Cancer Research and Treatment

Original Articles

The Synergistic Effect of PARP Inhibitors and Irinotecan in Small Cell Lung Cancer Cells: Songji Oh, Soyeon Kim, Bhumsuk Keam, Jeonghwan Youk, Tae Min Kim, Dong-Wan Kim, Miso Kim; Received August 1, 2024 Accepted January 6, 2025 Published online January 7, 2025; DOI: https://doi.org/10.4143/crt.2024.728 [Epub ahead of print]

Abstract PDF Supplementary Material PubReader ePub: Purpose
This study focused on combining irinotecan with poly(ADP-ribose) polymerase (PARP) inhibitors to explore the potential for novel combination therapeutics in small cell lung cancer (SCLC).
Materials and Methods
We selected 10 different SCLC cell lines with diverse mutational backgrounds in DNA damage response (DDR) pathway genes to evaluate the efficacy of the combination of three PARP inhibitors and irinotecan. After the cells were exposed to the drugs for seven days, cell viability was measured, and a combination index was calculated. Apoptotic signaling was assessed via western blot, and DNA damage was evaluated using an alkaline comet assay.
Results
We assessed the synergistic effects of PARP inhibitors and irinotecan in in vitro SCLC models, which revealed increased sensitivity, particularly in cells harboring BRCA mutations. However, even in cells lacking mutations in DDR pathway genes, the combination of the two drugs exhibited a synergistic effect. When treated with 50 nM irinotecan, the IC₅₀ fold changes for PARP inhibitors were as follows: olaparib, 1,649±4,049; talazoparib, 25±34.21; venadaparib, 336±596.01. This combination enhanced apoptosis signaling and increased p-chk1 and p-p53 protein levels. Additionally, the treatment of PARP inhibitor with irinotecan increased DNA damage, as visualized by the alkaline comet assay.
Conclusion
This study provides preclinical evidence of the potential clinical benefits of combining irinotecan with PARP inhibitors in SCLC. Further clinical investigations are warranted to validate these findings for the development of more effective and personalized therapeutic strategies for SCLC patients.

908 View
134 Download

Lung and Thoracic cancer

Targeting CD73 to Overcomes Resistance to First-Generation EGFR Tyrosine Kinase Inhibitors in Non–Small Cell Lung Cancer: Miso Kim, Soyeon Kim, Jeemin Yim, Bhumsuk Keam, Tae Min Kim, Yoon Kyung Jeon, Dong-Wan Kim, Dae Seog Heo; Cancer Res Treat. 2023;55(4):1134-1143. Published online May 23, 2023; DOI: https://doi.org/10.4143/crt.2023.311

Abstract PDF Supplementary Material PubReader ePub

Purpose
In patients with epidermal growth factor receptor (EGFR)-mutant non–small cell lung cancer (NSCLC), EGFR tyrosine kinase inhibitors (TKIs) improve response rate and survival. However, most patients eventually develop resistance. This study aimed to identify the role of CD73 in EGFR-mutant NSCLC and explore whether CD73 inhibition may serve as a therapeutic strategy in NSCLC patients with acquired resistance to EGFR-TKIs.
Materials and Methods
We evaluated the prognostic role of CD73 expression in EGFR-mutant NSCLC using tumor samples from a single institution. We silenced CD73 in EGFR-TKI–resistant cell lines using short hairpin RNA (shRNA) targeting CD73 and also transfected a vector alone as a negative control. Using these cell lines, cell proliferation and viability assays, immunoblot assays, cell cycle analysis, colony-forming assays, flow cytometry, and apoptosis analysis were performed.
Results
High expression of CD73 was associated with shorter survival in patients with metastatic EGFR-mutant NSCLC treated with first-generation EGFR-TKI. CD73 inhibition synergistically inhibited cell viability with first-generation EGFR-TKI treatment compared with the negative control. When CD73 inhibition and EGFR-TKI treatment were combined, G0/G1 cell cycle arrest was induced through the regulation of p21 and cyclin D1. In addition, the apoptosis rate was increased in CD73 shRNA-transfected cells treated with EGFR-TKI.
Conclusion
High expression of CD73 adversely affects the survival of patients with EGFR-mutant NSCLC. The study demonstrated that inhibiting CD73 in EGFR-TKI–resistant cell lines resulted in increased apoptosis and cell cycle arrest, which overcame the acquired resistance to first-generation EGFR-TKIs. Further research is needed to determine whether blocking CD73 plays a therapeutic role in EGFR-TKI–resistant patients with EGFR-mutant NSCLC.

