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6 "Ying Yang"
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Gastrointestinal cancer
The Oncogenic Role of TNFRSF12A in Colorectal Cancer and Pan-Cancer Bioinformatics Analysis
Chuyue Wang, Yingying Zhao, You Chen, Ying Shi, Zhiying Yang, Weili Wu, Rui Ma, Bo Wang, Yifeng Sun, Ping Yuan
Cancer Res Treat. 2025;57(1):212-228.   Published online August 9, 2024
DOI: https://doi.org/10.4143/crt.2024.408
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms.
Materials and Methods
Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A.
Results
TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer.
Conclusion
TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.
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Lung and Thoracic cancer
The Clinical Outcomes of Different First-Line EGFR-TKIs Plus Bevacizumab in Advanced EGFR-Mutant Lung Adenocarcinoma
Yen-Hsiang Huang, Kuo-Hsuan Hsu, Chun-Shih Chin, Jeng-Sen Tseng, Tsung-Ying Yang, Kun-Chieh Chen, Kang-Yi Su, Sung-Liang Yu, Jeremy J.W. Chen, Gee-Chen Chang
Cancer Res Treat. 2022;54(2):434-444.   Published online August 2, 2021
DOI: https://doi.org/10.4143/crt.2021.671
AbstractAbstract PDFPubReaderePub
Purpose
The aim of this study was to investigate the efficacy of various epidermal growth factor receptor (EGFR)–tyrosine kinase inhibitors (TKIs) plus bevacizumab in advanced EGFR-mutant lung adenocarcinoma patients.
Materials and Methods
From August 2016 to October 2020, we enrolled advanced lung adenocarcinoma patients harboring exon 19 deletion or L858R receiving gefitinib, erlotinib and afatinib plus bevacizumab as the first-line treatment for the purposes of analysis.
Results
A total of 36 patients were included in the final analysis. Three patients received gefitinib, 17 received erlotinib, and 16 received afatinib combined with bevacizumab as the first-line treatment. The objective response rate was 77.8%, and disease control rate was 94.4%. The overall median progression-free survival (PFS) was 16.4 months, while the median PFS was 17.1 months in patients with exon 19 deletion, and 16.2 months in patients with L858R mutation (p=0.311). Regarding the use of different EGFR-TKIs, the median PFS was 17.1 months in the erlotinib group and 21.6 months in the afatinib group (p=0.617). In patients with brain metastasis at baseline, the median PFS was 18.9 months in the erlotinib group and 16.4 months in the afatinib group (p=0.747). Amongst patients harboring exon 19 deletion, the median PFS was 16.2 months in the erlotinib group and not-reached in the afatinib group (p=0.141). In patients with L858R mutation, the median PFS was 18.9 months in the erlotinib group and 16.2 months in the afatinib group (p=0.481).
Conclusion
Our research demonstrates that not only erlotinib combined with bevacizumab, but also afatinib plus bevacizumab as first-line treatment, provides solid clinical efficacy in advanced EGFR-mutant lung adenocarcinoma patients.

