ReviewJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2017
Primary Double-Strike Therapy for Cancers to Overcome EGFR Kinase Inhibitor Resistance: Proposal from the Bench.
Review in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- A Multikinase Inhibitor AX-0085 Blocks FGFR1 Activation to Overcomes Osimertinib Resistance in Non-Small Cell Lung Cancer.Biomedicines · 2025Article
- Osimertinib in combination with anti-angiogenesis therapy presents a promising option for osimertinib-resistant non-small cell lung cancer.BMC medicine · 2024Article
- Recent Advances in Perioperative Immunotherapies in Lung Cancer.Biomolecules · 2023Review
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- Role of Small Molecule Targeted Compounds in Cancer: Progress, Opportunities, and Challenges.Frontiers in cell and developmental biology · 2021Review
- Estrogen ReceptorFrontiers in oncology · 2020Article
- For a better adjuvant strategy for resected lung cancer-lessons from treatment failure patterns of the ADJUVANT trial (CTONG 1104).Translational lung cancer research · 2019Article
- Targeting the reversible drug-tolerant state: aurora kinase A, is that the final answer?Translational cancer research · 2019Article
- Overcoming acquired resistance of gefitinib in lung cancer cells without T790M by AZD9291 or Twist1 knockdown in vitro and in vivo.Archives of toxicology · 2019Article
- Early-Stage NSCLC: Advances in Thoracic Oncology 2018.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2019Review
- Semaphorin 7A promotes EGFR-TKI resistance in EGFR mutant lung adenocarcinoma cells.JCI insight · 2018Article
- Targeted inhibitors of P-glycoprotein increase chemotherapeutic-induced mortality of multidrug resistant tumor cells.Scientific reports · 2018Article
- Trastuzumab emtansine delays and overcomes resistance to the third-generation EGFR-TKI osimertinib in NSCLC EGFR mutated cell lines.Journal of experimental & clinical cancer research : CR · 2017Article
- Concurrent epidermal growth factor receptor T790M secondary mutation and epithelial-mesenchymal transition in a lung adenocarcinoma patient with EGFR-TKI drug resistance.Thoracic cancer · 2017Article
- A case report ofRespiratory medicine case reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Diverse molecular mechanisms that confer acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) in lung cancers with sensitive EGFR mutations have been reported. However, it is not realistic to analyze for all these mechanisms at the time of resistance in clinical practice and establish adequate treatment targeting these numerous resistance mechanisms. Therefore, we believe that we should move our research focus from the exploration of "established" diverse resistance mechanisms to the elucidation of molecular mechanisms that enable cancer cells to remain alive at the early phase of the treatment. Here in this review, we summarize up-to-date molecular mechanisms that maintain residual tumor cells against EGFR TKI monotherapy in lung cancers with EGFR mutations. We classified these mechanisms into three categories. The first is a preexisting minor subpopulation with a resistance mechanism such as a pretreatment T790M mutation that can be detected by highly sensitivity methods. The second is the reversible drug-tolerant state that is often observed in cell line models and accounts for the lack of complete response and continued survival of cells exposed to EGFR TKIs in patients. And the last is the role of the microenvironment, including survival signaling from fibroblasts or dying cancer cells and the role of poor vascularization. Primary double-strike cancer therapy, or even initial multiple-strike therapy, to cancer cells that cotarget EGFR and survival mechanism(s) simultaneously would be a promising strategy to improve the outcomes of patients with EGFR mutations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.