Citations

Citations to this article as recorded by

Simultaneous blockade of the CD73/EGFR axis inhibits tumor growth
Keivan Ardeshiri, Hadi Hassannia, Ghasem Ghalamfarsa, Hanieh Jafary, Farhad Jadidi
IUBMB Life.2025;[Epub] CrossRef
Exploring the Expression of CD73 in Lung Adenocarcinoma with EGFR Genomic Alterations
Elodie Long-Mira, Christophe Bontoux, Guylène Rignol, Véronique Hofman, Sandra Lassalle, Jonathan Benzaquen, Jacques Boutros, Salomé Lalvée-Moret, Katia Zahaf, Virginie Lespinet-Fabre, Olivier Bordone, Sophia Maistre, Christelle Bonnetaud, Charlotte Cohen
Cancers.2025; 17(6): 1034. CrossRef
Comprehensive pan-cancer analysis of CD73: Explore its association with prognosis and tumor immune microenvironment
Chen Chen, Sasa Liu, Yanfen Ma
Heliyon.2024; 10(22): e40329. CrossRef

3,999 View
283 Download
3 Web of Science
3 Crossref

Acquired Resistance Mechanism of EGFR Kinase Domain Duplication to EGFR TKIs in Non–Small Cell Lung Cancer: Chaelin Lee, Miso Kim, Dong-Wan Kim, Tae Min Kim, Soyeon Kim, Sun-Wha Im, Yoon Kyung Jeon, Bhumsuk Keam, Ja-Lok Ku, Dae Seog Heo; Cancer Res Treat. 2022;54(1):140-149. Published online May 3, 2021; DOI: https://doi.org/10.4143/crt.2021.385

Abstract PDF Supplementary Material PubReader ePub

Purpose
Epidermal growth factor receptor kinase domain duplication (EGFR-KDD) is a rare and poorly understood oncogenic mutation in non–small cell lung cancer (NSCLC). We aimed to investigate the acquired resistance mechanism of EGFR-KDD against EGFR-TKIs.
Materials and Methods
We identified EGFR-KDD in tumor tissue obtained from a patient with stage IV lung adenocarcinoma and established the patient-derived cell line SNU-4784. We also established several EGFR-KDD Ba/F3 cell lines: EGFR-KDD wild type (EGFR-KDD^WT), EGFR-KDD domain 1 T790M (EGFR-KDD^D1T), EGFR-KDD domain 2 T790M (EGFR-KDD^D2T), and EGFR-KDD both domain T790M (EGFR-KDD^BDT). We treated the cells with EGFR tyrosine kinase inhibitors (TKIs) and performed cell viability assays, immunoblot assays, and ENU (N-ethyl-N-nitrosourea) mutagenesis screening.
Results
In cell viability assays, SNU-4784 cells and EGFR-KDD^WT Ba/F3 cells were sensitive to 2nd generation and 3rd generation EGFR TKIs. In contrast, the T790M-positive EGFR-KDD Ba/F3 cell lines (EGFR-KDD^T790M) were only sensitive to 3rd generation EGFR TKIs. In ENU mutagenesis screening, we identified the C797S mutation in kinase domain 2 of EGFR-KDD^BDT Ba/F3 cells. Based on this finding, we established an EGFR-KDD domain 1 T790M/domain 2 cis-T790M+C797S (EGFR-KDD^T/T+C) Ba/F3 model, which was resistant to EGFR TKIs and anti-EGFR monoclonal antibody combined with EGFR TKIs.
Conclusion
Our study reveals that the T790M mutation in EGFR-KDD confers resistance to 1st and 2nd generation EGFR TKIs, but is sensitive to 3rd generation EGFR TKIs. In addition, we identified that the C797S mutation in kinase domain 2 of EGFR-KDD^T790M mediates a resistance mechanism against 3rd generation EGFR TKIs.

Citations

Citations to this article as recorded by

Colorectal cancer harboring EGFR kinase domain duplication response to EGFR tyrosine kinase inhibitors
Tomohiro Kondo, Osamu Kikuchi, Yoshihiro Yamamoto, Tomohiko Sunami, Yafeng Wang, Keita Fukuyama, Tomoki Saito, Hideto Nakahara, Sachiko Minamiguchi, Masashi Kanai, Atsushi Sueyoshi, Manabu Muto
The Oncologist.2025;[Epub] CrossRef
A Constitutive EGFR Kinase Dimer to Study Inhibitor Pharmacology
Justin J. Kim, Ilse K. Schaeffner, David E. Heppner, Ciric To, Pasi A. Jänne, Tyler S. Beyett, Michael J. Eck
Molecular Pharmacology.2024; 105(2): 97. CrossRef
Tumor-associated Macrophages Mediate Gefitinib Resistance in Lung Cancer through HGF/c-met Signaling Pathway
Xiali Tang, Yu Chen, Demin Jiao, Xiang Liu, Jun Chen, Yongyang Liu, Chunyan Jiang, Qingyong Chen
Anti-Cancer Agents in Medicinal Chemistry.2024; 24(1): 30. CrossRef
Research progress on the role of bypass activation mechanisms in resistance to tyrosine kinase inhibitors in non-small cell lung cancer
Ziyang Jiang, Zhihan Gu, Xiaomin Yu, Tao Cheng, Bofu Liu
Frontiers in Oncology.2024;[Epub] CrossRef
Molecular Targets and Mechanisms of Casein-Derived Tripeptides Ile-Pro-Pro and Val-Pro-Pro on Hepatic Glucose Metabolism
Chenyang Wang, Lin Zheng, Mouming Zhao
Journal of Agricultural and Food Chemistry.2023; 71(48): 18802. CrossRef
Erlotinib

