted molecular imaging could be a feasible and adaptive alternative approach for the accurate diagnosis and complete resection of bladder cancer.

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Weyerer, Veronika, Markus Eckstein, Pamela L. Strissel, Adrian Wullweber, Fabienne Lange, Lars Tögel, Carol I. Geppert, et al. "TERT Promoter Mutation Analysis of Whole-Organ Mapping Bladder Cancers." Genes 12, no. 2 (February 5, 2021): 230. http://dx.doi.org/10.3390/genes12020230.

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Background: Multifocal occurrence is a main characteristic of urothelial bladder cancer (UBC). Whether urothelial transformation is caused by monoclonal events within the urothelium, or by polyclonal unrelated events resulting in several tumor clones is still under debate. TERT promoter mutations are the most common somatic alteration identified in UBC. In this study, we analyzed different histological tissues from whole-organ mapping bladder cancer specimens to reveal TERT mutational status, as well as to discern how tumors develop. Methods: Up to 23 tissues from nine whole-organ mapping bladder tumor specimens, were tested for TERT promoter mutations including tumor associated normal urothelium, non-invasive urothelial lesions (hyperplasia, dysplasia, metaplasia), carcinoma in situ (CIS) and different areas of muscle invasive bladder cancers (MIBC). The mutational DNA hotspot region within the TERT promoter was analyzed by SNaPshot analysis including three hot spot regions (−57, −124 or −146). Telomere length was measured by the Relative Human Telomere Length Quantification qPCR Assay Kit. Results: TERT promoter mutations were identified in tumor associated normal urothelium as well as non-invasive urothelial lesions, CIS and MIBC. Analysis of separate regions of the MIBC showed 100% concordance of TERT promoter mutations within a respective whole-organ bladder specimen. Polyclonal events were observed in five out of nine whole-organ mapping bladder cancers housing tumor associated normal urothelium, non-invasive urothelial lesions and CIS where different TERT promoter mutations were found compared to MIBC. The remaining four whole-organ mapping bladders were monoclonal for TERT mutations. No significant differences of telomere length were observed. Conclusions: Examining multiple whole-organ mapping bladders we conclude that TERT promoter mutations may be an early step in bladder cancer carcinogenesis as supported by TERT mutations detected in tumor associated normal urothelium as well as non-invasive urothelial lesions. Since mutated TERT promoter regions within non-invasive urothelial lesions are not sufficient alone for the establishment of cancerous growth, this points to the contribution of other gene mutations as a requirement for tumor development.

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Fujimoto, Kiyohide, Yoshitomo Chihara, Yoshihiko Hirao, and Kokichi Sugano. "S14-2 Risk factors and prediction of recurrence in superficial bladder cancer(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_2.

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22

Zhao, Zhankui, Yufeng Wang, J. Jillian Zhang, and Xin-Yun Huang. "Fascin Inhibitors Decrease Cell Migration and Adhesion While Increase Overall Survival of Mice Bearing Bladder Cancers." Cancers 13, no. 11 (May 30, 2021): 2698. http://dx.doi.org/10.3390/cancers13112698.

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Bladder cancer is one of the most common cancers in the world. Early stage bladder tumors can be surgically removed, but these patients usually have relapses. When bladder cancer becomes metastatic, survival is very low. There is an urgent need for new treatments for metastatic bladder cancers. Here, we report that a new fascin inhibitor decreases the migration and adhesion of bladder cancer cells. Furthermore, this inhibitor decreases the primary tumor growth and increases the overall survival of mice bearing bladder cancers, alone, as well as in combination with the chemotherapy medication, cisplatin, or the immune checkpoint inhibitor, anti-PD-1 antibody. These data suggest that fascin inhibitors can be explored as a new treatment for bladder cancers.

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Eshagh Hoseini, Seyed Jalal, Mohammad Heidari, and Hassan Fatemi Manesh. "Evaluation of secondary cancers, synchronous and metachronous with bladder cancer." Bionatura 7, no. 1 (February 15, 2022): 1–5. http://dx.doi.org/10.21931/rb/2022.07.01.6.