Citations

Citations to this article as recorded by  
  • Clinical outcome of bevacizumab or ramucirumab combined with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors as the first line therapy in susceptible EGFR‐mutated advanced non‐small‐cell lung
    Chia‐Yu Kuo, Ming‐Ju Tsai, Jen‐Yu Hung, Mei‐Hsuan Lee, Kuan‐Li Wu, Yu‐Chen Tsai, Cheng‐Hao Chuang, Chung‐Wen Huang, Chin‐Ling Chen, Chih‐Jen Yang, Inn‐Wen Chong
    The Kaohsiung Journal of Medical Sciences.2024; 40(5): 467.     CrossRef
  • Scorpiones, Scolopendra and Gekko Inhibit Lung Cancer Growth and Metastasis by Ameliorating Hypoxic Tumor Microenvironment via PI3K/AKT/mTOR/HIF-1α Signaling Pathway
    Qi-yuan Mao, Xue-qian Wang, Fei Lin, Ming-wei Yu, Hui-ting Fan, Qi Zheng, Lan-chun Liu, Chu-chu Zhang, Dao-rui Li, Hong-sheng Lin
    Chinese Journal of Integrative Medicine.2024; 30(9): 799.     CrossRef
  • Real-world clinical efficacy of bevacizumab biosimilar in patients with advanced non-small-cell lung cancer
    Wei-Fan Ou, Kuo-Hsuan Hsu, Jeng-Sen Tseng, Po-Hsin Lee, Kun-Chieh Chen, Yen-Hsiang Huang, Gee-Chen Chang, Tsung-Ying Yang
    Therapeutic Advances in Medical Oncology.2024;[Epub]     CrossRef
  • Bevacizumab plus erlotinib versus erlotinib alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials
    Ruijian Li, Weiyi Li, Fang Zhang, Shanshan Li
    European Journal of Medical Research.2023;[Epub]     CrossRef
  • Bevacizumab versus Ramucirumab in EGFR-Mutated Metastatic Non-Small-Cell Lung Cancer Patients: A Real-World Observational Study
    Wen-Chien Cheng, Yi-Cheng Shen, Chieh-Lung Chen, Wei-Chih Liao, Chia-Hung Chen, Hung-Jen Chen, Chih-Yen Tu, Te-Chun Hsia
    Cancers.2023; 15(3): 642.     CrossRef
  • Afatinib/bevacizumab/erlotinib

    Reactions Weekly.2023; 1952(1): 32.     CrossRef
  • Comprehensive analysis of prediction of the EGFR mutation and subtypes based on the spinal metastasis from primary lung adenocarcinoma
    Ran Cao, Huanhuan Chen, Huan Wang, Yan Wang, E-Nuo Cui, Wenyan Jiang
    Frontiers in Oncology.2023;[Epub]     CrossRef
  • When to add anti-angiogenesis drugs to EGFR-mutated metastatic non–small cell lung cancer patients: a real-world study from Taiwan
    Chieh-Lung Chen, Sing-Ting Wang, Wei-Chih Liao, Chia-Hung Chen, Chih-Yen Tu, Hung-Jen Chen, Te-Chun Hsia, Wen-Chien Cheng
    BMC Cancer.2022;[Epub]     CrossRef
  • State-of-the-Art Molecular Oncology of Lung Cancer in Taiwan
    Yung-Hung Luo, Kung-Hao Liang, Hsu-Ching Huang, Chia-I Shen, Chi-Lu Chiang, Mong-Lien Wang, Shih-Hwa Chiou, Yuh-Min Chen
    International Journal of Molecular Sciences.2022; 23(13): 7037.     CrossRef
  • Comparison of afatinib and erlotinib combined with bevacizumab in untreated stage IIIB/IV epidermal growth factor receptor-mutated lung adenocarcinoma patients: a multicenter clinical analysis study
    Suey-Haur Lee, Yu-Ching Lin, Li-Chung Chiu, Jia-Shiuan Ju, Pi-Hung Tung, Allen Chung-Cheng Huang, Shih-Hong Li, Yueh-Fu Fang, Chih-Hung Chen, Scott Chih-Hsi Kuo, Chin-Chou Wang, Cheng-Ta Yang, Ping-Chih Hsu
    Therapeutic Advances in Medical Oncology.2022;[Epub]     CrossRef
  • The efficacy and tolerability of combining pemetrexed-based chemotherapy with gefitinib in the first-line treatment of non-small cell lung cancer with mutated EGFR: A pooled analysis of randomized clinical trials
    Bi-Cheng Wang, Wen-Xuan Zhang, Bo-Hua Kuang, Guo-He Lin, Alessandro Rizzo
    PLOS ONE.2022; 17(10): e0275919.     CrossRef
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Gastrointestinal cancer
Hepatitis B Virus Core Protein Mediates the Upregulation of C5α Receptor 1 via NF-κB Pathway to Facilitate the Growth and Migration of Hepatoma Cells
Fanyun Kong, Yukai Tao, Dongchen Yuan, Ning Zhang, Qi Li, Tong Yu, Xiaoying Yang, Delong Kong, Xiaohui Ding, Xiangye Liu, Hongjuan You, Kuiyang Zheng, Renxian Tang
Cancer Res Treat. 2021;53(2):506-527.   Published online November 16, 2020
DOI: https://doi.org/10.4143/crt.2020.397
AbstractAbstract PDFPubReaderePub
Purpose
C5α receptor 1 (C5ΑR1) is associated with the development of various human cancers. However, whether it is involved in the development of hepatitis B virus (HBV)–related hepatocellular carcinoma (HCC) is poorly understood. We explored the expression, biological role, and associated mechanisms of C5AR1 in HBV-related hepatoma cells.