Reactions Weekly.2022; 1907(1): 208. CrossRef

9,650 View
340 Download
5 Web of Science
6 Crossref

Alterations in PD-L1 Expression Associated with Acquisition of Resistance to ALK Inhibitors in ALK-Rearranged Lung Cancer: Su-Jung Kim, Soyeon Kim, Dong-Wan Kim, Miso Kim, Bhumsuk Keam, Tae Min Kim, Yusoo Lee, Jaemoon Koh, Yoon Kyung Jeon, Dae Seog Heo; Cancer Res Treat. 2019;51(3):1231-1240. Published online December 31, 2018; DOI: https://doi.org/10.4143/crt.2018.486

Abstract PDF Supplementary Material PubReader ePub

Purpose
The purpose of this study was to evaluate the relationships between the resistance of anaplastic lymphoma kinase (ALK)‒positive non-small cell lung cancer (NSCLC) to ALK inhibitors and the programmed cell death-1/programmed cell death–ligand 1 (PD-L1) pathway, we evaluated alterations in PD-L1 following acquisition of resistance to ALK inhibitors in ALK-positive lung cancer.
Materials and Methods
We established ALK inhibitor-resistant cell lines (H3122CR1, LR1, and CH1) by exposing the parental H3122 ALK-translocated NSCLC cell line to ALK inhibitors. Then, the double-resistant cell lines H3122CR1LR1 and CR1CH1 were developed by exposing the H3122CR1 to other ALK inhibitors. We compared the alterations in PD-L1 expression levels using western blotting, flow cytometry, and quantitative polymerase chain reaction. We also investigated gene expression using RNA sequencing. The expression of PD-L1 in the tumors from 26 ALK-positive metastatic NSCLC patients (11 ALK inhibitor-naïve and 15 ALK inhibitor-resistant patients) was assessed by immunohistochemistry and analyzed.
Results
PD-L1 was expressed at higher levels in ALK inhibitor-resistant cell lines than in the ALK inhibitor-naïve parental cell line at the total protein, surface protein, and mRNA levels. Furthermore, PD-L1 expression in the double-resistant cell lines was much higher than that in the single resistant cell lines. RNA sequencing demonstrated that expression of immune-related genes were largely involved in ALK inhibitor resistance. The mean value of the PD-L1 H-score was 6.5 pre-treatment and 35.0 post-treatment, and the fold difference was 5.42 (p=0.163).
Conclusion
PD-L1 expression increased following acquisition of ALK inhibitor resistance in ALK-positive NSCLC cell lines and tumors.

