Genito-urinary Cancer

These results indicate useful properties of red deer antler stem cell culture medium that can control molecular and cellular mechanisms that halt carcinogenesis. All these can be considered targets for further cancer stem cell treatment or cancer diagnostic improvements.

Moreover, FlcnLiKO mice are more prone to develop diethylnitrosamine (DEN)- or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)- induced liver tumors with heterogenous histological features. Notably, depletion of TFE3, but not TFEB, in the liver of FlcnLiKO mice fully rescues the cancer phenotype and normalized mTORC1 signaling, highlighting TFE3 as the primary driver of liver cancer and mTORC1 hyperactivity in the absence of FLCN.

Although study of additional cases is necessary, these findings suggest that the downstream effects of TFE3-rearrangement are different in PHF1::TFE3-rearranged OFMTs, compared to other known TFE3-rearranged neoplasms. TFE3-rearranged OFMTs are epigenetically distinct, implying that the impact of TFE3-rearrangement may be lineage-dependent.

Research in bladder cancer investigates the role of activating transcription factor 3, known for its anti-tumor properties, and its link to metformin...Additional studies present a novel intervention approach for autoimmune diseases, advancements in artificial bone grafts to enhance bone regeneration, and the benefits of public hospital participation in oncological clinical trials. Finally, a study confirms the suitability of transthoracic echocardiography for diagnosing suspected acute aortic syndrome.

We found that high expression of CK17 promoted the proliferation, migration and invasion of bladder cancer cells and induced EMT through AKT-Ser473 phosphorylation. These findings suggest that CK17 is significantly associated with malignant progression and poor prognosis of bladder cancer patients, and it may become a new biological target for bladder cancer treatment.

Our research shed light on the controversial and tumor-specific role of HSP70s. More in detail, we have identified HSPA8 and HSPA9 as potential prognostic and therapeutic targets involved in several biological processes leading to tumorigenesis, including nucleic acid maturation, cell signaling, vesicle trafficking, mitochondrial structure and function, and protein maturation.

Our findings suggest that combining Orai3 downregulation with autophagy inhibition may enhance the efficacy of oxaliplatin in treating prostate cancer. This combinatorial approach could hold potential for overcoming resistance and improving therapeutic outcomes.

Especially, C2 showed superior efficacy against ARF877L/T878A mutants compared to darolutamide and enzalutamide. Furthermore, C2 demonstrated excellent oral bioavailability, indicating the potential to enhance in vivo efficacy and to serve as a promising therapeutic option for PCa treatment.

YKL-40 was associated with the risks of liver and bladder cancers, clearly outperforming CRP for these cancers. This suggests distinct prognostic roles for YKL-40 and CRP, and highlights YKL-40 as a promising biomarker for liver cancer.

These findings reveal promising biomarkers and mechanistic insights, offering a new perspective on predicting ICI response and opening up exciting possibilities for more personalized immunotherapy strategies in NSCLC and MIBC.

Our comprehensive approach provides a novel tool to identify disease-relevant functions of genes of interest (GOI) in large datasets. This integrated approach offers a valuable framework for understanding the role of the expression variation of a GOI in complex diseases and for informing on targeted therapeutic strategies.

In this first report to quantify FAP protein in benign prostate and primary tumours, using standard large tissue sections, we clarify that FAP is present in all primary prostatic carcinomas, supporting its potential clinical relevance. The finding of high levels of FAP within PIA supports the injury/regeneration model for its pathogenesis and suggests that it harbours a protumourigenic stroma, yet ​high levels of FAP in benign regions could lead to false-positive FAP-based molecular imaging results in clinically localised prostate cancer.

Our study reports the first CD28 bsAb targeting Nectin-4 and highlights the potential of CD28 × Nectin-4 bsAbs as a new immunotherapeutic modality. The findings support the clinical development of RNDO-564 in patients with locally advanced and metastatic UC and other Nectin-4 positive malignancies.

The identification of fisetin as a NUF2 inhibitor offers a promising therapeutic strategy for targeting NUF2 to impede PCa growth. NUF2 may thus serve as a valuable prognostic biomarker and a potential therapeutic target for PCa.

KIF14 down-regulates cell cycle proteins CyclinD1 and CDK4 to facilitate the proliferation of ccRCC cells, suggesting its potential as a therapeutic target and prognostic biomarker in ccRCC.

Survival curve analysis revealed that a decrease in CD4 + T, CD8 + T and CD3 + T cells after surgery led to a decrease in the survival rate of patients, but the results were not statistically significant. CD4 + T, CD8 + T and CD3 + T cells decreased before and after surgery in patients with malignant tumors of the urinary system complicated with AIDS, and CD8 + T cells had a statistically significant effect on patient prognosis compared with other immune indices.

Notably, STEAP proteins are recognized as potential biomarkers and therapeutic targets in human cancers, particularly prostate cancer. This review outlines the structural features and functional roles of STEAP proteins in various diseases, including cancers, insulin resistance, non-alcoholic fatty liver disease (NAFLD), and benign prostatic hyperplasia, with a focus on their potential for therapeutic intervention.

The cytotoxic effects of rosmarinic acid@Se-TiO2-GO nanoparticles on prostate cancer cells appear to be mediated through the generation of oxidative stress and induction of apoptosis. The unique formulation of these nanoparticles holds promise for future prostate cancer treatment strategies.

