Background and objective Bladder cancer presents a significant challenge in clinical practice. This review aims to investigate trends in BC drug trials globally and in China from 2010 to 2025, with particular emphasis on the period form 2010 to 2019, as 2018 marked the advent of the immunotherapy era. Methods Data were extracted from clinical trial registries, regulatory databases (including the CDE platform), and scientific publications. Eligibility criteria included clinical trials evaluating systemic therapies for BC. Quality assessment was performed using the Cochrane Risk of Bias Tool and MINORS criteria. Key findings and limitations Between 2010 and 2019, 448 BC trials were identified globally, with a compound annual growth rate of 17.8%. The United States, China, and Japan were the leading countries in terms of the number of trials. China contributed 13 registered BC drugs, involving 33 trials, that primarily focused on chemical agents in Phase II studies. Globally, 131 BC agents were studied, including 63 biopharmaceuticals (48% of which were antibody-based, predominantly PD-1/PD-L1 inhibitors) and 68 chemotherapies. From 2020 to 2025, overall trends remained; similar, with chemotherapy continuing to dominate and the United States, China, Japan, and European countries remaining the primary contributors. However, limitations such as potential reporting bias and varying methodological quality should be taken into account. Conclusion and clinical implications Chemotherapy remains a cornerstone in BC treatment, while biopharmaceutical agents are emerging as promising alternatives. The rapid expansion of immune checkpoint inhibitors and novel modalities, such as antibody-drug conjugates, represents a shift in therapeutic strategies. China's increasing involvement in clinical trials and advancements in biopharmaceutical research capacity suggest substantialsignificant potential for future contributions to this evolving landscape. Clinicians should consider incorporating biological agents into treatment algorithms while remaining vigilant about resistance mechanisms.

Interleukin-7 (IL7) plays a pivotal role in T cell biology; however, its therapeutic potential is constrained by its short half-life. Conventional chemical biotinylation frequently results in random modifications that compromise its bioactivity. This study endeavors to establish a prokaryotic system for the site-specific biotinylation of IL7 utilizing AviTag and underscores its advantages over random biotinylation in retaining functionality. A recombinant plasmid (pET-Dual-His-IL7-avi-birA) was constructed to coexpress AviTag-fused IL7 and BirA ligase, which was subsequently transformed into Escherichia coli BL21-(DE3). Optimal expression conditions were determined as follows: cultivation at 37 °C with shaking at 200 rpm for 12 h following induction with 0.5 mM IPTG in the presence of 80 μM biotin. The expressed protein, predominantly localized in inclusion bodies, was purified using Ni-NTA resin supplemented with 250 mM imidazole. Biotinylation efficiency was confirmed through Western blot analysis and native polyacrylamide gel electrophoresis (PAGE). Functional characterization encompassed T cell proliferation and apoptosis assays employing CCK-8 methodology and flow cytometry, respectively, alongside comparative analyses against chemically randomized biotinylated IL7. Site-specifically biotinylated IL7 (biotin-IL7) was successfully generated and purified. It specifically bound streptavidin and retained T cell proliferative activity comparable to native IL7. Compared with randomly biotinylated IL7, site-specific exhibited stronger induction of T cell proliferation, less interference with antibody binding, and more effective downregulation of T cell apoptosis. The AviTag/BirA-based biotinylation system provides an efficient, economical, and scalable method for producing functional biotin-IL7 with enhanced stability and targeting potential. The key advantages of site-specific over random biotinylation were confirmed: preservation of IL7's bioactivity, reduction of functional interference, and enhancement of therapeutic efficacy. This approach offers a paradigm for optimizing small therapeutic proteins, particularly in cancer immunotherapy, while highlighting the need to improve soluble expression and biotinylation efficiency.

