Topic Editors

Department of Urology, Goethe-University Frankfurt, Interdisciplinary Science Building, Building 25A, Room 404, Theodor-Stern-Kai 7, D-60590 Frankfurt / Main, Germany
Institute of Pharmaceutical Biology, Goethe University Frankfurt, 60438 Frankfurt am Main, Germany

Novel Approaches in Bladder Cancer Treatment

Abstract submission deadline
closed (31 January 2023)
Manuscript submission deadline
closed (30 April 2023)
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Topic Information

Dear Colleagues,

Bladder cancer is the ninth most common malignant ailment and the fourteenth most common cause of cancer death worldwide. Over the past decades, novel and potent agents have been developed and approved. However, although innovative approaches, such as targeted therapy and/or immunotherapy, have provided benefits for tumor patients, many challenges, such as low response rate and drug resistance, remain overt. Extensive research is required to refine and optimize the current bladder cancer treatment protocols. Dissatisfaction with the conventional treatment has meanwhile driven many cancer patients to seek “non-conventional” care options, including natural products, mind and body practices, or other non-conventional health approaches. From the scientists’ side, innovative and “risky” projects are under investigation focusing on cancer stem cell targeting, selective photodynamic technology, or anticancer vaccine therapy, among others. The purpose of this Special Issue is to collect original research articles and reviews on non-conventional medicine for bladder cancer. Both clinical trials and preclinical studies (in vitro and in vivo) are welcome that do not reflect the mainstream of cancer treatment but which are rather original and may open the mind for unconventional strategies.

Prof. Dr. Roman Blaheta
Prof. Dr. Beatrice E. Bachmeier
Topic Editors

Keywords

  • bladder cancer
  • non-mainstream treatment
  • complementary medicine
  • plant compounds
  • stem cell targeting
  • anticancer vaccination
  • photodynamic therapy

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Biomolecules
biomolecules
6.064 5.7 2011 16.6 Days 2300 CHF
Cancers
cancers
6.575 5.8 2009 17.4 Days 2600 CHF
Current Oncology
curroncol
3.109 3.5 1994 19.6 Days 1800 CHF
International Journal of Molecular Sciences
ijms
6.208 6.9 2000 15.9 Days 2500 CHF
Onco
onco
- - 2021 15.0 days * 1000 CHF

* Median value for all MDPI journals in the second half of 2022.


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Published Papers (4 papers)

