Majed Al Fayi^*†, Ahmad Alamri^*, Prasanna Rajagopalan^*†

Oncology Research, Vol.28, No.2, pp. 177-189, 2020, DOI:10.3727/096504019X15746768080428

Abstract Drug discovery research to fight lung cancer is incessantly challenged by drug resistance. In this study, we used drug-resistant lung cancer stem like cells (A549-CS) to compare the efficacy of standard drugs like cisplatin (DDP) and gemcitabine (GEM) with a novel arylidene derivative IOX-101. A549-CS was derived from regular A549 cells by growing in special media. Resistance proteins were detected using Western blotting. Cell proliferations were assessed by MTT assay. Cytokine release was enumerated using enzyme-linked immunosorbent assay. The effect of drugs on apoptosis and cell cycle was studied with flow cytometry protocols. Apoptosis-related proteins, caspases, and other signaling protein… More >

Nahathai Dukaew^*†, Teruaki Konishi^‡§, Kongthawat Chairatvit^¶, Narongchai Autsavapromporn^#, Noppamas Soonthornchareonnon^**, Ariyaphong Wongnoppavich^†

Oncology Research, Vol.28, No.2, pp. 161-175, 2020, DOI:10.3727/096504019X15736439848765

Abstract Radiotherapy (RT) is an important treatment for non-small cell lung cancer (NSCLC). However, the major obstacles to successful RT include the low radiosensitivity of cancer cells and the restricted radiation dose, which is given without damaging normal tissues. Therefore, the sensitizer that increases RT efficacy without dose escalation will be beneficial for NSCLC treatment. Eurycomalactone (ECL), an active quassinoid isolated from Eurycoma longifolia Jack, has been demonstrated to possess anticancer activity. In this study, we aimed to investigate the effect of ECL on sensitizing NSCLC cells to X-radiation (X-ray) as well as the underlying mechanisms. The results showed that ECL… More >

ZiJun Liao^*†, Qi Zheng^†, Ting Wei^‡, YanBing Zhang^†, JieQun Ma^†, Zheng Zhao^§, HaiFeng Sun^§, KeJun Nan^*

Oncology Research, Vol.28, No.2, pp. 147-159, 2020, DOI:10.3727/096504019X15732109856009

Abstract MicroRNAs (miRNAs) play crucial roles in tumorigenesis and tumor progression. miR-561 has been reported to be downregulated in gastric cancer and affects cancer cell proliferation and metastasis. However, the role and underlying molecular mechanism of miR-561 in human non-small cell lung cancer (NSCLC) remain unknown and need to be further elucidated. In this study, we discovered that miR-561 expression was downregulated in human NSCLC tissues and cell lines. The overexpression of miR-561 inhibited NSCLC cell proliferation and cell cycle G1 /S transition and induced apoptosis. The inhibition of miR-561 facilitated cell proliferation and G1 /S transition and suppressed apoptosis. miR-561… More >

Lu, Xiaoqin¹, Wang, Fuying¹, Fu, Meizhou², Li, Yuankun¹, Wang, Lijun¹

Oncology Research, Vol.28, No.2, pp. 135-146, 2020, DOI:10.3727/096504019X15719983040135

Abstract This article was wihdrawn by the authors with the following Withdrawal Statement - The integrity of the current study is not acceptable. The authors intend to enrich the study to make it more valuable. Thus, the authors want to withdraw the current study. Please accept our apologies for this inconvenience and we hope for your understanding. Yours sincerely (on behalf of the authors), Xiaoqin Lu. More >

Jianping Xu, Xiaoyan Liu, Sheng Yang, Yuankai Shi

Oncology Research, Vol.28, No.2, pp. 127-133, 2020, DOI:10.3727/096504019X15707896762251

Abstract Apatinib, an oral small molecular receptor tyrosine kinase inhibitor (TKI) developed first in China, exerts antiangiogenic and antineoplastic function through selectively binding and inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2). In this study, we aimed to explore the efficacy and safety profile of apatinib monotherapy, or combined with chemotherapy or endothelial growth factor receptor (EGFR)-TKI in heavily pretreated non-small cell lung cancer (NSCLC) patients with brain metastases. We performed a retrospective analysis for relapsed NSCLC patients with brain metastases from our institute, who received apatinib (250 mg or 500 mg p.o. qd) monotherapy, or combination with EGFR-TKI or chemotherapy… More >

Xiuhua Weng^*1, Shaohong Luo^*1, Shen Lin^*, Lixian Zhong^†, Meiyue Li^*, Rao Xin^*, Pinfang Huang^*, Xiongwei Xu^*

Oncology Research, Vol.28, No.2, pp. 117-125, 2020, DOI:10.3727/096504019X15707883083132

