Kidney Cancer

GPNMB serves as an important auxiliary marker for diagnosis of FLCN-mutation-associated low-grade eosinophilic renal tumors. Clinical, molecular, and genetic testing should be integrated to assess potential association with BHD syndrome, for making a precise diagnosis.

Functional status and symptom control were maintained in most patients during treatment, based on routine clinical assessment. These findings suggest that cabozantinib may represent a clinically meaningful treatment option for selected patients with metastatic chRCC and support its further evaluation in this rare disease subtype.

These differences may reflect the limitations of body mass index as a biological indicator of obesity, together with variations in systemic inflammation, body composition, and treatment context. Here, we summarize current knowledge on obesity-driven immunometabolic rewiring in RCC and outline key priorities for the field, including obesity-relevant preclinical models, biomarkers of visceral adiposity and systemic inflammation, and clinical trials targeting immunometabolism.

The patient underwent radical nephrectomy followed by biomarker-guided FLOT (fluorouracil, leucovorin, oxaliplatin, and docetaxel) chemotherapy combined with camrelizumab immunotherapy, achieving a progression-free survival of approximately 7 months, accompanied by a temporary decline in tumor markers. Therapeutically, while the identified biomarker provided a rationale for precision therapy, the resulting clinical benefit was limited and transient. This suggests that the aggressive biology and spatial heterogeneity typical of CUP can attenuate the long-term efficacy of biomarker-guided interventions.

Although 66.3% reported familiarity with the WHO classification, 33.6% cited barriers such as rapid updates, financial constraints, and workload.ConclusionsMarked global disparities persist in renal tumor diagnostics. While IHC is widely accessible, advanced molecular tools and novel biomarkers remain unevenly distributed, underscoring the need for targeted educational and resource-sharing strategies.

PRSS is a rare malignant tumor with a poor prognosis that presents significant diagnostic challenges. Our immunohistochemical panel (SS18-SSX, TLE1, INI1) enhances diagnostic accuracy and may assist in the triage of cases requiring molecular confirmation.

The report underlines the importance of genetic evaluation and long-term surveillance for patients and at-risk relatives. Genetic testing for the FLCN (Folliculin) gene was initiated and results were consistent with Birt-Hogg-Dubé syndrome.

P2, N=146, Recruiting, Jinling Hospital, China

MMP-2 rs243865, particularly the TT genotype, may serve as a genetic susceptibility marker for RCC and may interact with lifestyle and clinical factors including smoking, alcohol drinking, and hypertension. Further large-scale studies are warranted to validate these observations and clarify the biological mechanisms underlying MMP-2-mediated RCC carcinogenesis.

Grade 3-4 treatment-emergent adverse events occurred in 46.8% of patients, and treatment discontinuation due to toxicity was reported in 6.5%. These findings demonstrate that cabozantinib plus nivolumab provides clinically meaningful and durable antitumor activity with manageable toxicity across diverse histologic subtypes in advanced nccRCC, supporting further prospective evaluation of cabozantinib plus nivolumab in advanced nccRCC.

In this Mini Review, we summarize the current treatment landscape of MRTK, examine why conventional multimodal therapy remains necessary but insufficient, discuss the preclinical model landscape that supports therapeutic translation, and define major priorities required to move the field toward renal-specific precision care. We argue that the next meaningful advance will depend on collaborative trials that integrate molecular profiling, faithful experimental models, rational combinations, and correlative biomarker studies from diagnosis onward.

Using the Seahorse XFe96 analyzer we also showed reduced glycolytic capacity and reserve in RCC4-ATF4 KO cells. Collectively, our results demonstrate that ATF4 regulates glycolysis in ccRCC, supporting ATF4 as a therapeutic target.