ReviewCancers2023
Resistance of Lung Cancer to EGFR-Specific Kinase Inhibitors: Activation of Bypass Pathways and Endogenous Mutators.
Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07486648 (The Safety and Efficacy of Osimertinib Plus Capivasertib in EGFRm Advanced Non-small Cell Lung Cancer), which is not on this map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
The Safety and Efficacy of Osimertinib Plus Capivasertib in EGFRm Advanced Non-small Cell Lung Cancer (NSCLC) Participants With PIK3CA/AKT1/PTEN Alterations Who Had Progressed on First-line Osimertinib Monotherapy or Plus Chemotherapy: a First-in-human, Phase Ib/Ⅱa Study (PRECISION)
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Diagnostic performance of machine learning-based radiomics models for predicting epidermal growth factor receptor mutation status in lung adenocarcinoma in Chinese patients: A systematic review and meta-analysis.The Journal of international medical research · 2026Pooled it
- Rewiring oncogenic signalling to precision ablation of metastatic cancer.Nature biomedical engineering · 2026Article
- Machine learning-guided drug repurposing for EGFR inhibition using scaffold-split validation, docking, and molecular dynamics.Journal of computer-aided molecular design · 2026Article
- Mitochondrial oxidative phosphorylation inhibition by 9α,11α-dihydroxy-kaurenoic acid promotes ROS-associated apoptosis and suppresses cancer stemness in non-small cell lung cancer.Scientific reports · 2026Article
- Leveraging conformational ensembles in allosteric drug discovery.Trends in pharmacological sciences · 2026Review
- Updated incidence of EGFR mutation in Middle Eastern patients with non-small cell lung cancer: a 7-year study in a Lebanese institution.BMC cancer · 2026Article
- A Darwinian Perspective on Tumor Evolution.International journal of biological sciences · 2026Review
- Strategies to Overcome Resistance to Osimertinib in EGFR-Mutated Lung Cancer.International journal of molecular sciences · 2025Review
- The Intricate Web of MicroRNAs in Modulating EGFR-TKI Resistance in Non-Small Cell Lung Cancer: A Comprehensive Review.Cancer management and research · 2025Review
- A bispecific antibody targeting EGFR and AXL delays resistance to osimertinib.Cell reports. Medicine · 2024Article
- A case of PhBMC medical genomics · 2024Article
- Role of MARK2 in the nervous system and cancer.Cancer gene therapy · 2024Review
- Targeting c-Met in breast cancer: From mechanisms of chemoresistance to novel therapeutic strategies.Current research in pharmacology and drug discovery · 2024Review
- Targeting HER3 to overcome EGFR TKI resistance in NSCLC.Frontiers in immunology · 2023Review
- Repurposing Antifungal Drugs for Oral Cancer Treatment: Mechanistic Insights and Clinical Potential-A Narrative Review.Journal of International Society of Preventive & Community DentistryReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Epidermal growth factor receptor (EGFR)-specific tyrosine kinase inhibitors (TKIs) have changed the landscape of lung cancer therapy. For patients who are treated with the new TKIs, the current median survival exceeds 3 years, substantially better than the average 20 month survival rate only a decade ago. Unfortunately, despite initial efficacy, nearly all treated patients evolve drug resistance due to the emergence of either new mutations or rewired signaling pathways that engage other receptor tyrosine kinases (RTKs), such as MET, HER3 and AXL. Apparently, the emergence of mutations is preceded by a phase of epigenetic alterations that finely regulate the cell cycle, bias a mesenchymal phenotype and activate antioxidants. Concomitantly, cells that evade TKI-induced apoptosis (i.e., drug-tolerant persister cells) activate an intrinsic mutagenic program reminiscent of the SOS system deployed when bacteria are exposed to antibiotics. This mammalian system imbalances the purine-to-pyrimidine ratio, inhibits DNA repair and boosts expression of mutation-prone DNA polymerases. Thus, the net outcome of the SOS response is a greater probability to evolve new mutations. Deeper understanding of the persister-to-resister transformation, along with the development of next-generation TKIs, EGFR-specific proteolysis targeting chimeras (PROTACs), as well as bispecific antibodies, will permit delaying the onset of relapses and prolonging survival of patients with EGFR
Indexed as
Identifiers
What OpenQuestion holds
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.