Photothermal therapy (PTT) for solid prostate cancer (PCa) is often limited by poor intratumoral penetration and rapid DNA repair. Herein, we engineered a PSMA-targeted gas nanomotor that couple deep tumor penetration with DNA repair sensitization for enhanced photothermal/NO therapy. BLM helicase inhibitor ML216 and nitric oxide donor BNN6 were co-encapsulated with phase-change material and loaded into single-pore hollow polydopamine nanoparticles, followed by surface conjugation with anti-PSMA nanobodies (VHH) to yield M/B@PDA‑VHH NPs. VHH-mediated recognition confers active targeting toward PSMA-positive PCa cells. Under near-infrared irradiation, the nanoparticles show high photothermal conversion and trigger on-demand release of NO and ML216. NO generation propels nanomotor movement, markedly improving transport across endothelial barriers, penetration into 3D tumor spheroids, and distribution in PCa tissues in vivo. Photothermal/NO treatment induces DNA damage and promote apoptosis. Released ML216 inhibits BLM helicase, leading to replication fork stalling and accumulation of double-strand breaks, and concomitantly suppresses AKT/mTOR signaling via dephosphorylation of p‑AKT and p‑PRAS40. These effects disrupt DNA repair and amplify oxidative damage, restoring therapeutic sensitivity. In vitro and in vivo studies show strong tumor growth inhibition with minimal systemic toxicity. This gas-propelled platform offers a strategy to overcome stromal barriers and resistance in solid PCa.

BackgroundBladder cancer, the most common malignancy of the urinary system, is associated with poor prognosis due to its metastatic potential, invasive behavior, and immune evasion. Intercellular adhesion molecule 5 (ICAM5), a member of the immunoglobulin superfamily, regulates cell adhesion and has been implicated in tumor progression. However, its biological function in bladder cancer remains unclear.MethodsIn this study, we analyzed data from The Cancer Genome Atlas (TCGA) and UCSC Xena databases to investigate ICAM5 expression, prognostic significance, genetic mutations, methylation, immune profiles, and regulatory functions in bladder cancer. Weighted Gene Coexpression Network Analysis (WGCNA) and Gene Set Cancer Analysis (GSCA) were employed to explore ICAM5-related pathways.ResultsOur findings demonstrated that ICAM5 expression was significantly upregulated in bladder cancer and associated with advanced disease features, including higher TNM stages, pathological grades, and aggressive molecular subtypes. Furthermore, ICAM5 influenced the immune microenvironment, regulated methylation, and modulated immune checkpoint expression, contributing to immunotherapy resistance. Mechanistically, ICAM5 promoted epithelial-mesenchymal transition (EMT), proliferation, and metastasis.ConclusionsICAM5 serves as a novel prognostic biomarker and potential therapeutic target in bladder cancer, orchestrating EMT progression, reshaping the immune microenvironment, and driving resistance to immunotherapy.

Zinc oxide nanoparticles (ZnO NPs), known for their distinct physicochemical properties and potent antibacterial activity, offer a promising alternative to address the global antibiotic resistance crisis. Their antibacterial performance can be precisely modulated by tuning their physical and chemical properties. In this study, we investigated how doping with transition metals and lanthanide elements alters key properties of ZnO NPs—such as size, morphology, and surface defects—and evaluated the corresponding effects on antibacterial activity. Departing from commonly reported wire/rod-like ZnO micro/nanostructures, we employed a simple hydrothermal doping method to synthesize Cu-doped (Cu-ZnO), Mn-doped (Mn-ZnO), and Ce-doped ZnO (Ce-ZnO) NPs. Antibacterial efficacy was assessed in vitro using agar diffusion and plate coating assays, and in vivo via a skin infection model. Undoped ZnO formed irregular rod-shaped crystals, whereas the doped variants exhibited distinct morphologies: Cu-ZnO showed a mesoporous urchin-like structure with an average size of ∼227 nm and Cu ions predominantly in Cu⁺/Cu²⁺ states; Mn-ZnO displayed a denser cauliflower-like shape (∼87 nm) with Mn mainly present as Mn²⁺/Mn⁴⁺; and Ce-ZnO adopted a cauliflower-like morphology (∼220 nm) with Ce in Ce³ ⁺/Ce⁴⁺ states. Doping introduced noticeable lattice defects in all samples. In vitro enzymatic simulation experiments revealed that Cu-ZnO, Mn-ZnO, and Ce-ZnO could generate •OH under photocatalytic conditions. Both in vivo and in vitro antibacterial tests demonstrated that all doped ZnO NPs possessed good antibacterial activity, with Cu-ZnO exhibiting the strongest effect. These findings indicate that metal doping significantly enhances the antibacterial performance of ZnO NPs, positioning them as a highly promising alternative to conventional antibiotics.