Materials and Methods
The expression of C5ΑR1 mediated by HBV and HBV core protein (HBc) was detected in hepatoma cells. The function of nuclear factor кB (NF-κB) pathway in HBc-induced C5AR1 expression was assessed. The roles of C5ΑR1 in the activation of intracellular signal pathways, the upregulation of inflammatory cytokines, and the growth and migration of hepatoma cells mediated by HBc, were investigated. The effect of C5α in the development of HCC mediated by C5AR1 was also measured.
Results
C5ΑR1 expression was increased in HBV-positive hepatoma cells. Dependent on HBc, HBV enhanced the expression of C5ΑR1 at the mRNA and protein levels. Besides, HBc could promote C5ΑR1 expression via the NF-κB pathway. Based on the C5ΑR1, HBc facilitated the activation of JNK and ERK pathways and the expression and secretion of interleukin-6 in hepatoma cells. Furthermore, C5ΑR1 was responsible for enhancing the growth and migration of hepatoma cells mediated by HBc. Except these, C5α could promote the malignant development of HBc-positive HCC via C5AR1.
Conclusion
We provide new insight into the mechanisms of hepatocarcinogenesis mediated by HBc. C5ΑR1 has a significant role in the functional abnormality of hepatoma cells mediated by HBc, and might be utilized as a potential therapeutic target for HBV-related HCC.

Citations

Citations to this article as recorded by  
  • Phenazine biosynthesis-like domain-containing protein (PBLD) and Cedrelone promote antiviral immune response by activating NF-ĸB
    Peili Hou, Hongchao Zhu, Fengyun Chu, Yan Gao, Xiaonan Sun, Fuzhen Zhang, Xiaomeng Wang, Yueyue Feng, Xingyu Li, Yu Liu, Jun Wang, Xiaoyun Wang, Daniel Chang He, Hongmei Wang, Hongbin He
    Nature Communications.2025;[Epub]     CrossRef
  • Hepatitis B virus core protein stabilizes RANGAP1 to upregulate KDM2A and facilitate hepatocarcinogenesis
    Hong-Juan You, Li-Hong Ma, Xing Wang, Yu-Xin Wang, Huan-Yang Zhang, En-Si Bao, Yu-Jie Zhong, Xiang-Ye Liu, De-Long Kong, Kui-Yang Zheng, Fan-Yun Kong, Ren-Xian Tang
    Cellular Oncology.2024; 47(2): 639.     CrossRef
  • Colchicine-mediated selective autophagic degradation of HBV core proteins inhibits HBV replication and HBV-related hepatocellular carcinoma progression
    Hui Zhang, Xiameng Su, Leirong Gu, Ming Tan, Yuting Liu, Kexin Xu, Jihua Ren, Juan Chen, Zhihong Li, Shengtao Cheng
    Cell Death Discovery.2024;[Epub]     CrossRef
  • Hepatitis B virus X protein increases LASP1 SUMOylation to stabilize HER2 and facilitate hepatocarcinogenesis
    Hongjuan You, Dongchen Yuan, Qi Li, Ning Zhang, Delong Kong, Tong Yu, Xiangye Liu, Xiaomei Liu, Rui Zhou, Fanyun Kong, Kuiyang Zheng, Renxian Tang
    International Journal of Biological Macromolecules.2023; 226: 996.     CrossRef
  • PLK3 promotes the proneural–mesenchymal transition in glioblastoma via transcriptional regulation of C5AR1
    Shuo Yu, Lin Lv, Yang Li, Qian Ning, Tingting Liu, Tinghua Hu
