Oncology Research Editorial Office

Oncology Research, Vol.32, No.8, pp. 1377-1377, 2024, DOI:10.32604/or.2024.055033

Abstract This article has no abstract. More >

XIAOBI HUANG^1,#, CHUNYUAN CHEN², YONGYANG CHEN^1,#, HONGLIAN ZHOU¹, YONGHUA CHEN¹, ZHONG HUANG¹, YULIU XIE¹, BAIYANG LIU¹, YUDONG GUO¹, ZHIXIONG YANG¹, GUANGHUA CHEN^3,*, WENMEI SU^1,4,*

Oncology Research, Vol.32, No.7, pp. 1185-1195, 2024, DOI:10.32604/or.2023.030771

Abstract Background: Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes. Their dysregulation has been closely associated with tumorigenesis. LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer. However, the mechanism underlying its function in cancer progression remains poorly understood. Methods: Here, the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines, clinical samples, and xenografts. Results: We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients, whereas knockdown of LINC00265 inhibited proliferation… More >

Iftikhar Naseer^1,2, Tehreem Masood^1,2, Sheeraz Akram^3,*, Zulfiqar Ali⁴, Awais Ahmad³, Shafiq Ur Rehman³, Arfan Jaffar^1,2

CMC-Computers, Materials & Continua, Vol.79, No.3, pp. 4963-4977, 2024, DOI:10.32604/cmc.2024.050204

Abstract Lung cancer is a leading cause of global mortality rates. Early detection of pulmonary tumors can significantly enhance the survival rate of patients. Recently, various Computer-Aided Diagnostic (CAD) methods have been developed to enhance the detection of pulmonary nodules with high accuracy. Nevertheless, the existing methodologies cannot obtain a high level of specificity and sensitivity. The present study introduces a novel model for Lung Cancer Segmentation and Classification (LCSC), which incorporates two improved architectures, namely the improved U-Net architecture and the improved AlexNet architecture. The LCSC model comprises two distinct stages. The first stage involves… More >

Mutasem K. Alsmadi^*

CMC-Computers, Materials & Continua, Vol.79, No.3, pp. 5175-5200, 2024, DOI:10.32604/cmc.2024.044065

Abstract Lung cancer is among the most frequent cancers in the world, with over one million deaths per year. Classification is required for lung cancer diagnosis and therapy to be effective, accurate, and reliable. Gene expression microarrays have made it possible to find genetic biomarkers for cancer diagnosis and prediction in a high-throughput manner. Machine Learning (ML) has been widely used to diagnose and classify lung cancer where the performance of ML methods is evaluated to identify the appropriate technique. Identifying and selecting the gene expression patterns can help in lung cancer diagnoses and classification. Normally,… More >

Huang Li, Li Fang, Deng Pengbo, Hu Chengping

Oncology Research, Vol.24, No.6, pp. 405-413, 2016, DOI:10.3727/096504016X14685034103437

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More >

Wang Weihua, Chen Jie, Dai Jinhua, Zhang Burong, Wang Feng, Sun Yizhe

Oncology Research, Vol.24, No.5, pp. 345-351, 2016, DOI:10.3727/096504016X14685034103194

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More >

Xuexin Gao^*, Xuezhen Gao^†, Chao Li^*, Yukun Zhang^*, Lei Gao^‡

Oncology Research, Vol.24, No.5, pp. 337-343, 2016, DOI:10.3727/096504016X14666990347671

Abstract Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G₀/G₁ phase in More >

Yaqiong Tian^*1, Zengli Zhang^†1, Liyun Miao^*, Zhimin Yang^‡, Jie Yang^*, Yinhua Wang^§, Danwen Qian^¶, Hourong Cai^*, Yongsheng Wang^*

Oncology Research, Vol.24, No.5, pp. 295-303, 2016, DOI:10.3727/096504016X14648701447814

Abstract Recently, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have revolutionized nonsmall cell lung cancer (NSCLC) treatment. However, resistance remains a major obstacle. Anexelekto (AXL) is a member of receptor tyrosine kinases (RTKs) and shares the same downstream signaling pathways with EGFR, such as PI3K/AKT and MAPK/ERK. AXL overexpression in resistant tumors has been implicated in many previous studies in vitro and in vivo. In this study, we further examined whether expression of AXL and its downstream targets increased in gefitinib-resistant PC9 cells (PC9GR). In addition, we hypothesize that knocking down AXL in PC9GR and… More >

Xuguang Wang^*, Zhe Chen^†

Oncology Research, Vol.24, No.4, pp. 271-277, 2016, DOI:10.3727/096504016X14666990347473

Abstract Cullin 4B (CUL4B), a scaffold protein that assembles CRL4B ubiquitin ligase complexes, was found to be overexpressed in many types of tumors. However, the expression pattern and role of CUL4B in non-small cell lung cancer (NSCLC) remain largely unknown. Therefore, in the present study, we investigated the role of CUL4B in NSCLC, and the underlying mechanism was also explored. Our results showed that CUL4B was highly expressed in NSCLC cell lines. Silencing CUL4B obviously inhibited proliferation and migration/invasion of NSCLC cells, and it also suppressed the epithelial–mesenchymal transition (EMT) progress in NSCLC cells. Furthermore, knockdown More >

Shengchao Zhang, Jun Yuan, Ruheng Zheng

Oncology Research, Vol.24, No.4, pp. 263-269, 2016, DOI:10.3727/096504016X14666990347392

Abstract Recently, deubiquitinating enzymes (DUBs) are emerging as new regulators in cancer progression. However, understanding of the involvement of DUBs in non-small cell lung cancer (NSCLC) is just beginning. In this study, we investigated the expression and biological function of ubiquitin-specific peptidase 17 (USP17) in NSCLC progression in vitro and in vivo. We found that the expression of USP17 was higher than in a normal control. We further efficiently depleted USP17 expression in two different NSCLC cells, A549 and H1299. The anchorage-independent growth ability of these cells, estimated by soft agar colony formation assay, was significantly More >