Targeted therapy enhances tumor elimination while reducing adverse effects by integrating multiple tumoricidal mechanisms. Low molecular weight (LMW) ligands, offering faster pharmacokinetics and improved tumor permeability, present a viable alternative to antibodies. This study presents a novel nanomedicine for prostate cancer therapy, leveraging mesoporous silica nanoparticles (MSN) as the nanocarrier to encapsulate manganese dioxide (MnO2) and doxorubicin (DOX). The resultant nanoparticles are further coated with a polydopamine (PDA) layer and covalently conjugated with glucose oxidase (GOx), forming the MSN@Mn@PDA-GOx/DOX hybrid system (hereafter termed SMPG/DOX NPs). LMW ligands (small-molecule inhibitor DCL and nanobody VHH) targeting prostate-specific membrane antigen (PSMA) were conjugated to create DCL-SMPG/DOX and VHH-SMPG/DOX. Mn2+-mediated Fenton-like reactions converted H2O2 into toxic hydroxyl radicals (·OH) under acidic conditions, enabling chemodynamic therapy (CDT). GOx-generated H2O2 and gluconic acid disrupted nutrient supply, inducing tumor starvation therapy (ST). The increased H2O2 and acidity amplified the Fenton-like reaction, creating a "ROS storm" that synergistically enhanced chemotherapy. LMW targeting improved tumor specificity, efficacy, and reduced side effects. In vitro, DCL-SMPG/DOX showed superior tumor cell internalization and cytotoxicity compared to VHH-SMPG/DOX. In vitro, the cellular internalization rates of VHH-SMPG/DOX and DCL-SMPG/DOX were 34.1

Background:Bladder cancer (BC) is a common malignancy characterized by high recurrence and poor prognosis. HOXB7, a member of the HOX gene family, is aberrantly expressed in various tumors, but its role in BC remains unclear. Methods:HOXB7 expression in BC was analyzed using public databases (GEPIA, UALCAN) and validated by immunohistochemistry on a tissue microarray of 36 BC patients. In vitro experiments using BC cell lines (5637 and T24) were conducted to investigate the effects of HOXB7 knockdown or overexpression on cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT). Western blotting and rescue assays with ERK pathway modulators (Ro67-7476 and PD98059) were performed to assess the involvement of the H-Ras/Raf-1/MEK/ERK signaling cascade. Xenograft mouse models were employed to evaluate tumorigenicity in vivo. Results:HOXB7 was significantly upregulated in BC tissues and cell lines, correlating with advanced tumor stage and poor overall survival. HOXB7 silencing inhibited BC cell proliferation, migration, invasion, and EMT, while promoting apoptosis. Conversely, HOXB7 overexpression produced the opposite effects. Mechanistically, HOXB7 activated the H-Ras/Raf-1/MEK/ERK pathway, as indicated by increased phosphorylation of MEK and ERK. These effects were reversed by pharmacological inhibition or activation of ERK signaling. In vivo, HOXB7 knockdown suppressed tumor growth and ERK pathway activation. Conclusion:This study provides the first comprehensive experimental evidence that HOXB7 drives BC progression via activation of the H-Ras/Raf-1/MEK/ERK pathway. These findings highlight HOXB7 as a potential prognostic biomarker and therapeutic target in BC. Furthermore, our results lay the foundation for future investigations into the broader molecular and immunological networks modulated by HOXB7 in BC.

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma, presenting significant challenges in diagnosis and treatment. Despite recent advancements in targeted therapies and immune checkpoint inhibitors, drug resistance remains a major obstacle in metastatic ccRCC. As a member of the AAA + ATPase superfamily, TRIP13 has been implicated in tumorigenesis across various cancers. however, its specific role and underlying mechanisms in ccRCC are not yet fully understood. This study aimed to explore the functional role and mechanisms of TRIP13 in ccRCC progression and its potential as a therapeutic target. Bioinformatics analyses were conducted to assess the expression, prognostic significance, clinical relevance, and oncogenic role of TRIP13 in ccRCC patients. In vitro, cell viability, cycle progression, apoptosis, and migration/invasion were evaluated using CCK-8, colony formation, EdU, flow cytometry, wound healing, and transwell assays. In vivo tumorigenic potential was assessed through a nude mouse xenograft model. Protein expression and interactions were analyzed by western blotting, co-immunoprecipitation, and RT-qPCR. We demonstrated that TRIP13 was significantly upregulated in ccRCC tissues and correlates with poor prognosis, advanced tumor grade, and metastasis. Additionally, we uncovered an interdependent relationship between TRIP13 expression, immune cell infiltration, immune checkpoints, and drug resistance. Functional assays revealed that TRIP13 promotes ccRCC cell proliferation, migration, and invasion in vitro, as well as tumorigenesis in vivo. Mechanistically, TRIP13 activates the PI3K/AKT/mTOR pathway and enhances cell proliferation, migration, invasion, and the epithelial-mesenchymal transition (EMT) process by upregulating NUSAP1. TRIP13 is upregulated in ccRCC and may serve as a novel prognostic biomarker for patient survival and treatment response. Additionally, TRIP13 enhances ccRCC cell proliferation, invasion, and EMT via the PI3K/AKT/mTOR pathway, while its expression is closely linked to immune cell infiltration and immune checkpoint regulation, offering new insights for immunotherapeutic approaches in ccRCC.