    Molecular Biology Reports.2023; 50(10): 8249.     CrossRef
  • The role of UXT in tumors and prospects for its application in hepatocellular carcinoma
    Zhengwang Wang, Shaojian Mo, Pengzhe Han, Lu Liu, Ziang Liu, Xifeng Fu, Yanzhang Tian
    Future Oncology.2022; 18(29): 3335.     CrossRef
  • C5aR1 promotes the progression of colorectal cancer by EMT and activating Wnt/β-catenin pathway
    Duo Xu, Meirong Li, Longyan Ran, Xiaochen Li, Xingwang Sun, Tao Yin
    Clinical and Translational Oncology.2022; 25(2): 440.     CrossRef
  • The Complement System: A Potential Therapeutic Target in Liver Cancer
    Meng Yuan, Li Liu, Chenlin Wang, Yan Zhang, Jiandong Zhang
    Life.2022; 12(10): 1532.     CrossRef
  • A Pleiotropic Role of the Hepatitis B Virus Core Protein in Hepatocarcinogenesis
    Caroline Lefeuvre, Hélène Le Guillou-Guillemette, Alexandra Ducancelle
    International Journal of Molecular Sciences.2021; 22(24): 13651.     CrossRef
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Pediatric cancer
Effectiveness and Safety of Dabrafenib in the Treatment of 20 Chinese Children with BRAFV600E-Mutated Langerhans Cell Histiocytosis
Ying Yang, Dong Wang, Lei Cui, Hong-Hao Ma, Li Zhang, Hong-Yun Lian, Qing Zhang, Xiao-Xi Zhao, Li-Ping Zhang, Yun-Ze Zhao, Na Li, Tian-You Wang, Zhi-Gang Li, Rui Zhang
Cancer Res Treat. 2021;53(1):261-269.   Published online September 15, 2020
DOI: https://doi.org/10.4143/crt.2020.769
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
We sought to investigate the effectiveness and safety of dabrafenib in children with BRAFV600E-mutated Langerhans cell histiocytosis (LCH).
Materials and Methods
A retrospective analysis was performed on 20 children with BRAFV600E-mutated LCH who were treated with dabrafenib.
Results
The median age at which the patients started taking dabrafenib was 2.3 years old (range, 0.6 to 6.5 years). The ratio of boys to girls was 2.3:1. The median follow-up time was 30.8 months (range, 18.9 to 43.6 months). There were 14 patients (70%) in the risk organ (RO)+ group and six patients (30%) in the RO group. All patients were initially treated with traditional chemotherapy and then shifted to targeted therapy due to poor control of LCH or intolerance to chemotherapy. The overall objective response rate and the overall disease control rate were 65% and 75%, respectively. During treatment, circulating levels of cell-free BRAFV600E (cfBRAFV600E) became negative in 60% of the patients within a median period of 3.0 months (range, 1.0 to 9.0 months). Grade 2 or 3 adverse effects occurred in five patients.
Conclusion
Some children with BRAFV600E-mutated LCH may benefit from monotherapy with dabrafenib, especially high-risk patients with concomitant hemophagocytic lymphohistiocytosis and intolerance to chemotherapy. The safety of dabrafenib is notable. A prospective study with a larger sample size is required to determine the optimal dosage and treatment duration.

