ArticleNPJ precision oncology2021
A tyrosine kinase inhibitor-induced interferon response positively associates with clinical response in EGFR-mutant lung cancer.
Article in NPJ precision oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Therapeutic vaccines for NSCLC: From mechanisms to clinical translation.Chinese medical journal pulmonary and critical care medicine · 2026Review
- KMT2D loss drives adeno-to-squamous transition and sensitizes TKI-resistant lung cancer to AURKA inhibition.Cell death and differentiation · 2026Article
- Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr-mutated lung cancer.Molecular oncology · 2026Article
- Neoadjuvant afatinib in a patient with locally advanced lung adenocarcinoma harboring an NPTN-NRG1 fusion: a case report.World journal of surgical oncology · 2026Article
- WNT inhibition activates interferon stimulated gene expression by alleviating epigenetic repression of endogenous retroviruses.Scientific reports · 2026Article
- Mitochondrial niches of residual disease in EGFR-mutant NSCLC: immune-constrained persistence and therapeutic interception.Frontiers in immunology · 2026Review
- EGFR: New Insights on Its Activation and Mutation in Tumor and Tumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- A Prospective Exploratory Study of Functional Immunity Assessed by Pretreatment Interferon Gamma Release Assay in Relation to Different Systemic Therapies in Patients With Advanced-Stage NSCLC.JTO clinical and research reports · 2025Article
- EGFR TKIs suppress MUC1 glycosylation through the PI3K/AKT/SP1/C1GALT1 pathway to enhance TnMUC1 CAR-T efficacy in EGFR-mutant NSCLC.Cell reports. Medicine · 2025Article
- Anti-galectin-9 therapy synergizes with EGFR inhibition to reprogram the tumor microenvironment and overcome immune evasion.Journal for immunotherapy of cancer · 2025Article
- Prolonged progression-free survival on epidermal growth factor receptor-tyrosine kinase inhibitors predicts superior response to atezolizumab-based therapy over chemotherapy in epidermal growth factor receptor-mutated non-small-cell lung cancer following progression.ESMO real world data and digital oncology · 2025Article
- Single-Cell RNA Sequencing in Unraveling Acquired Resistance to EGFR-TKIs in Non-Small Cell Lung Cancer: New Perspectives.International journal of molecular sciences · 2025Review
- Enhancing immunotherapy efficacy in colorectal cancer: targeting the FGR-AKT-SP1-DKK1 axis with DCC-2036 (Rebastinib).Cell death & disease · 2025Article
- Resistance signatures manifested in early drug response across cancer types and species.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- CYpHER: Catalytic extracellular targeted protein degradation with high potency and durable effect.bioRxiv : the preprint server for biology · 2024Article
- Cancer/testis antigen CAGE mediates osimertinib resistance in non-small cell lung cancer cells and predicts poor prognosis in patients with pulmonary adenocarcinoma.Scientific reports · 2023Article
- Stratification of non-small cell lung adenocarcinoma patients with EGFR actionable mutations based on drug-resistant stem cell genes.iScience · 2023Article
- Novel EGFR-mutant mouse models of lung adenocarcinoma reveal adaptive immunity requirement for durable osimertinib response.Cancer letters · 2023Article
- Durable responses to alectinib in murine models of EML4-ALK lung cancer requires adaptive immunity.NPJ precision oncology · 2023Article
- Circulating immune response proteins predict the outcome following disease progression of osimertinib treated epidermal growth factor receptor-positive non-small cell lung cancer patients.Translational lung cancer research · 2023Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Tyrosine kinase inhibitors (TKIs) targeting EGFR-mutant lung cancers promote a range of tumor regression responses to yield variable residual disease, a likely incubator for acquired resistance. Herein, rapid transcriptional responses induced by TKIs early in treatment that associate with the range of patient responses were explored. RNAseq was performed on EGFR mutant cell lines treated in vitro with osimertinib and on tumor biopsies of eight EGFR mutant lung cancer patients before and after 2 weeks of TKI treatment. Data were evaluated for gene expression programs altered upon TKI treatment. Chemokine and cytokine expression were measured by ELISA and quantitative RT-PCR. IκB Kinase (IKK) and JAK-STAT pathway dependence was tested with pharmacologic and molecular inhibitors. Tumor sections were stained for the T-cell marker CD3. Osimertinib stimulated dynamic, yet wide-ranging interferon (IFN) program regulation in EGFR mutant cell lines. IL6 and CXCL10 induction varied markedly among the EGFR mutant cell lines and was sensitive to IKK and JAK-STAT inhibitors. Analysis of matched patient biopsy pairs revealed marked, yet varied enrichment of IFN transcriptional programs, effector immune cell signatures and T-cell content in treated tumors that positively correlated with time to progression in the patients. EGFR-specific TKIs induce wide-ranging IFN response program activation originating within the cancer cell. The strong association of IFN program induction and duration of clinical response indicates that the TKI-induced IFN program instructs variable recruitment and participation of immune cells in the overall therapeutic response.
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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.