PAULINA CHMIEL^1,2, ALEKSANDRA SłOWIKOWSKA^1,2, ŁUKASZ BANASZEK^1,2, ANNA SZUMERA-CIEćKIEWICZ³, BARTłOMIEJ SZOSTAKOWSKI¹, MATEUSZ J. SPAłEK^1,4,*, TOMASZ ŚWITAJ¹, PIOTR RUTKOWSKI¹, ANNA M. CZARNECKA¹

Oncology Research, Vol.32, No.7, pp. 1141-1162, 2024, DOI:10.32604/or.2024.050350

Abstract Inflammatory myofibroblastic tumor (IMT) is a rare neoplasm with intermediate malignancy characterized by a propensity for recurrence but a low metastatic rate. Diagnostic challenges arise from the diverse pathological presentation, variable symptomatology, and lack of different imaging features. However, IMT is identified by the fusion of the anaplastic lymphoma kinase (ALK) gene, which is present in approximately 70% of cases, with various fusion partners, including ran-binding protein 2 (RANBP2), which allows confirmation of the diagnosis. While surgery is the preferred approach for localized tumors, the optimal long-term treatment for advanced or metastatic disease is difficult… More >

Baohong Yang^*1, Aiying Qin^†1, Kongyuan Zhang^‡, Haipeng Ren^*, Shuzhen Liu^*, Xiaolei Liu^§, Xiangpo Pan^¶, Guohua Yu^*

Oncology Research, Vol.25, No.9, pp. 1601-1606, 2017, DOI:10.3727/096504017X14928634401178

Abstract Epithelial growth factor receptor (EGFR) mutations are present in 10%–26% of non-small cell lung cancer (NSCLC) tumors and are associated with the response to tyrosine kinase inhibitors (TKIs). This study aimed to detect and quantify the presence of circulating tumor cells (CTCs) in EGFR-mutant NSCLC patients and investigate their possible role in providing prognostic information. Enrolled patients received erlotinib (150 mg) or gefitinib (250 mg) orally once daily as the first-line treatment. Serial blood samples were taken at baseline (CTC-d0) and on day 28 (CTC-d28) following the initiation of erlotinib/gefitinib for detection of CTCs using… More >

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… 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 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 More >