Citations

Citations to this article as recorded by

Immunomodulatory role of oncogenic alterations in non-small cell lung cancer: a review of implications for immunotherapy
Maritza Ramos-Ramírez, Enrique Caballe-Pérez, José Lucio-Lozada, Eunice Romero-Nuñez, Cesar Castillo-Ruiz, Lorena Dorantes-Sánchez, Diana Flores-Estrada, Gonzalo Recondo, Pedro Barrios-Bernal, Luis Cabrera-Miranda, Heyman Bravo-Dominguez, Norma Hernández-
Cancer and Metastasis Reviews.2025;[Epub] CrossRef
Association of PD-L1 expression and clinical outcomes in ROS1 - rearranged advanced non-small cell lung cancer treated with crizotinib
Huixian Zhang, Ziheng Zhang, Ningning Yan, Xingya Li
Frontiers in Oncology.2024;[Epub] CrossRef
Co-Occurrence of ALK rearrangement and KRAS G12C mutation in NSCLC: Report of two cases
M Siringo, F Larocca, A Spagnuolo, G Gentile, M Anile, D Diso, D Santini, A Gelibter
Current Problems in Cancer: Case Reports.2024; 14: 100291. CrossRef
Characterizing the immune tumor microenvironment in ALK fusion-positive lung cancer: state-of-the-art and therapeutical implications
Marco Sposito, Serena Eccher, Luca Pasqualin, Ilaria Mariangela Scaglione, Alice Avancini, Daniela Tregnago, Ilaria Trestini, Jessica Insolda, Adele Bonato, Stefano Ugel, Lisa Derosa, Michele Milella, Sara Pilotto, Lorenzo Belluomini
Expert Review of Clinical Immunology.2024; 20(8): 959. CrossRef
Comparing Genomic Profiles of ALK Fusion-Positive and ALK Fusion-Negative Nonsmall Cell Lung Cancer Patients
Wenchao Xia, Jing Yang, Hongbin Li, Ling Li, Jinfeng Liu
Global Medical Genetics.2024; 11(02): 175. CrossRef
Changes of tumor microenvironment in non-small cell lung cancer after TKI treatments
Shanshan Chen, Jingyi Tang, Fen Liu, Wei Li, Ting Yan, Dangang Shangguan, Nong Yang, Dehua Liao
Frontiers in Immunology.2023;[Epub] CrossRef
High PD-L1 Expression Correlates with an Immunosuppressive Tumour Immune Microenvironment and Worse Prognosis in ALK-Rearranged Non-Small Cell Lung Cancer
Xia Tian, Yalun Li, Qin Huang, Hao Zeng, Qi Wei, Panwen Tian
Biomolecules.2023; 13(6): 991. CrossRef
Spoilt for choice: different immunosuppressive potential of anaplastic lymphoma kinase inhibitors for non small cell lung cancer
Annkristin Heine, Stefanie Andrea Erika Held, Solveig Nora Daecke, Chrystel Flores, Peter Brossart
Frontiers in Immunology.2023;[Epub] CrossRef
Anaplastic lymphoma kinase-special immunity and immunotherapy
Ye Guo, Hanfei Guo, Yongfei Zhang, Jiuwei Cui
Frontiers in Immunology.2022;[Epub] CrossRef
The quantum leap in therapeutics for advanced ALK+ non-small cell lung cancer and pursuit to cure with precision medicine
Malinda Itchins, Nick Pavlakis
Frontiers in Oncology.2022;[Epub] CrossRef
Successful Treatment with Brigatinib after Alectinib-Induced Hemolytic Anemia in Patients with Metastatic Lung Adenocarcinoma—A Case Series
Rola El Sayed, Mustapha Tehfe, Normand Blais
Current Oncology.2022; 30(1): 518. CrossRef
The role of immunotherapy in fusion-driven lung cancer
Aaron C. Tan, Johan Chan, Mustafa Khasraw
Expert Review of Anticancer Therapy.2021; 21(5): 461. CrossRef
ARIH1 signaling promotes anti-tumor immunity by targeting PD-L1 for proteasomal degradation
Youqian Wu, Chao Zhang, Xiaolan Liu, Zhengfu He, Bing Shan, Qingxin Zeng, Qingwei Zhao, Huaying Zhu, Hongwei Liao, Xufeng Cen, Xiaoyan Xu, Mengmeng Zhang, Tingjun Hou, Zhe Wang, Huanhuan Yan, Shuying Yang, Yaqin Sun, Yanying Chen, Ronghai Wu, Tingxue Xie,
Nature Communications.2021;[Epub] CrossRef
Pan-cancer Analysis of Tumor Mutational Burden and Homologous Recombination DNA Damage Repair Using Targeted Next-Generation Sequencing
Hai-Yun Wang, Ling Deng, Ying-Qing Li, Xiao Zhang, Ya-Kang Long, Xu Zhang, Yan-Fen Feng, Yuan He, Tao Tang, Xin-Hua Yang, Fang Wang
Cancer Research and Treatment.2021; 53(4): 973. CrossRef
Multiplexed electrokinetic sensor for detection and therapy monitoring of extracellular vesicles from liquid biopsies of non-small-cell lung cancer patients
Sara Cavallaro, Petra Hååg, Siddharth S. Sahu, Lorenca Berisha, Vitaliy O. Kaminskyy, Simon Ekman, Rolf Lewensohn, Jan Linnros, Kristina Viktorsson, Apurba Dev
Biosensors and Bioelectronics.2021; 193: 113568. CrossRef
Enhanced histone H3 acetylation of the PD-L1 promoter via the COP1/c-Jun/HDAC3 axis is required for PD-L1 expression in drug-resistant cancer cells
Haifang Wang, Chen Fu, Jun Du, Hongsheng Wang, Rui He, Xiaofeng Yin, Haixia Li, Xin Li, Hongxia Wang, Kui Li, Lei Zheng, Zongcai Liu, Yurong Qiu
Journal of Experimental & Clinical Cancer Research.2020;[Epub] CrossRef
Emerging Roles of ALK in Immunity and Insights for Immunotherapy
Lan Wang, Vivian Wai Yan Lui
Cancers.2020; 12(2): 426. CrossRef
Utility of PD‐L1 immunocytochemistry using body‐fluid cell blocks in patients with non‐small‐cell lung cancer
Seung Geun Song, Jonghoon Lee, Jaemoon Koh, Sehui Kim, Doo Hyun Chung, Yoon Kyung Jeon
Diagnostic Cytopathology.2020; 48(4): 291. CrossRef
RNA Sequencing in Comparison to Immunohistochemistry for Measuring Cancer Biomarkers in Breast Cancer and Lung Cancer Specimens
Maxim Sorokin, Kirill Ignatev, Elena Poddubskaya, Uliana Vladimirova, Nurshat Gaifullin, Dmitriy Lantsov, Andrew Garazha, Daria Allina, Maria Suntsova, Victoria Barbara, Anton Buzdin
Biomedicines.2020; 8(5): 114. CrossRef
PLAC8 overexpression correlates with PD-L1 upregulation and acquired resistance to chemotherapies in gallbladder carcinoma
Ke Gong, Zi-Jun Gong, Pin-Xiang Lu, Xiao-ling Ni, Sheng Shen, Han Liu, Ji-Wen Wang, De-Xiang Zhang, Hou-Bao Liu, Tao Suo
Biochemical and Biophysical Research Communications.2019; 516(3): 983. CrossRef
The efficacy of immune checkpoint inhibitors in anaplastic lymphoma kinase‐positive non‐small cell lung cancer
Ja Yoon Heo, Changhee Park, Bhumsuk Keam, Chan‐Young Ock, Miso Kim, Tae Min Kim, Dong‐Wan Kim, Se Hyun Kim, Yu Jung Kim, Jong Seok Lee, Dae Seog Heo
Thoracic Cancer.2019; 10(11): 2117. CrossRef

