Yinling Hu

Abstract Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy; however, their use is frequently associated with immune-related adverse events (irAEs). In this study, anti-PD-L1 therapy exacerbates muscle wasting in tumor-bearing male mice despite its anti-tumor efficacy, accompanied by an accumulation of CD8+ T cells in muscle. Single-cell RNA sequencing identifies these cells as tissue-resident memory-like CD49a+ CD8+ T cells.

Abstract Pancreatic ductal adenocarcinoma (PDAC) emerges from mutant KRAS-harboring but dormant low-grade pancreatic intraepithelial neoplasia (PanIN). To examine the role of oxidative stress, a putative PDAC risk factor, we established an organoid-based transformation system. Although the prototypic oxidant H2O2 induced organoid transformation, its effect was nonmutational and was mediated by the oxidant-responsive transcription factor NRF2, which induced the histone methyltransferase EZH2.

1. Introduction Human lung cancer is still a leading cause of cancer mortality. Non-small cell lung carcinoma (NSCLC), which represents 80–90% of human lung cancer, includes lung adenocarcinoma (ADC) (50%), squamous cell carcinoma (SCC) (35%), and large cell carcinoma (15%) [1]. Lung SCC and ADC derive from different lung epithelial cells and exhibit distinct causes, morphology, and gene expression patterns [1,2,3,4].