Background:IGFL1, a member of the insulin growth factor-like family, plays a potential role in tumorigenesis. This study aimed to investigate IGFL1 expression and its prognostic and immunological significance across cancers, with experimental validation in bladder cancer (BLCA). Methods:Data from TCGA, GTEx, and TIMER2.0 were analyzed to assess IGFL1 expression across cancers and its associations with prognosis, immune subtypes, immune infiltration, and tumor-related genomic features. Drug sensitivity data were also evaluated. Given BLCA's high mutation burden, limited treatment options, and strong IGFL1 dysregulation observed in pan-cancer analysis, we selected it for experimental validation. In vitro and in vivo experiments were conducted to validate the oncogenic role of IGFL1 in BLCA and explore its underlying mechanisms. Results:IGFL1 was significantly overexpressed in 10 tumor types and associated with advanced stage and grade in BLCA. High IGFL1 expression correlated with poor prognosis in OV, SARC, HNSC, PAAD, UCEC, KIRC, and BLCA. IGFL1 expression was linked to features of the tumor microenvironment in several cancers. In BLCA tissues, IGFL1 levels were markedly elevated. Knockdown of IGFL1 in 5637 and ScaBER cells reduced proliferation, migration, and epithelial-mesenchymal transition (EMT)-related protein expression; overexpression had the opposite effect. In vivo, IGFL1 silencing suppressed xenograft tumor growth, decreased Ki67 expression, increased apoptosis, and enhanced CD4⁺ and CD8⁺ T-cell infiltration. Mechanistic analysis suggested that IGFL1's effects are mediated through the JAK2/STAT3 signaling pathway. Conclusion:IGFL1 promotes tumor progression and immune modulation in multiple cancers, particularly in BLCA. Its oncogenic and immunosuppressive roles, mediated through the JAK2/STAT3 axis, support its potential as a prognostic biomarker and therapeutic target.

Background: Deafness autosomal dominant 2A (DFNA2A) is related to non-syndromic genetic hearing impairment. The KCNQ4 (Potassium Voltage-Gated Channel Subfamily Q Member 4) can lead to DFNA2A. In this study, we report a case of autosomal dominant non-syndromic hearing loss with six family members as caused by a novel variant in the KCNQ4 gene. Methods: The whole-exome sequencing (WES) and pure tone audiometry were performed on the proband of the family. Sanger sequencing was conducted on family members to determine if the novel variant in the KCNQ4 gene was present. Evolutionary conservation analysis and computational tertiary structure protein prediction of the wild-type KCNQ4 protein and its variant were then performed. In addition, voltage-gated channel activity of the wild-type KCNQ4 protein and its variant were tested using whole-cell patch clamp. Results: It was observed that the proband had inherited autosomal dominant, non-syndromic sensorineural hearing loss as a trait. A novel co-segregating heterozygous missense variant (c.902C>A, p.Ala301Asp) of the KCNQ4 gene was identified in the proband and other five affected family members. This variant was predicted to cause an alanine-to-aspartic acid substitution at position 301 in the KCNQ4 protein. The alanine at position 301 is well conserved across different species. Whole-cell patch clamp showed that there was a significant difference between the WT protein currents and the mutant protein currents in the voltage-gated channel activity. Conclusion: In the present study, performing WES in conjunction with Sanger sequencing enhanced the detection of a novel, potentially causative variant (c301 A>G; p.Ala301Asp) in exon 6 of the KCNQ4 gene. Therefore, our findings contributed to the mutation spectrum of the KCNQ4 gene and may be useful in the diagnosis and gene therapy of deafness autosomal dominant 2A.