Citations

Citations to this article as recorded by  
  • Genetic Landscape and Its Prognostic Impact in Children With Langerhans Cell Histiocytosis
    Chan-Juan Wang, Lei Cui, Shuang-Shuang Li, Hong-Hao Ma, Dong Wang, Hong-Yun Lian, Yun-Ze Zhao, Li-Ping Zhang, Wei-Jing Li, Qing Zhang, Xiao-Xi Zhao, Ying Yang, Xiao-Tong Huang, Wei Liu, Yi-Zhuo Wang, Wan-Shui Wu, Tian-You Wang, Rui Zhang, Zhi-Gang Li
    Archives of Pathology & Laboratory Medicine.2025; 149(2): 175.     CrossRef
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    Emmanuel Lee Boniao, Richard C. Allen, Gangadhara Sundar
    Orbit.2024; 43(5): 656.     CrossRef
  • Treatment of children with refractory/relapse high risk langerhans cell histiocytosis with the combination of cytarabine, vindesine and prednisone
    Wenqian Wang, Jian Ge, Honghao Ma, Hongyun Lian, Lei Cui, Yunze Zhao, Zhigang Li, Tianyou Wang, Rui Zhang
    BMC Pediatrics.2024;[Epub]     CrossRef
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    Jiaying Lei, Wenxia Wang, Danna Lin, Chengguang Zhu, Wenguang Jia, Wenjun Weng, Xiaoshan Liu, Yuhan Ma, Zhixuan Wang, Lihua Yang, Xiangling He, Yunyan He, Yang LI
    Journal of Cancer Research and Clinical Oncology.2024;[Epub]     CrossRef
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    Xinshun Ge, Wenxin Ou, Ang Wei, Hongyun Lian, Honghao Ma, Lei Cui, Dong Wang, Liping Zhang, Xiaoman Wang, Lejian He, Rui Zhang, Tianyou Wang
    BMC Pediatrics.2024;[Epub]     CrossRef
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    Isaac Hauk, Ignacio Gonzalez‐Gomes, Deepak Chellapandian, Jonathan Metts, Peter H. Shaw
    Pediatric Blood & Cancer.2024;[Epub]     CrossRef
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    Paul G. Kemps, F. J. Sherida H. Woei-A-Jin, Patrick Schöffski, Thomas Tousseyn, Isabelle Vanden Bempt, Friederike A. G. Meyer-Wentrup, Natasja Dors, Natasha K. A. van Eijkelenburg, Marijn A. Scheijde-Vermeulen, Ingrid M. Jazet, Maarten Limper, Margot Jak,
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    Zi-Jing Zhao, Hong-Yun Lian, Wei-Jing Li, Qing Zhang, Hong-Hao Ma, Dong Wang, Yun-Ze Zhao, Ting Zhu, Hua-Lin Li, Xiao-Tong Huang, Tian-You Wang, Rui Zhang, Lei Cui, Zhi-Gang Li
    Jornal de Pediatria.2024;[Epub]     CrossRef
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    Xue-Lian Wang, Chun-Xiao Fang, Min-Xia Chen, Hua-Mei Yang, Lan-Hui She, Yu Gong, Yi Xu, Wei-Qiang Xiao, Jin-Sheng Tian, Bin Ai, Li Huang, Xu-Fang Li
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    Evgeniy F. Khynku, Maria K. Monaenkova, Olga B. Tamrazova, Alexey V. Taganov, Мarina А. Gureeva, Gayane E. Bagramova, Anton V. Molochkov
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  • Dabrafenib, alone or in combination with trametinib, in BRAF V600–mutated pediatric Langerhans cell histiocytosis
    James A. Whitlock, Birgit Geoerger, Ira J. Dunkel, Michael Roughton, Jeea Choi, Lisa Osterloh, Mark Russo, Darren Hargrave
    Blood Advances.2023; 7(15): 3806.     CrossRef
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    Anke Elisabeth Barnbrock, Caroline Hutter, Konrad Bochennek, Milen Minkov, Thomas Lehrnbecher
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    Benjamin H. Durham, Oshrat Hershkovitz-Rokah, Omar Abdel-Wahab, Mariko Yabe, Young Rock Chung, Gilad Itchaki, Maayan Ben-Sasson, Vered A. Asher-Guz, David Groshar, Seyram A. Doe-Tetteh, Tina Alano, David B. Solit, Ofer Shpilberg, Eli L. Diamond, Roei D. M