Abstract To evaluate the cost–utility of pembrolizumab versus chemotherapy as the first-line setting for metastatic nonsmall cell lung cancer (NSCLC) from the US health care system perspective, a Markov model was developed to compare the lifetime cost and effectiveness of pembrolizumab versus chemotherapy for untreated metastatic NSCLC, based on the clinical data derived from phase III randomized controlled trial (KEYNOTE- 042; ClinicalTrials.gov; NCT02220894). Weibull distribution was fitted to simulate the parametric survival functions. Drug costs were collected from official websites, and utility values were obtained from published literature. Total costs, quality-adjusted life years (QALYs), and incremental cost-effectiveness ratios (ICERs) were computed… More >

Ya-Sian Chang^*†‡§, Chieh-Min Chang^†‡, Chien-Yu Lin^¶#, Dy-San Chao^†, Hsi-Yuan Huang^†, Jan-Gowth Chang^{*†‡**††}

Oncology Research, Vol.28, No.2, pp. 107-116, 2020, DOI:10.3727/096504019X15698362825407

Abstract The genomic landscape of breast cancer (BC) is complex. The purpose of this study was to decipher the mutational profiles of Taiwanese patients with BC using next-generation sequencing. We performed whole-exome sequencing on DNA from 24 tumor tissue specimens from BC patients. Sanger sequencing was used to validate the identified variants. Sanger sequencing was also performed on paired adjacent nontumor tissues. After genotype calling and algorithmic annotations, we identified 49 deleterious variants in canonical cancer-related genes in our BC cohort. The most frequently mutated genes were PIK3CA (16.67%), FKBP9 (12.5%), TP53 (12.5%), ATM (8.33%), CHEK2 (8.33%), FOXO3 (8.33%), NTRK1… More >

Nikhil Gadewal^*1, Rohit Kumar^†1, Swapnil Aher^†, Anagha Gardane^†, Tarang Gaur^†, Ashok K. Varma^*‡§, Navin Khattry^¶, Syed K. Hasan^†§¶

Oncology Research, Vol.28, No.3, pp. 321-330, 2020, DOI:10.3727/096504020X15816752427321

Abstract Acute myeloid leukemia (AML) with NPM1 mutation is a disease driving genetic alteration with good prognosis. Although it has been suggested that NPM1 mutation induces chemosensitivity in leukemic cells, the underlying cause for the better survival of NPM1 mutated patients is still not clear. Mutant NPM1 AML has a unique microRNA and their target gene (mRNA) signature compared to wild-type NPM1. Dynamic regulation of miRNA–mRNA has been reported to influence the prognostic outcome. In the present study, in silico expression data of miRNA and mRNA in AML patients was retrieved from genome data commons, and differentially expressed miRNA and mRNA… More >

Jianing Xu^*†, Qiyu Bo^‡, Xiang Zhang^§, Dapeng Lei^†, Jue Wang^*, Xinliang Pan^†

Oncology Research, Vol.28, No.3, pp. 311-319, 2020, DOI:10.3727/096504020X15801233454611

Abstract Hypopharyngeal squamous cell carcinoma (HSCC) remains one of the most lethal malignancies in the head and neck. Long noncoding RNA (lncRNA) HOXA11-AS is proven to function as an oncogene and a therapeutic target in various tumors. Our previous study and others have demonstrated that HOXA11-AS is one of the most upregulated lncRNAs in HSCC. However, the role of HOXA11-AS in HSCC has not yet been identified. The current study demonstrated that the expression of HOXA11-AS was significantly upregulated in HSCC tumors and was positively associated with lymph node metastasis. Moreover, functional experiments revealed that HOXA11-AS knockdown suppressed the proliferation and… More >

Minhua Wu^*1, Xubin Deng^†1, Yu Zhong^‡1, Li Hu^*, Xiujuan Zhang^§, Yanqin Liang^*, Xiaofang Li^¶, Xiaoxia Ye^*

Oncology Research, Vol.28, No.3, pp. 299-309, 2020, DOI:10.3727/096504020X15796890809840

Abstract MafF is a member of the basic leucine zipper (bZIP) transcription factor Maf family and is commonly downregulated in multiple cancers. But the expression and function of MafF in hepatocellular carcinoma (HCC) remain unclear. In this study, we investigated the relationship between endogenous MafF expression and HCC progression and explored the regulatory mechanism of MafF expression in HCC. We found that MafF decreased in HCC tissues and cells. Lentivirus-mediated MafF overexpression inhibited HCC cell proliferation and induced cell apoptosis. Bioinformatics analysis and luciferase assay identified MafF as a direct target of miR-224-5p. RNA pull-down assay demonstrated that circular RNA circ-ITCH… More >