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Article
Targeting Pro-Survival Autophagy Enhanced GSK-3β Inhibition-Induced Apoptosis and Retarded Proliferation in Bladder Cancer Cells
Curr. Oncol. 2023, 30(6), 5350-5365; https://doi.org/10.3390/curroncol30060406 - 28 May 2023
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Abstract
Advanced bladder cancer (BC) (local invasive and/or metastatic) is not curable even with cytotoxic chemotherapy, immune checkpoint inhibitors, and targeted treatment. Targeting GSK-3β is a promising novel approach in advanced BC. The induction of autophagy is a mechanism of secondary resistance to various [...] Read more.
Advanced bladder cancer (BC) (local invasive and/or metastatic) is not curable even with cytotoxic chemotherapy, immune checkpoint inhibitors, and targeted treatment. Targeting GSK-3β is a promising novel approach in advanced BC. The induction of autophagy is a mechanism of secondary resistance to various anticancer treatments. Our objectives are to investigate the synergistic effects of GSK-3β in combination with autophagy inhibitors to evade GSK-3β drug resistance. Small molecule GSK-3β inhibitors and GSK-3β knockdown using siRNA promote the expression of autophagy-related proteins. We further investigated that GSK-3β inhibition induced the nucleus translocation of transcription factor EB (TFEB). Compared to the GSK-3β inhibition alone, its combination with chloroquine (an autophagy inhibitor) significantly reduced BC cell growth. These results suggest that targeting autophagy potentiates GSK-3β inhibition-induced apoptosis and retarded proliferation in BC cells. Full article
(This article belongs to the Topic Novel Approaches in Bladder Cancer Treatment)
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Review
New Approaches to Targeting Epigenetic Regulation in Bladder Cancer
Cancers 2023, 15(6), 1856; https://doi.org/10.3390/cancers15061856 - 20 Mar 2023
Viewed by 799
Abstract
Epigenetics is a growing field and in bladder cancer, it is of particular interest in advanced or metastatic disease. As opposed to genetic mutations in which the nucleotide sequence itself is altered, epigenetic alterations refer to changes to the genome that do not [...] Read more.
Epigenetics is a growing field and in bladder cancer, it is of particular interest in advanced or metastatic disease. As opposed to genetic mutations in which the nucleotide sequence itself is altered, epigenetic alterations refer to changes to the genome that do not involve nucleotides. This is of great interest in cancer research because epigenetic alterations are reversible, making them a promising target for pharmacological agents. While chemoimmunotherapy is the mainstay for metastatic disease, there are few alternatives for patients who have progressed on first- or second-line treatment. By targeting reversible epigenetic alterations, novel epigenetic therapies are important potential treatment options for these patients. A search of clinical registries was performed in order to identify and collate epigenetic therapies currently in human trials. A literature search was also performed to identify therapies that are currently in preclinical stages, whether this be in vivo or in vitro models. Twenty-five clinical trials were identified that investigated the use of epigenetic inhibitors in patients with bladder cancer, often in combination with another agent, such as platinum-based chemotherapy or pembrolizumab. The main classes of epigenetic inhibitors studied include DNA-methyltransferase (DNMT) inhibitors, histone deacetylase (HDAC) inhibitors, and histone methyltransferase (HMT) inhibitors. At present, no phase 3 clinical trials have been registered. Few trials have published results, though DNMT inhibitors have shown the most promise thus far. Many patients with advanced or metastatic bladder cancer have limited treatment options, particularly when first- or second-line chemoimmunotherapy fails. Epigenetic alterations, which are common in bladder cancer, are potential targets for drug therapies, and these epigenetic agents are already in use for many cancers. While they have shown promise in pre-clinical trials for bladder cancer, more research is needed to assess their benefit in clinical settings. Full article
(This article belongs to the Topic Novel Approaches in Bladder Cancer Treatment)
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Article
Hypomethylation of CLDN4 Gene Promoter Is Associated with Malignant Phenotype in Urinary Bladder Cancer
Int. J. Mol. Sci. 2022, 23(12), 6516; https://doi.org/10.3390/ijms23126516 - 10 Jun 2022
Cited by 1 | Viewed by 1223
Abstract
The tight junction (TJ) protein claudin-4 (CLDN4) is overexpressed in bladder urothelial carcinoma (BUC) and correlates with cancer progression. However, the mechanism of CLDN4 upregulation and promotion of malignant phenotype is not clear. Here, we analyzed 157 cases of BUC and investigated the [...] Read more.
The tight junction (TJ) protein claudin-4 (CLDN4) is overexpressed in bladder urothelial carcinoma (BUC) and correlates with cancer progression. However, the mechanism of CLDN4 upregulation and promotion of malignant phenotype is not clear. Here, we analyzed 157 cases of BUC and investigated the hypomethylation of CpG island in the CLDN4 promoter DNA and its correlation with cancer progression. In hypomethylated cases, CLDN4 expression, cell proliferation, stemness, and epithelial-mesenchymal transition were increased. Treatment of three human BUC cell lines with the demethylating agent aza-2′-deoxycytidine (AZA) led to excessive CLDN4 expression, and, specifically, to an increase in CLDN4 monomer that is not integrated into the TJ. The TJ-unintegrated CLDN4 was found to bind integrin β1 and increase stemness, drug resistance, and metastatic ability of the cells as well as show an anti-apoptosis effect likely via FAK phosphorylation, which reduces upon knockdown of CLDN4. Thus, CLDN4 is overexpressed in BUC by an epigenetic mechanism and the high expression enhances the malignant phenotype of BUC via increased levels of TJ-unintegrated CLDN4. CLDN4 promoter DNA methylation is expected to be a novel indicator of BUC malignant phenotype and a new therapeutic target. Full article
(This article belongs to the Topic Novel Approaches in Bladder Cancer Treatment)
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Communication
Gold Glyconanoparticles Combined with 91–99 Peptide of the Bacterial Toxin, Listeriolysin O, Are Efficient Immunotherapies in Experimental Bladder Tumors
Cancers 2022, 14(10), 2413; https://doi.org/10.3390/cancers14102413 - 13 May 2022
Cited by 3 | Viewed by 1485
Abstract
This study presents proof of concept assays to validate gold nanoparticles loaded with the bacterial peptide 91–99 of the listeriolysin O toxin (GNP-LLO91–99 nanovaccines) as immunotherapy for bladder tumors. GNP-LLO91–99 nanovaccines showed adjuvant abilities as they induce maturation and activation of [...] Read more.
This study presents proof of concept assays to validate gold nanoparticles loaded with the bacterial peptide 91–99 of the listeriolysin O toxin (GNP-LLO91–99 nanovaccines) as immunotherapy for bladder tumors. GNP-LLO91–99 nanovaccines showed adjuvant abilities as they induce maturation and activation of monocyte-derived dendritic cells (MoDCs) to functional antigen-presenting cells in healthy donors and patients with melanoma or bladder cancer (BC), promoting a Th1 cytokine pattern. GNP-LLO91–99 nanovaccines were also efficient dendritic cell inducers of immunogenic tumor death using different bladder and melanoma tumor cell lines. The establishment of a pre-clinical mice model of subcutaneous BC confirmed that a single dose of GNP-LLO91–99 nanovaccines reduced tumor burden 4.7-fold and stimulated systemic Th1-type immune responses. Proof of concept assays validated GNP-LLO91–99 nanovaccines as immunotherapy by comparison to anti-CTLA-4 or anti-PD-1 antibodies. In fact, GNP-LLO91–99 nanovaccines increased percentages of CD4+ and CD8+ T cells, B cells, and functional antigen-presenting DCs in tumor-infiltrated lymphocytes, while they reduced the levels of myeloid-derived suppressor cells (MDSC) and suppressor T cells (Treg). We conclude that GNP-LLO91–99 nanovaccines can work as monotherapies or combinatory immunotherapies with anti-CTLA-4 or anti-PD-1 antibodies for solid tumors with high T cell infiltration, such as bladder cancer or melanoma. Full article
(This article belongs to the Topic Novel Approaches in Bladder Cancer Treatment)
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