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    Marie Bellouard, Jean Donadieu, Pauline Thiebot, Etienne Giroux Leprieur, Philippe Saiag, Isabelle Etting, Pamela Dugues, Emuri Abe, Jean-Claude Alvarez, Islam-Amine Larabi
    Pharmaceutics.2023; 16(1): 5.     CrossRef
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    Oussama Abla
    Hematology.2023; 2023(1): 386.     CrossRef
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    Ja-Feng Yao, Dong Wang, Hong-Hao Ma, Hong-Yun Lian, Li Zhang, Tian-You Wang, Zhi-Gang Li, Jin Jiang, Lei Cui, Rui Zhang
    The Journal of Pediatrics.2022; 244: 194.     CrossRef
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    Dong Wang, Xi-Hua Chen, Ang Wei, Chun-Ju Zhou, Xue Zhang, Hong-Hao Ma, Hong-Yun Lian, Li Zhang, Qing Zhang, Xiao-Tong Huang, Chan-Juan Wang, Ying Yang, Wei Liu, Tian-You Wang, Zhi-Gang Li, Lei Cui, Rui Zhang
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    Jagadeesh Menon, Ashwin Rammohan, Mukul Vij, Naresh Shanmugam, Mohamed Rela
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    延泽 刘
    Advances in Clinical Medicine.2022; 12(09): 8499.     CrossRef
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    Jin Kyung Suh, Sunghan Kang, Hyery Kim, Ho Joon Im, Kyung-Nam Koh
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    Ying Yang, Dong Wang, Na Li, Honghao Ma, Hongyun Lian, Lei Cui, Qing Zhang, Xiaoxi Zhao, Liping Zhang, Yunze Zhao, Chanjuan Wang, Li Zhang, Tianyou Wang, Zhigang Li, Rui Zhang
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The Association of Acquired T790M Mutation with Clinical Characteristics after Resistance to First-Line Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in Lung Adenocarcinoma
Yen-Hsiang Huang, Kuo-Hsuan Hsu, Jeng-Sen Tseng, Kun-Chieh Chen, Chia-Hung Hsu, Kang-Yi Su, Jeremy J. W. Chen, Huei-Wen Chen, Sung-Liang Yu, Tsung-Ying Yang, Gee-Chen Chang
Cancer Res Treat. 2018;50(4):1294-1303.   Published online January 4, 2018
DOI: https://doi.org/10.4143/crt.2017.512
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
The main objective of this study was to investigate the relationship among the clinical characteristics and the frequency of T790M mutation in advanced epidermal growth factor receptor (EGFR)‒mutant lung adenocarcinoma patients with acquired resistance after firstline EGFR‒tyrosine kinase inhibitor (TKI) treatment.
Materials and Methods
We enrolled EGFR-mutant stage IIIB-IV lung adenocarcinoma patients, who had progressed to prior EGFR-TKI therapy, and evaluated their rebiopsy EGFR mutation status.
Results
A total of 205 patients were enrolled for analysis. The overall T790M mutation rate of rebiopsy was 46.3%. The T790M mutation rates among patients with exon 19 deletion mutation, exon 21 L858R point mutation, and other mutations were 55.0%, 37.3%, and 27.3%, respectively. Baseline exon 19 deletion was associated with a significantly higher frequency of T790M mutation (adjusted odds ratio, 2.14; 95% confidence interval [CI], 1.20 to 3.83; p=0.010). In the exon 19 deletion subgroup, there was a greater prevalence of T790M mutation than other exon 19 deletion subtypes in patients with the Del E746-A750 mutation (61.6% vs. 40.6%; odds ratio, 2.35; 95% CI, 1.01 to 5.49; p=0.049). The progression-free survival (PFS) of first-line TKI treatment > 11 months was also associated with a higher T790M mutation rate (54.1% vs. 39.3%; adjusted odds ratio, 1.82; 95% CI, 1.02 to 3.25; p=0.044). Patients who underwent rebiopsy at metastatic sites had more chance to harbor T790M mutation (52.6% vs. 33.8%; adjusted odds ratio, 1.97; 95% CI, 1.06 to 3.67; p=0.032).