9,886 View
291 Download
23 Web of Science
21 Crossref

Acquired Resistance of MET-Amplified Non-small Cell Lung Cancer Cells to the MET Inhibitor Capmatinib: Seulki Kim, Tae Min Kim, Dong-Wan Kim, Soyeon Kim, Miso Kim, Yong-Oon Ahn, Bhumsuk Keam, Dae Seog Heo; Cancer Res Treat. 2019;51(3):951-962. Published online October 10, 2018; DOI: https://doi.org/10.4143/crt.2018.052

Abstract PDF Supplementary Material PubReader ePub

Purpose
Amplified mesenchymal-epithelial transition factor, MET, is a receptor tyrosine kinase (RTK) that has been considered a druggable target in non-small cell lung cancer (NSCLC). Although multiple MET tyrosine kinase inhibitors (TKIs) are being actively developed for MET-driven NSCLC, the mechanisms of acquired resistance to MET-TKIs have not been well elucidated. To understand the mechanisms of resistance and establish therapeutic strategies, we developed an in vitro model using the MET-amplified NSCLC cell line EBC-1.
Materials and Methods
We established capmatinib-resistant NSCLC cell lines and identified alternative signaling pathways using 3′ mRNA sequencing and human phospho-RTK arrays. Copy number alterations were evaluated by quantitative polymerase chain reaction and cell proliferation assay; activation of RTKs and downstream effectors were compared between the parental cell line EBC-1 and the resistant cell lines.
Results
We found that EBC-CR1 showed an epidermal growth factor receptor (EGFR)‒dependent growth and sensitivity to afatinib, an irreversible EGFR TKI. EBC-CR2 cells that had overexpression of EGFR-MET heterodimer dramatically responded to combined capmatinib with afatinib. In addition, EBC-CR3 cells derived from EBC-CR1 cells that activated EGFR with amplified phosphoinositide-3 kinase catalytic subunit α (PIK3CA) were sensitive to combined afatinib with BYL719, a phosphoinositide 3-kinase α (PI3Kα) inhibitor.
Conclusion
Our in vitro studies suggested that activation of EGFR signaling and/or genetic alteration of downstream effectors like PIK3CA were alternative resistance mechanisms used by capmatinib-resistant NSCLC cell lines. In addition, combined treatments with MET, EGFR, and PI3Kα inhibitors may be effective therapeutic strategies in capmatinib-resistant NSCLC patients.