Purpose: The objective of this study was to examine the expression and role of Centromere protein W (CENPW) in bladder cancer (BLCA), as well as its potential mechanistic impact on the progression of BLCA. Methods: In this study, we conducted a comparative analysis of the mRNA expression level of CENPW in BLCA tissues and adjacent normal tissues using data from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Additionally, we investigated the association between CENPW expression and patient prognosis. Furthermore, we performed in vitro and in vivo experiments to assess the impact of CENPW knockdown on various tumor biological phenotypes in BLCA. Finally, we conducted an analysis to elucidate the underlying mechanisms responsible for the observed phenotypic alterations in BLCA. Results: The expression of CENPW was found to be upregulated in BLCA, and its higher expression was associated with a poorer disease-specific survival (DSS). CENPW was found to have close associations with the cell cycle, mitosis, and DNA replication. In vitro and in vivo experiments demonstrated that the inhibition of CENPW led to a suppression of BLCA progression. Specifically, the knockdown of CENPW resulted in cell cycle arrest phase and induced apoptosis in BLCA by potentially inactivating the signal transducer and activator of transcription3 (STAT3) signaling pathway. Conclusion: CENPW has the potential to function as a molecular marker indicating an unfavorable prognosis in BLCA. Additionally, CENPW exhibits promise as a novel therapeutic target for BLCA.

Apoptosis as a common form of programmed cell death, plays a crucial role in tumor therapy. Celastrol and erianin are natural compounds extracted from plants. Celastrol exhibits cytotoxic effects on various tumor cells through mechanisms such as ferroptosis and apoptosis, while erianin significantly inhibits the growth and metastasis of cancer cells. However, the high toxicity of celastrol and the low water solubility of both compounds hinder their clinical applications. In this study, nanoparticles (CEN) self-assembled from celastrol and erianin were designed to enhance drug solubility and tumor-targeting capability. These nanoparticles significantly inhibited the proliferation of tumor cells while effectively killing the entire tumor cell population. Additionally, using activity-based protein profiling (ABPP) and a celastrol-probe (cel-p), Annexin A2 was identified as the target of celastrol in 4 T1 cells. Proteomics was subsequently used to evaluate the changes in protein expression induced by CEN. In a mouse model of breast cancer, CEN demonstrated superior tumor-targeting ability and prolonged action due to the enhanced permeability and retention (EPR) effect, resulting in better therapeutic efficacy with lower systemic toxicity. In conclusion, this study provides a novel reference for the treatment of breast cancer.

Natural killer (NK) cell therapy is emerging as a cancer treatment. NK cells are innate cytotoxic lymphocytes that act as first-line responders to kill target cells without prior encounters. NK cells recognize cancer cells, virus-infected cells, and other types of stressed cell through a reservoir of germline-encoded receptors. NK cells are safe for allogeneic applications. Therefore, they are the ideal off-the-shelf cell, which overcome the low efficiency issue caused by the patient-by-patient nature of autologous cell therapy. Unlike T cells, NK cells cannot form a strong immune memory; therefore, they suffer from short in vivo persistence. However, different from T cells, NK cells have a reservoir of innate immune receptors targeting a variety of malignant cells. In addition, they can utilize antibody guidance in target recognition. With suitable engineering, NK cells can function as universal anticancer drugs that are not restricted to HLA and cancer types, which will benefit the large cohort of patients with rare cancer types and patients with no convenient drug targets for precision and personalized medicine. Here, we summarize and discuss the designs of current anticancer NK cell therapies.

BACKGROUND:Attenuated live bacterial therapy and medical BSA materials have their own advantages in anti-cancer research, and their combination is expected to overcome some of the disadvantages of conventional anti-cancer therapeutics.METHODS AND OBJECTIVE:Utilizing the high affinity between biotin and streptavidin, BSA modification on the surface of Escherichia coli (E. coli) was achieved. Then, the adhesion and targeting abilities of BSA modified E. coli was explored on different bladder cancer cells, and the underlying mechanism was also investigated.RESULTS:BSA modification on the surface of E. coli enhances its ability to adhere and target cancer cells, and we speculate that these characteristics are related to the expression of SPARC in different bladder cancer cell lines.CONCLUSION:BSA and live bacteria have their own advantages in anti-cancer research. In this study, we found that E. coli surface-modified by BSA had stronger adhesion and targeting effects on bladder cancer cells with high expression of SPARC. These findings pave the way for the future studies exploring the combination of BSA combined with live bacteria for cancer therapy.