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The number of bladder cancer survivors worldwide is increasing due to the advancement of diagnostic methods and bladder cancer treatment. Besides, bladder cancer is the sixth most common cancer in Iran. Nowadays, many secondary cancers have been proven with bladder cancer. This study focused on synchronous and metachronous cancers with bladder cancer. This study was performed retrospectively. A total of 276 patients with a definitive diagnosis of bladder cancer were included in the study. Tumors were diagnosed using ultrasound and cystoscopy. Out of 276 patients with bladder tumor, 240 underwent resection, 25 underwent radical cystectomy, and 31 underwent chemotherapy in addition to resection. The mean age of patients was 65±3.9 years. Among the patients, 184 were male (67%), and 92 were female (33%). Smoking was the most common known risk factor. There were 165 smokers, 135 of whom were male and 30 female. Sixty-nine patients had no known risk factor (P <0.05). Gastric cancer was the most common secondary cancer with bladder cancer in all individuals (5.7%). Prostate cancer (20%) in men and cervical cancer (11.9%) in women was the most common secondary cancer simultaneous with bladder cancer. Given the importance of SPC as a cause of cancer death, early detection and screening of primary cancer survivors will increase patients' life expectancy and quality of life.

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Song, Cheeun, Seung Ju Jang, Woo Hyeok Jeon, Sejung Maeng, Jong Hyun Tae, and In Ho Chang. "Nanomedicines for Therapy of Bladder Cancer." Korean Journal of Urological Oncology 20, no. 4 (November 30, 2022): 235–47. http://dx.doi.org/10.22465/kjuo.2022.20.4.235.

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Bladder cancer is one of most common malignant urinary tract tumor types, and transurethral resection of nonmuscle invasive bladder cancer followed by intravesical instillation of immunochemotherapy is the standard treatment approach to minimize recurrence and delay progression of bladder cancer. In general, conventional intravesical immunochemotherapy lacks selectivity for tumor tissues and the effect of drug is reduced with the excretion of urine leading to frequent administration and bladder irritation symptoms. Recently, nanomedicines which adhere to the bladder tumors for a long time, and continuously and efficiently release drug to bladder cancers may overcome all the above problems. Moreover, the advances in nanomedicine based targeted therapy have led to significant improvements in drug efficacy and precision of targeted drug delivery. This review shows the available nano-systems of targeted drug delivery to bladder cancer tissues.

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25

Beachy, Philip A., Kris B. Prado, Aaron M. Kershner, Karim Mrouj, Bernard M. Kiss, Hua Dong, Ozgu Aydogdu, Ye Tian, and Joseph C. Liao. "Abstract IA001: Cellular and molecular underpinnings of field cancerization and progression to invasive carcinoma in bladder cancer." Clinical Cancer Research 30, no. 10_Supplement (May 17, 2024): IA001. http://dx.doi.org/10.1158/1557-3265.bladder24-ia001.

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Abstract Two major concerns in clinical management of bladder cancer are: (i) the high frequency of recurrence; and (ii) the morbidity and mortality associated with progression to invasive disease (invasive urothelial carcinoma, IUC). To gain a better understanding of these issues we have used the murine BBN (N-butyl-N-(4-hydroxylbutyl) nitrosamine) experimental model of bladder cancer, as well as tissue samples from normal human bladders and from bladders of patients at various stages of bladder cancer formation and progression. We have documented in the BBN model a CIS-like stage, prior to invasion, in which clonal expansion from a single cell occupies a significant fraction of the urothelium. With this experimental murine model alongside observations from patient samples and data from The Cancer Genome Atlas (TCGA), we have ascertained that a key event in progression of pre-invasive to invasive carcinoma is the silencing of the Sonic hedgehog (Shh) member of the Hedgehog gene family. Silencing-associated invasion appears due to the loss of SHH-induced differentiation signals, which when present slow growth and block invasion. Despite the consistent loss of SHH expression in invasive murine and human bladder cancers, however, TCGA data show few if any mutations in the SHH gene of IUC cells. Instead, our studies of patient samples and cancer-derived cell lines reveal that the loss of SHH expression is due to tighter chromosomal packaging and reduced accessibility of a bladder-specific enhancer located ~200 kb upstream of the SHH transcription start site. We have found that inhibitors of certain chromatin-modifying enzymes, including an FDA-approved drug, are capable of re-activating SHH expression, and are testing the possibility that these drugs may block or reverse invasion of urothelial carcinoma. The high frequency of bladder cancer recurrence is thought to result from field cancerization, that is, an increased probability of new cancer formation in apparent normal urothelium, even after successful resection of the primary tumor. To understand the basis for this field effect, we compared apparent normal urothelium from cancer patients to truly normal urothelium from bladders never affected by malignancy. We found that apparent normal samples display a dramatically increased basal character in transcriptomic assays, using as a metric of basalization an index constructed from single cell RNA-seq analysis of normal urothelium. We and others have demonstrated previously by lineage tracing and cell ablation studies in the BBN model that IUC arises from basal stem cells of the urothelium. The basalization of urothelium distant from the primary tumor that we observe thus may account for the increased probability of cancer formation in the apparent normal urothelium of bladder cancer patients. We have found that several FDA-approved antagonists of EGF signaling can reverse this basalization in the mouse BBN model as well as in organoid culture, and that these drugs dramatically reduce the formation of tumors following BBN exposure. Citation Format: Philip A. Beachy, Kris B. Prado, Aaron M. Kershner, Karim Mrouj, Bernard M. Kiss, Hua Dong, Ozgu Aydogdu, Ye Tian, Joseph C. Liao. Cellular and molecular underpinnings of field cancerization and progression to invasive carcinoma in bladder cancer [abstract]. In: Proceedings of the AACR Special Conference on Bladder Cancer: Transforming the Field; 2024 May 17-20; Charlotte, NC. Philadelphia (PA): AACR; Clin Cancer Res 2024;30(10_Suppl):Abstract nr IA001.