In comparison with TIMP1-overexpressing cells, TIMP1-knockdown cells demonstrated a 12.3% decrease in Fe2+ concentration after erastin treatment, a 37.8% reduction in malondialdehyde (MDA) levels, an 113.7% increase in GPX4 expression, and a 78.9% rise in the GSH/GSSG ratio. Our findings indicate that TIMP1 overexpression promotes ferroptosis by modulating critical markers such as GPX4 and TFRC, thereby significantly reducing metastatic potential in prostate cancer cells. Our results highlight TIMP1's role in regulating ferroptosis pathways, which are crucial for tumor progression, and exposes a potential therapeutic target for prostate cancer management.

This facilitates delivery of eukaryotic initiation factor 6 (eIF6), a key 60S biogenesis factor, which binds to CRNDEUCE through a sequence element adjacent to the UCE. These findings highlight the functional versatility of snoRNA sequences and expand the known mechanisms through which noncoding RNAs orchestrate ribosome biogenesis.

Differences in the ratios of GG/GC and GG/(GC+CC) genotypes also suggested a potential association between the C allele and PCa (p-value <0.1), and the combined affected (PCa+BPH) group (p-value <0.04). The small sample size and sampling from one ethnic group are limitations of this study.

P1, N=269, Completed, Exelixis | Active, not recruiting --> Completed

P=N/A, N=14000, Completed, Fondazione del Piemonte per l'Oncologia | Recruiting --> Completed

P2, N=25, Completed, Ohio State University Comprehensive Cancer Center | Active, not recruiting --> Completed

P3, N=387, Completed, Sumitomo Pharma Switzerland GmbH | Active, not recruiting --> Completed

P2, N=15, Recruiting, University of Texas Southwestern Medical Center | Not yet recruiting --> Recruiting

P3, N=522, Completed, Hoffmann-La Roche | Active, not recruiting --> Completed

P=N/A, N=60, Recruiting, Western University, Canada | Not yet recruiting --> Recruiting

In addition to uncovering a prominent role for VAV2-Rac1 as an effector pathway mediating EGFR-driven proliferative and migratory responses in prostate cancer cells, our findings underscore the potential prognostic value of VAV2 in human prostate cancer progression. Implications: This study highlights VAV2's central role in prostate cancer cell proliferation and migration and its potential prognostic value in disease progression.

Findings are consistent with the hypothesis of altered tumorigenesis for cancers developing in an environment of immunosuppression.

PD-1-positive TIIC score of TN and tumor necrosis may efficiently predict recurrence in pT1b ccRCC.

This review focuses on these probes, their biologic targets, and the applications or potential applications for their use in the assessment of various neoplasms, including both probes available for commercial use-such as somatostatin receptor ligands in neuroendocrine tumors, prostate-specific membrane antigen ligands in prostate cancer, norepinephrine analogs in neural crest tumors like neuroblastoma, and estrogen analogs in breast cancer-and others in clinical development, such as fibroblast-activating protein inhibitors, C-X-C chemokine receptor type 4 ligands, and monoclonal antibodies targeting receptor tyrosine kinases, CD4-positive or CD8-positive tumor-infiltrating lymphocytes, tumor-associated macrophages, and cancer stem cell biomarkers. These developments represent a major step toward the integration of molecular imaging as a powerful tool in precision medicine, with an expectedly significant impact on patient management and outcome.

Finally, gene-disease and gene-drug association, highlighted correlated diseases and their promising inhibitors. In conclusion, the identified novel biomarkers and associated pathways, provides a comprehensive insight into the molecular mechanisms, prognosis, and potential clinical applications for the diagnosis and therapeutic interventions of ACC.

The addition of the ROS inhibitor N-acetylcysteine (NAC) upregulated the expression level of Bcl-2 protein, decreased p38 phosphorylation, increased ERK phosphorylation and restored the levels of PI3K and p-mTOR after ChA treatment. These suggest that ChA induces apoptosis by regulating oxidative stress, MAPK, and PI3K-AKT-mTOR signaling pathways in T-24 cells.

TGFb1 levels in urine after PN are related to the number of sutures. Reduced number of sutures in tumor bed has a positive effect on short term eGFR changes possibly by reducing tumor bed fibrogenic healing response as well as preserving renal parenchymal volume.

Our findings underscore the importance of targeting IL-8 as a therapeutic strategy to overcome treatment resistance and improve outcomes for urological cancer patients. Further research into IL-8-targeted therapies and their integration into clinical practice is urgently needed to enhance the treatment landscape for urological cancers.

In Chinese populations, PCa risk and clinical features may result from individual genes, gene-gene interactions, and gene-environment interactions. These findings provide important insights into the relationship between genetic susceptibility and PCa risk in Chinese men.

P1/2, N=47, Recruiting, University of California, San Francisco | Not yet recruiting --> Recruiting

P1, N=15, Recruiting, South Metropolitan Health Service | Not yet recruiting --> Recruiting

P=N/A, N=1950, Recruiting, Australian and New Zealand Urogenital and Prostate Cancer Trials Group | Not yet recruiting --> Recruiting

P3, N=280, Active, not recruiting, University Medical Center Groningen | Recruiting --> Active, not recruiting | Trial completion date: Dec 2024 --> Dec 2027 | Trial primary completion date: Dec 2024 --> Oct 2027

P=N/A, N=4500, Enrolling by invitation, Fondazione del Piemonte per l'Oncologia | Not yet recruiting --> Enrolling by invitation | Trial primary completion date: Jan 2026 --> Jun 2026