Conclusion
PFS of first-line EGFR-TKI, rebiopsy site, EGFR exon 19 deletion and its subtype Del E746- A750 mutation are associated with the frequency of T790M mutation.

Citations

Citations to this article as recorded by  
  • RELAY, Erlotinib Plus Ramucirumab in Untreated, EGFR-Mutated, Metastatic NSCLC: Outcomes by EGFR Exon 19 Deletion Variants
    Kazumi Nishino, Jin-Yuan Shih, Kazuhiko Nakagawa, Martin Reck, Edward B. Garon, Michelle Carlsen, Tomoko Matsui, Carla Visseren-Grul, Ernest Nadal
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    Yan-Jei Tang, John Wen-Cheng Chang, Chen-Yang Huang, Yueh-Fu Fang, Ching-Fu Chang, Cheng-Ta Yang, Chih-Hsi Scott Kuo, Ping-Chih Hsu, Chiao-En Wu
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    Kyung Soo Hong, Jinmo Cho, Jong Geol Jang, Min Hye Jang, June Hong Ahn
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Intercalated Treatment Following Rebiopsy Is Associated with a Shorter Progression-Free Survival of Osimertinib Treatment
Jeng-Sen Tseng, Tsung-Ying Yang, Kun-Chieh Chen, Kuo-Hsuan Hsu, Yen-Hsiang Huang, Kang-Yi Su, Sung-Liang Yu, Gee-Chen Chang
Cancer Res Treat. 2018;50(4):1164-1174.   Published online December 11, 2017
DOI: https://doi.org/10.4143/crt.2017.460
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Epidermal growth factor receptor (EGFR) T790M mutation serves as an important predictor of osimertinib efficacy. However, little is known about how it works among patients with various timings of T790M emergence and treatment.
Materials and Methods
Advanced EGFR-mutant lung adenocarcinoma patients with positive T790M mutation in tumor were retrospectively enrolled and observed to determine the outcomes of osimertinib treatment. We evaluated the association between patients’ characteristics and the efficacy of osimertinib treatment, particularly with respect to the timing of T790M emergence and osimertinib prescription.
Results
A total of 91 patients were enrolled, including 14 (15.4%) with primary and 77 (84.6%) with acquired T790M mutation. The objective response rate and disease controlratewere 60.9% and 85.1%, respectively. The median progression-free survival (PFS) and overall survival were 11.5 months (95% confidence interval [CI], 9.0 to 14.0) and 30.4 months (95% CI, 11.3 to 49.5), respectively. There was no significant difference in response rate and PFS between primary and acquired T790M populations. In the acquired T790M subgroup, patientswho received osimertinib after T790M had been confirmed by rebiopsy had a longer PFS than those with intercalated treatments between rebiopsy and osimertinib prescription (14.0 months [95% CI, 9.0 to 18.9] vs. 7.2 months [95% CI, 3.7 to 10.8]; adjusted hazard ratio, 0.48 [95% CI, 0.24 to 0.98; p=0.043]). Rebiopsy timing did not influence the outcome.
Conclusion
Osimertinib prescription with intercalated treatment following rebiopsy but not the timing of T790M emergence influenced the treatment outcome. We suggest that it is better to start osimertinib treatment once T790M mutation has been confirmed by biopsy.

Citations

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    Targeted Oncology.2019; 14(4): 433.     CrossRef
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