Kidney Cancer

In contrast, under standard low-Cu conditions, CTR1 remains required for cellular Cu uptake and CuCOX metallation. Together, these findings define context-dependent Cu trafficking pathways in renal cancer and establish SEC-ICP-MS as a sensitive platform for assessing CuCOX metallation and mitochondrial metabolism, with potential applications in biomarker discovery and therapeutic targeting in RCC.

All patients with follow-up data were alive without evidence of disease progression. Our findings expand the clinical, histologic, immunohistochemical, and molecular spectrum of ELOC-mutated RCC and further support its classification as a distinct renal neoplasm.

Third, we perform a cistrome-wide association study in ccRCC, validating five established RCC risk loci and identifying six novel loci, including a locus at 12q24 linked to SCARB1 that was functionally validated. These datasets provide new perspectives on the role of developmental pathways in ccRCC tumorigenesis, insights into epigenetic mechanisms of ccRCC heritability, and a comprehensive epigenomic atlas for the research community.

P1/2, N=83, Recruiting, Essen Biotech

P=N/A, N=91, Completed, Institute of Oncology Ljubljana

Next-generation sequencing-based molecular profiling had clinical utility in two-thirds of patients, and the greatest benefit was within the broad category of ccRCN. Our results suggest that GPNMB expression was helpful in separating ELOC-RCCfms from M/TSC-RCCfms. Other benefits of NGS include subtyping high-grade RCC/RCC type not otherwise specified and identification of rare phenotypes.

Given the role of sex hormones in metabolic regulation, we examined the expression of estrogen (ER), androgen (AR), and progesterone (PR) receptors...The dedifferentiation and browning of adipocytes, altered adipocytokine expression, and increased lactate production observed in hRAN reflect the metabolic stress imposed by the tumor environment. Here, we provide evidence, using an ex vivo model, of a dynamic partnership between human adipose tissue and ccRCC tumors.

RARγ also acts as a co-factor to Smad3 and reduced or enhanced TGFβ-driven and Smad3-mediated events when liganded and non-liganded, respectively. Collectively the findings support the view that RARγ plays a crucial role in controlling stem and progenitor cell behavior.

Macrophage CD68 staining in the tubulointerstitial area increased and was associated with clinical and laboratory parameters such as eGFR and proteinuria. Additionally, MEST-C histological parameters, such as segmental glomerulosclerosis (S0/S1), tubular atrophy/interstitial fibrosis (T0/T1/T2), and crescents (C0/C1/C2), were associated with a higher number of CD68+ cells.

These findings led to the diagnosis of primary renal adenosarcoma. This case highlights the diagnostic challenge of distinguishing this rare tumor from more common renal malignancies and underscores the importance of imaging-pathologic correlation.

Notably, targeting CDK13 with the small-molecule inhibitor 1NM-PP1 potentiates METTL16 depletion-mediated anticancer effects. Our findings establish a kinase-RNA modifier axis that links CDK13 to epitranscriptomic control of lipid metabolism, positioning the CDK13-METTL16-ACLY pathway as a promising target for precision therapies against ccRCC.

Additionally, a cell-permeable peptide has been designed to disrupt the ternary complex and inhibit ccRCC progression in tumor cells and patient-derived xenografts. Thus, our findings not only provide new insights into the prominent role of PRAME in mediating C/EBPβ and EZH2 regulation of NTN4 and tumor metastasis, but also highlight a promising strategy for ccRCC therapy by targeting the C/EBPβ-PRAME-EZH2 complex.