KAIWEN TIAN^#, HANZHONG CHEN^#, QIANQIAN WANG, FENGLIAN JIANG, CHUNXIANG FENG, TENG LI, XIAOYONG PU, YANLIN TANG^*, JIUMIN LIU^*

BIOCELL, Vol.48, No.5, pp. 817-834, 2024, DOI:10.32604/biocell.2024.048737

Abstract Background: The incidence of clear cell renal cell carcinoma (ccRCC) is globally high; however, despite the introduction of innovative drug therapies, there remains a lack of effective biomarkers for evaluating treatment response. Recently, Caspase recruiting domain-containing protein 11 (CARD11) has garnered attention due to its significant association with tumor development and the immune system. Methods: The expression of CARD11 mRNA and protein in ccRCC were analyzed by public database and immunohistochemistry. The focus of this study is on the epigenomic modifications of CARD11, its expression of ccRCC immunophenotype, and its correlation with response to immunotherapy and targeted therapy. Furthermore, to… More > Graphic Abstract

WEIXUE WANG^#, TONGTONG WANG^#, YAN ZHANG, TING DENG, HAIYANG ZHANG^*, YI BA^*

Oncology Research, Vol.32, No.3, pp. 489-502, 2024, DOI:10.32604/or.2023.046676

Abstract Different from necrosis, apoptosis, autophagy and other forms of cell death, ferroptosis is a mechanism that catalyzes lipid peroxidation of polyunsaturated fatty acids under the action of iron divalent or lipoxygenase, leading to cell death. Apatinib is currently used in the third-line standard treatment of advanced gastric cancer, targeting the anti-angiogenesis pathway. However, Apatinib-mediated ferroptosis in vascular endothelial cells has not been reported yet. Tumor-secreted exosomes can be taken up into target cells to regulate tumor development, but the mechanism related to vascular endothelial cell ferroptosis has not yet been discovered. Here, we show that exosomes secreted by gastric cancer… More >

Xinwen Wang, Fupeng Zhang, Xi Yang, Meiping Xue, Xiaoli Li, Yu Gao, Likun Liu

Oncology Research, Vol.27, No.8, pp. 871-877, 2019, DOI:10.3727/096504018X15426271404407

Abstract Second-generation irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), afatinib, has been approved for treating EGFR mutant lung cancer patients, but the mechanism of acquired resistance to afatinib has not been well studied. In this study, we established afatinib acquired resistant cell lines. Gene array technology was used to screen changes in gene expression between afatinib-resistant lung cancer cells and parental cells. Our results showed that secreted phosphoprotein 1 (SPP1) was significantly increased in afatinib-resistant lung cancer cells. To study the effect of SPP1 on afatinib resistance, siSPP1 was used to knock down SSP1 in afatinib-resistant lung cancer… More >