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Prado, Kris, Kiran Gollapudi, Christopher King, Michael L. Steinberg, and Arnold I. Chin. "Bladder preservation in the treatment of muscle-invasive bladder cancer." Bladder 1, no. 1 (December 2, 2014): 5. http://dx.doi.org/10.14440/bladder.2014.37.

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27

Kim, Jae Heon, Ji Sung Shim, Tae Il Noh, Hong Jae Ahn, Jae Hyun Bae, and Jae Young Park. "Concurrent Bladder Lymphoma and Bladder Cancer Presenting as Metastatic Bladder Cancer." World Journal of Men's Health 30, no. 2 (2012): 141. http://dx.doi.org/10.5534/wjmh.2012.30.2.141.

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28

Peate, Ian. "Bladder cancer." British Journal of Healthcare Assistants 13, no. 6 (June 2, 2019): 271–77. http://dx.doi.org/10.12968/bjha.2019.13.6.271.

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This article is the one in the cancer series that discusses bladder cancer. Bladder cancer can occur in men and women; however, in the UK, there are more men with bladder cancer than women. It is also a disease of the older person. This article provides an introduction that discusses the condition. An overview of the anatomy of the bladder and ureters is provided. In 2015, bladder cancer was the 10th most common cancer in the UK and was responsible for 3% of all new cancer cases. Diagnosis and treatment options are discussed, with an emphasis on ensuring that the patient is key in any decisions that are made about treatment regimens. The importance of follow-up after treatment is also discussed. A glossary of terms is provided and five multiple-choice questions are included to enhance learning and application to practice.

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Kim, Hak Soo, Soo Yong Choi, Sung Eun Kim, Kihoon Lee, Hyun Ju Lee, Gil Hyun Kang, and Hoon Yu. "Bladder Malakoplakia Mimicking Bladder Cancer." Korean Journal of Medicine 92, no. 5 (October 1, 2017): 476–79. http://dx.doi.org/10.3904/kjm.2017.92.5.476.

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30

Sonpavde, Guru P. "Bladder Cancer." Hematology/Oncology Clinics of North America 35, no. 3 (June 2021): i. http://dx.doi.org/10.1016/s0889-8588(21)00049-6.

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31

_, _. "Bladder Cancer." Journal of the National Comprehensive Cancer Network 4, no. 10 (November 2006): 984. http://dx.doi.org/10.6004/jnccn.2006.0083.

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An estimated 61,420 new cases of urinary bladder cancer will be diagnosed in the United States in 2006, making it the fourth most common cancer in men and the ninth most common neoplasm in women. Because the median age of diagnosis is 65 years, medical comorbidities are a frequent consideration. The clinical spectrum of bladder cancer can be divided into 3 categories: noninvasive tumors, invasive lesions, and metastatic lesions. These categories differ in prognosis, management, and therapeutic goals, and these guidelines discuss management strategies to achieve the best possible outcomes. For the most recent version of the guidelines, please visit NCCN.org

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Montie, James E., Peter E. Clark, Mario A. Eisenberger, Rizk El-Galley, Richard E. Greenberg, Harry W. Herr, Gary R. Hudes, et al. "Bladder Cancer." Journal of the National Comprehensive Cancer Network 7, no. 1 (January 2009): 8–39. http://dx.doi.org/10.6004/jnccn.2009.0002.

