CD70, a member of the tumor necrosis factor family, has been implicated in various cellular processes associated with tumorigenesis. Despite its known expression in certain cancers, a detailed pan-cancer analysis and functional validation in clear cell renal cell carcinoma (ccRCC) have not been comprehensively explored. We conducted a pan-cancer analysis using publicly available databases to investigate the expression and prognostic significance of CD70 across various cancer types. For functional validation, immunohistochemistry was performed on ccRCC and adjacent normal tissues to evaluate CD70 expression levels. Additionally, ccRCC organoid model was developed and subjected to CAR-T cell cytotoxicity assays to evaluate the efficacy of targeting CD70 in vitro. The pan-cancer analysis revealed elevated expression of CD70 in several cancer types, including ccRCC, where it correlated with poor prognosis. Immunohistochemical analysis confirmed significant overexpression of CD70 in ccRCC tissues compared to normal tissues. In the ccRCC organoid model, CAR-T cells targeting CD70 demonstrated effective cytotoxicity against organoids expressing CD70. The overexpression of CD70 across diverse cancer types underscores its potential as a universal biomarker. Importantly, our findings underscore the clinical relevance of CD70 as a critical oncogenic factor and a promising therapeutic target in ccRCC, with implications for advancing personalized medicine.

Studies have shown that the circulating tumor cell (CTC) is a necessary condition for the invasion and distant metastasis of renal cell carcimona (RCC). However, few CTCs-related gene mutations have been developed which could promote the metastasis and implantation of RCC. The objective of this study is to explore the potential driver gene mutations that promote RCC metastasis and implantation based on CTCs culture. Fifteen patients with primary mRCC and three healthy subjects were included, and peripheral blood was obtained. After the preparation of synthetic biological scaffolds, peripheral blood CTCs were cultured. Successful cultured CTCs were applied to construct CTCs-derived xenograft (CDX) models, followed by DNA extraction, whole exome sequencing (WES) and bioinformatics analysis. Synthetic biological scaffolds were constructed based on previously applied techniques, and peripheral blood CTCs culture was successfully performed. We then constructed CDX models and performed WES, and explored the potential driver gene mutations that may promote RCC metastasis and implantation. Bioinformatics analysis showed that KAZN and POU6F2 may be closely related to the prognosis of RCC. We successfully performed the culture of peripheral blood CTCs and, on this basis we initially explored the potential driver mutations for the metastasis and implantation of RCC.

Aim: Tumor flare reaction (TFR) is characterized by an increase in tumor size during immunotherapy, often resembling disease progression. This study explores the relationship between anti‐tumor drugs and tumor flare reaction (TFR) through the FAERS database to assist clinicians in better patient management. Methods: We analyzed the FAERS database to identify TFR cases reported from Q1 2004 to Q3 2024. For signal detection, we employed disproportionality analysis with four algorithms—reported odds ratio (ROR), proportional reporting ratio (PRR), Bayesian confidence propagation neural network (BCPNN), and empirical Bayes geometric mean (EBGM). These algorithms assessed statistical correlations between anticancer drugs and TFR, based on a 2 × 2 contingency table framework. Results: From Q1 2004 to Q3 2024, 566 TFR cases were recorded in the FAERS database. The incidence of TFR peaked in 2023, with the highest increase in cases from 2021 to 2022, at 4.9%. A total of 28 anticancer drugs were identified as strongly associated with TFR, of which only 4 are explicitly listed in the medication instructions as having TFR‐related adverse reactions. Lenalidomide was the most frequent drug causing TFR, accounting for 38% of all TFR reports. Conclusions: Our findings highlight the key associations between treatment drugs and TFR, particularly targeted therapies such as Rituximab, which are not explicitly marked for this side effect in the FAERS database. The study emphasizes the need for clinicians to closely monitor TFR in patients receiving certain cancer treatments and improve therapeutic strategies to mitigate TFR risks, ensuring safer cancer treatment outcomes.

Primary aldosteronism (PA) is a leading cause of secondary hypertension, but the lack of representative preclinical models hampers translational research and imaging evaluation. We aimed to establish a patient-derived organoids-based xenograft (PDOX) model of PA and to assess its imaging characteristics using [18F]AlF-NOTA-pentixather PET/CT, with validation in clinical patients. Adrenal tissues from patients with PA were used to generate adrenal organoids in vitro. After serial passaging, these organoids were implanted subcutaneously into immunodeficient mice to establish PA PDOX models. The xenografted mice were subjected to [18F]AlF-NOTA-pentixather PET/CT to evaluate tracer uptake and lesion detectability. In parallel, clinical PA patients underwent [18F]AlF-NOTA-pentixather PET/CT to assess the imaging performance in a clinical setting. The PDOX models successfully engrafted and proliferated in vivo, maintaining key pathological features of PA. [18F]AlF-NOTA-pentixather PET/CT imaging in the PDOX models demonstrated high and specific tracer uptake in xenografted lesions, with strong concordance to histopathological findings. In clinical PA patients, [18F]AlF-NOTA-pentixather PET/CT also showed excellent performance in localizing PA lesions and provided valuable diagnostic information. We established a novel PDOX model of PA and demonstrated the effectiveness of [18F]AlF-NOTA-pentixather PET/CT in both preclinical and clinical applications. This approach provides a robust translational platform for mechanistic studies and for advancing precision imaging and therapy in PA.