Citations

Citations to this article as recorded by

Quinoline-Based FDA-Approved Drugs: Synthetic Route and Clinical Uses
Devesh Chandra, Sachin Sachin, Shourabh Rav, Upendra Sharma
Synlett.2025;[Epub] CrossRef
Immunohistochemical characteristics and potential therapeutic regimens of hepatoid adenocarcinoma of the stomach: a study of 139 cases
Xuesong Yang, Yan Wu, Anqiang Wang, Xiuli Ma, Kai Zhou, Ke Ji, Xin Ji, Ji Zhang, Xiaojiang Wu, ZhongWu Li, Zhaode Bu
The Journal of Pathology: Clinical Research.2024;[Epub] CrossRef
My battle with cancer. Part 1
Mikhail V. Blagosklonny
Oncoscience.2024; 11: 1. CrossRef
SOS2 modulates the threshold of EGFR signaling to regulate osimertinib efficacy and resistance in lung adenocarcinoma
Patricia L. Theard, Amanda J. Linke, Nancy E. Sealover, Brianna R. Daley, Johnny Yang, Katherine Cox, Robert L. Kortum
Molecular Oncology.2024; 18(3): 641. CrossRef
Synthetic approaches and application of representative clinically approved fluorine-enriched anti-cancer medications
He-Nan Liu, Ying Zhu, Yuan Chi, Fei-Fei Sun, Li-Shen Shan, Ya-Tao Wang, Bing Dai
European Journal of Medicinal Chemistry.2024; 276: 116722. CrossRef
Multifunctional dendrimer-peptide conjugates for MET receptor-specific imaging of cancer cells
Jin Woong Lee, Kwangok P. Nickel, Rachel L. Minne, Justin J. Jeffery, Eduardo Aluicio-Sarduy, Carter Kim, DaWon Kim, Piper A. Rawding, Michael J. Poellmann, Narsimha Mamidi, Jonathan W. Engle, Jung Heon Lee, Hansoo Park, Reinier Hernandez, Randall J. Kimp
Nano Today.2024; 59: 102509. CrossRef
Non-small cell lung carcinoma (NSCLC): Implications on molecular pathology and advances in early diagnostics and therapeutics
Hafiza Padinharayil, Jinsu Varghese, Mithun Chacko John, Golgodu Krishnamurthy Rajanikant, Cornelia M. Wilson, Minnatallah Al-Yozbaki, Kaviyarasi Renu, Saikat Dewanjee, Rupa Sanyal, Abhijit Dey, Anirban Goutam Mukherjee, Uddesh Ramesh Wanjari, Abilash Val
Genes & Diseases.2023; 10(3): 960. CrossRef
Synergistic therapeutic potential of alpelisib in cancers (excluding breast cancer): Preclinical and clinical evidences
Yuhao Ye, Zhiyu Huang, Maoqing Zhang, Jiayue Li, Yiqiong Zhang, Chenghua Lou
Biomedicine & Pharmacotherapy.2023; 159: 114183. CrossRef
Quinolines: Privileged Scaffolds for Developing New Anti‐neurodegenerative Agents
M.Sc.Shivani Chauhan, Tarana Umar, Manpreet K. Aulakh
ChemistrySelect.2023;[Epub] CrossRef
A multiparametric fluorescent visualization approach for detecting drug resistance in living cancer cells
Zhilan Zhou, Ya Wang, Zhengtao Shao, Guixi Zhang, Hang Jiang, Yiyuan Tang, Zening Huang, Yingdi Zhu, Juan Li
Talanta.2023; 259: 124564. CrossRef
Targeting MET: Discovery of Small Molecule Inhibitors as Non-Small Cell Lung Cancer Therapy
Chaofan Wang, Xiaoyun Lu
Journal of Medicinal Chemistry.2023; 66(12): 7670. CrossRef
Current Indications and Future Landscape of Bispecific Antibodies for the Treatment of Lung Cancer
Hugo Arasanz, Luisa Chocarro, Leticia Fernández-Rubio, Ester Blanco, Ana Bocanegra, Miriam Echaide, Ibone Labiano, Ana Elsa Huerta, Maria Alsina, Ruth Vera, David Escors, Grazyna Kochan
International Journal of Molecular Sciences.2023; 24(12): 9855. CrossRef
An Observatory for the MET Oncogene: A Guide for Targeted Therapies
Dogus M. Altintas, Paolo M. Comoglio
Cancers.2023; 15(18): 4672. CrossRef
Advances of clinically approved small-molecule drugs for the treatment of non-small cell lung cancer
Zhen-Xi Niu, Ya-Tao Wang, Nan Lu, Jin-Feng Sun, Peng Nie, Piet Herdewijn
European Journal of Medicinal Chemistry.2023; 261: 115868. CrossRef
Epigenetic regulation in lung cancer
Shahin Ramazi, Maedeh Dadzadi, Zahra Sahafnejad, Abdollah Allahverdi
MedComm.2023;[Epub] CrossRef
SOS1 and KSR1 modulate MEK inhibitor responsiveness to target resistant cell populations based on PI3K and KRAS mutation status
Brianna R. Daley, Heidi M. Vieira, Chaitra Rao, Jacob M. Hughes, Zaria M. Beckley, Dianna H. Huisman, Deepan Chatterjee, Nancy E. Sealover, Katherine Cox, James W. Askew, Robert A. Svoboda, Kurt W. Fisher, Robert E. Lewis, Robert L. Kortum