Accurate and precise localization of intracellular nucleic acids is crucial for regulating genetic information transcription and diagnosing diseases. Although intracellular nucleic acid imaging methods are available for various cell types, their widespread utilization is impeded by the intricate nature of the process and its exorbitant cost. Recently, numerous intracellular nucleic acid labeling techniques based on clustered regularly interspaced short palindromic repeats (CRISPR) have been established due to their modularity, flexibility, and specificity. In this work, we present various CRISPR methods that are currently employed for visualizing intracellular genomic sequences and RNA, based on their detection principles and application scenarios. Furthermore, we discuss the advantages and drawbacks of the existing CRISPR imaging methods, as well as future research directions. We anticipate that with continued refinement, more advanced CRISPR-based imaging techniques can be developed to better elucidate the localization and dynamics of intracellular nucleic acids, thereby providing a powerful tool for molecular biology research and clinical molecular pathology diagnosis.

Anti-cancer drugs with various mechanisms emerge in succession, but most of free therapeutics are accompanied by some disadvantages, such as poor safety and effectiveness, inability to target tumor cells, and short circulation time. Nanotechnology provides new solutions for overcoming the intrinsic limits of free therapeutics and navigating biological barriers. Considerable technological and clinical success have been achieved in cancer nanomedicines, but the main obstacle to the clinical translation of nanomedicine is an incomplete understanding of the requirements of clinical trials in new and established research scientists and the latest research of nanomedicine in clinicians. In this review, by searching the authoritative database, we introduce the progress and challenges of nanomedicines that have entered the clinical market or are ubiquitous in clinical trials for cancer therapy, including lipid-based nanoparticles, polymeric nanoparticles and albumin-based nanoparticles. Furthermore, we introduce several biomolecule-based nanomedicines that are promising for clinical application in the future, including biomimetic membranes, viruslike particles and DNA-based nanomachine, and highlight their advanced nanoparticle designs, advantages and challenges.

Abstract Objective: Validating the feasibility of surface modification of Escherichia coli (E. coli) with bovine serum albumin (BSA), and propose a approach of protein modification on living bacterial surface to to develop a new antitumor therapeutic strategy. Methods: Based on the advantages of live bacteria and albumin in drug delivery and antitumor therapy, E. coli and BSA were used as the live bacteria and target protein, respectively. Through the bridging action of biotin and streptavidin, the surface of E. coli was modified by BSA. To enhance the chemotaxis ability, tumor adhesion and targeting ability of E. coli vector, we report a new method of using living bacterial surface protein modification as a tool to develop a promising antitumor therapeutic strategy. Results: BSA modification on the surface of E. coli was feasible and enhanced the tumor targeting ability and adhesion capacity of E. coli to tumor cells. Conclusion: Protein modification on the surface of living bacteria was effective and easy, and the novel strategy would enable the development of a new model of live bacteria as anti-tumor therapy.

Cell therapy is a distinguished targeted immunotherapy with great potential to treat solid tumors in the new era of cancer treatment. Cell therapy products include genetically engineered cell products and non-genetically engineered cell products. Several recent cell therapies, especially chimeric antigen receptor (CAR)-T cell therapies, have been approved as novel treatment strategies for cancer. Many clinical trials on cell therapies, in the form of cell therapy alone or in combination with other treatments, in solid tumors, have been conducted or ongoing. However, there are still challenges since adverse events and the limited efficacy of cell therapies have also been observed. Here, we concisely summarize the clinical milestones of the conducted and ongoing clinical trials of cell therapy, introduce the evolution of CARs, discuss the challenges and limitations of these therapeutic modalities taking CAR-T as the main focus, and analyze the disparities in the regulatory policies in different countries.

The differential diagnosis of renal tumors and abscesses is crucial owing to their different treatments. Although antibacterial administration and radiological examination are excellent means for distinction, misdiagnosis is common and may lead to severe consequences, such as the need for nephrectomy. Here, we report a case involving a 52-year-old Asian woman with a renal mass for which a differential diagnosis was challenging. The mass persisted after administration of intravenous antibiotic therapy for 1 month. A computed tomography scan indicated an inflammatory lesion, whereas magnetic resonance imaging suggested a diagnosis of a tumor. Despite these indications, a right renal abscess was suspected during robot-assisted laparoscopic surgery, and nephron-sparing surgery was performed, which allowed confirmation of the final pathological result by biopsy specimen. Postoperatively, the mass gradually decreased in size after antibiotic therapy for a further month. This case, in which a renal abscess mimicked a tumor and the patient almost underwent a nephrectomy, highlights the need for caution in establishing therapeutic schedules for patients with inaccurate diagnoses. The management strategies for such patients must be reviewed and improved.