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Clark, Peter E., Neeraj Agarwal, Matthew C. Biagioli, Mario A. Eisenberger, Richard E. Greenberg, Harry W. Herr, Brant A. Inman, et al. "Bladder Cancer." Journal of the National Comprehensive Cancer Network 11, no. 4 (April 2013): 446–75. http://dx.doi.org/10.6004/jnccn.2013.0059.

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34

Fernandes, Tanya. "Bladder cancer." Nursing Standard 23, no. 37 (May 20, 2009): 58. http://dx.doi.org/10.7748/ns2009.05.23.37.58.c7194.

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35

Badalament, Robert A., and Edward W. Schervish. "Bladder cancer." Postgraduate Medicine 100, no. 2 (August 1996): 217–30. http://dx.doi.org/10.3810/pgm.1996.08.60.

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36

Arrabal Polo, Miguel Ángel, and María del Carmen Cano García. "Bladder Cancer." ACTUALIDAD MEDICA 101, no. 798 (August 31, 2016): 140–41. http://dx.doi.org/10.15568/am.2016.798.ao01.

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37

DiGiulio, Sarah. "Bladder Cancer." Oncology Times 36, no. 9 (May 2014): 40. http://dx.doi.org/10.1097/01.cot.0000449873.28652.1a.

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38

Moyer, Paula, and Crystal Phend. "Bladder Cancer." Oncology Times 27, no. 21 (November 2005): 24. http://dx.doi.org/10.1097/01.cot.0000291281.93657.eb.

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39

Mead, G. M. "Bladder cancer." Current Opinion in Oncology 2, no. 3 (June 1990): 514–19. http://dx.doi.org/10.1097/00001622-199002030-00012.

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40

Mead, G. M. "Bladder cancer." Current Opinion in Oncology 2, no. 3 (June 1990): 514–19. http://dx.doi.org/10.1097/00001622-199006000-00012.

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41

Ozen, Haluk. "Bladder cancer." Current Opinion in Oncology 4, no. 3 (June 1992): 435–41. http://dx.doi.org/10.1097/00001622-199206000-00003.

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Özen, Haluk. "Bladder cancer." Current Opinion in Oncology 8, no. 3 (May 1996): 259. http://dx.doi.org/10.1097/00001622-199605000-00016.

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Özen, Haluk. "Bladder cancer." Current Opinion in Oncology 9, no. 3 (May 1997): 295–300. http://dx.doi.org/10.1097/00001622-199709030-00013.

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Özen, Haluk. "Bladder cancer." Current Opinion in Oncology 10, no. 3 (May 1998): 273–78. http://dx.doi.org/10.1097/00001622-199805000-00016.

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Özen, Haluk. "Bladder cancer." Current Opinion in Oncology 11, no. 3 (May 1999): 207. http://dx.doi.org/10.1097/00001622-199905000-00013.

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Özen, Haluk, and M. Craig Hall. "Bladder cancer." Current Opinion in Oncology 12, no. 3 (May 2000): 255–59. http://dx.doi.org/10.1097/00001622-200005000-00012.

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Patton, Suzanne E., M. Craig Hall, and Haluk Ozen. "Bladder cancer." Current Opinion in Oncology 14, no. 3 (May 2002): 265–72. http://dx.doi.org/10.1097/00001622-200205000-00003.

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Borden,, Lester S., Peter E. Clark, and M. Craig Hall. "Bladder cancer." Current Opinion in Oncology 15, no. 3 (May 2003): 227–33. http://dx.doi.org/10.1097/00001622-200305000-00009.

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Borden, Lester S., Peter E. Clark, and M. Craig Hall. "Bladder cancer." Current Opinion in Oncology 16, no. 3 (May 2004): 257–62. http://dx.doi.org/10.1097/00001622-200405000-00012.

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Badalament, Robert A., and Joseph R. Drago. "Bladder cancer." Postgraduate Medicine 88, no. 4 (September 15, 1990): 63–70. http://dx.doi.org/10.1080/00325481.1990.11704753.

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