Proceedings of the National Academy of Sciences.2023;[Epub] CrossRef
KRAS and MET in non-small-cell lung cancer: two of the new kids on the ‘drivers’ block
Juan Esteban Garcia-Robledo, Rafael Rosell, Alejandro Ruíz-Patiño, Carolina Sotelo, Oscar Arrieta, Lucia Zatarain-Barrón, Camila Ordoñez, Elvira Jaller, Leonardo Rojas, Alessandro Russo, Diego de Miguel-Pérez, Christian Rolfo, Andrés F. Cardona
Therapeutic Advances in Respiratory Disease.2022;[Epub] CrossRef
MET Exon 14 Splice-Site Mutations Preferentially Activate KRAS Signaling to Drive Tumourigenesis
Daniel Lu, Amy Nagelberg, Justine LM Chow, Yankuan T Chen, Quentin Michalchuk, Romel Somwar, William W. Lockwood
Cancers.2022; 14(6): 1378. CrossRef
hOA-DN30: a highly effective humanized single-arm MET antibody inducing remission of ‘MET-addicted’ cancers
Ilaria Martinelli, Chiara Modica, Cristina Chiriaco, Cristina Basilico, James M. Hughes, Simona Corso, Silvia Giordano, Paolo M. Comoglio, Elisa Vigna
Journal of Experimental & Clinical Cancer Research.2022;[Epub] CrossRef
PIK3CAMutations Drive Therapeutic Resistance in Human Epidermal Growth Factor Receptor 2–Positive Breast Cancer
Aryana R. Rasti, Amy Guimaraes-Young, Farrah Datko, Virginia F. Borges, Dara L. Aisner, Elena Shagisultanova
JCO Precision Oncology.2022;[Epub] CrossRef
Protein tyrosine kinase inhibitor resistance in malignant tumors: molecular mechanisms and future perspective
Yang Yang, Shuo Li, Yujiao Wang, Yi Zhao, Qiu Li
Signal Transduction and Targeted Therapy.2022;[Epub] CrossRef
MET Signaling Pathways, Resistance Mechanisms, and Opportunities for Target Therapies
Solange Rivas, Arnaldo Marín, Suraj Samtani, Evelin González-Feliú, Ricardo Armisén
International Journal of Molecular Sciences.2022; 23(22): 13898. CrossRef
Advances in the Lung Cancer Immunotherapy Approaches
Hafiza Padinharayil, Reema Rose Alappat, Liji Maria Joy, Kavya V. Anilkumar, Cornelia M. Wilson, Alex George, Abilash Valsala Gopalakrishnan, Harishkumar Madhyastha, Thiyagarajan Ramesh, Ezhaveni Sathiyamoorthi, Jintae Lee, Raja Ganesan
Vaccines.2022; 10(11): 1963. CrossRef
A comprehensive review on the biological interest of quinoline and its derivatives
Basavarajaiah Suliphuldevara Matada, Raviraj Pattanashettar, Nagesh Gunavanthrao Yernale
Bioorganic & Medicinal Chemistry.2021; 32: 115973. CrossRef
Combination of HGF/MET-targeting agents and other therapeutic strategies in cancer
Fatemeh Moosavi, Elisa Giovannetti, Godefridus J. Peters, Omidreza Firuzi
Critical Reviews in Oncology/Hematology.2021; 160: 103234. CrossRef
Novel Therapies for Metastatic Non-Small Cell Lung Cancer with MET Exon 14 Alterations: A Spotlight on Capmatinib
Aaron Tan, Tracy J Loh, Xue Lin Kwang, Gek San Tan, Kiat Hon Lim, Daniel SW Tan
Lung Cancer: Targets and Therapy.2021; Volume 12: 11. CrossRef
Discovery of Potent, Selective Triazolothiadiazole-Containing c-Met Inhibitors
Qing Tang, Alex M. Aronov, David D. Deininger, Simon Giroux, David J. Lauffer, Pan Li, Jianglin Liang, Kira McGinty, Steven Ronkin, Rebecca Swett, Nathan Waal, Diane Boucher, Pamella J. Ford, Cameron S. Moody
ACS Medicinal Chemistry Letters.2021; 12(6): 955. CrossRef
Tyrosine Kinase Inhibitors, Antibody-Drug Conjugates, and Proteolysis-Targeting Chimeras: The Pharmacology of Cutting-Edge Lung Cancer Therapies
Jennifer W. Carlisle, R. Donald Harvey
American Society of Clinical Oncology Educational Book.2021; (41): e286. CrossRef
Response to crizotinib in a patient with MET‐amplified hepatocellular carcinoma
Qinglian Chen, Chunfeng Xie, Kunliang Feng, Haijun Huang, Chengming Xiong, Tengjiao Lin, Wenjing Wang, Mian Xu, Xianwei Yang, Chong Zhong
Hepatology Research.2021; 51(11): 1164. CrossRef
New FDA oncology small molecule drugs approvals in 2020: Mechanism of action and clinical applications
Thais Cristina Mendonça Nogueira, Marcus Vinicius Nora de Souza
Bioorganic & Medicinal Chemistry.2021; 46: 116340. CrossRef
Genetic evolution to tyrosine kinase inhibitory therapy in patients with EGFR-mutated non-small-cell lung cancer
Alex Martinez-Marti, Enriqueta Felip, Francesco Mattia Mancuso, Ginevra Caratú, Judit Matito, Paolo Nuciforo, Irene Sansano, Nely Diaz-Mejia, Susana Cedrés, Ana Callejo, Patricia Iranzo, Nuria Pardo, Josep Maria Miquel, Alejandro Navarro, Ana Vivancos, Mi
British Journal of Cancer.2021; 125(11): 1561. CrossRef
A Biparatopic Antibody–Drug Conjugate to Treat MET-Expressing Cancers, Including Those that Are Unresponsive to MET Pathway Blockade
John O. DaSilva, Katie Yang, Oliver Surriga, Thomas Nittoli, Arthur Kunz, Matthew C. Franklin, Frank J. Delfino, Shu Mao, Feng Zhao, Jason T. Giurleo, Marcus P. Kelly, Sosina Makonnen, Carlos Hickey, Pamela Krueger, Randi Foster, Zhaoyuan Chen, Marc W. Re
Molecular Cancer Therapeutics.2021; 20(10): 1966. CrossRef
Development and full validation of an LC–MS/MS methodology to quantify capmatinib (INC280) following intragastric administration to rats
Xiaoguang Fan, Guanghu Yang, Wenjuan Cui, Qin Liu, Zhaolong Zhang, Zhikun Zhang
Biomedical Chromatography.2020;[Epub] CrossRef
A Randomized-Controlled Phase 2 Study of the MET Antibody Emibetuzumab in Combination with Erlotinib as First-Line Treatment for EGFR Mutation–Positive NSCLC Patients
Giorgio Scagliotti, Denis Moro-Sibilot, Jens Kollmeier, Adolfo Favaretto, Eun Kyung Cho, Heidrun Grosch, Martin Kimmich, Nicolas Girard, Chun-Ming Tsai, Te-Chun Hsia, Matteo Brighenti, Christian Schumann, Xuejing Aimee Wang, Sameera R. Wijayawardana, Aaro
Journal of Thoracic Oncology.2020; 15(1): 80. CrossRef
Targeted Therapy and Checkpoint Immunotherapy in Lung Cancer
Roberto Ruiz-Cordero, Walter Patrick Devine
Surgical Pathology Clinics.2020; 13(1): 17. CrossRef
Meta-analysis of functional expression and mutational analysis of c-Met in various cancers
Murugesan Sivakumar, Murugesan Jayakumar, Palaniappan Seedevi, Palaniappan Sivasankar, Muthu Ravikumar, Sundharaiyya Surendar, Tamilselvi Murugan, Shahid S. Siddiqui, Sivakumar Loganathan
Current Problems in Cancer.2020; 44(4): 100515. CrossRef
Targeting the HGF/MET Axis in Cancer Therapy: Challenges in Resistance and Opportunities for Improvement
Xing Huang, Enliang Li, Hang Shen, Xun Wang, Tianyu Tang, Xiaozhen Zhang, Jian Xu, Zengwei Tang, Chengxiang Guo, Xueli Bai, Tingbo Liang
Frontiers in Cell and Developmental Biology.2020;[Epub] CrossRef
Statins use and its impact in EGFR‐TKIs resistance to prolong the survival of lung cancer patients: A Cancer registry cohort study in Taiwan
Phung‐Anh Nguyen, Chih‐Cheng Chang, Cooper J. Galvin, Yao‐Chin Wang, Soo Yeon An, Chih‐Wei Huang, Yu‐Hsiang Wang, Min‐Huei Hsu, Yu‐Chuan (Jack) Li, Hsuan‐Chia Yang
Cancer Science.2020; 111(8): 2965. CrossRef
A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
Kenneth J. Finn, Scott E. Martin, Jeff Settleman
Cancer Research.2020; 80(1): 79. CrossRef
Emerging therapies for non-small cell lung cancer
Chao Zhang, Natasha B. Leighl, Yi-Long Wu, Wen-Zhao Zhong
Journal of Hematology & Oncology.2019;[Epub] CrossRef
Capmatinib for the treatment of non-small cell lung cancer
Johan Filip Vansteenkiste, Charlotte Van De Kerkhove, Els Wauters, Pierre Van Mol
Expert Review of Anticancer Therapy.2019; 19(8): 659. CrossRef
Afatinib Overcomes Pemetrexed-Acquired Resistance in Non-Small Cell Lung Cancer Cells Harboring an EML4-ALK Rearrangement
Ji-Hyun Kwon, Kui-Jin Kim, Ji Hea Sung, Koung Jin Suh, Ji Yun Lee, Ji-Won Kim, Se Hyun Kim, Jeong-Ok Lee, Jin Won Kim, Yu Jung Kim, Keun-Wook Lee, Jee Hyun Kim, Soo-Mee Bang, Soyeon Kim, Sung-Soo Yoon, Jong Seok Lee
Cells.2019; 8(12): 1538. CrossRef
DYRK1A inhibition suppresses STAT3/EGFR/Met signalling and sensitizes EGFR wild‐type NSCLC cells to AZD9291
Yang‐ling Li, Ke Ding, Xiu Hu, Lin‐wen Wu, Dong‐mei Zhou, Ming‐jun Rao, Neng‐ming Lin, Chong Zhang
Journal of Cellular and Molecular Medicine.2019; 23(11): 7427. CrossRef
MiR-1246 Promotes Metastasis and Invasion of A549 cells by Targeting GSK-3β‒Mediated Wnt/β-Catenin Pathway
Fan Yang, Hairong Xiong, Li Duan, Qian Li, Xin Li, Yongqin Zhou
Cancer Research and Treatment.2019; 51(4): 1420. CrossRef

13,209 View
583 Download
45 Web of Science
44 Crossref

First
Prev
Page of 1
Next
Last

Search