"Gefitinib"

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                            1
                            2023NIHR HTA programme
                            Review Analysis
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                            Gefitinib and methotrexate to resolve tubal ectopic pregnancy: the GEM3 RCT Text onlyJournals LibraryNHS NIHR - National Institute for Health and Care ResearchSelectEMEGHRHSDRHTAPGfARPHR AdvancedJournalsEfficacy and Mechanism EvaluationGlobal Health ResearchHealth and Social Care Delivery ResearchHealth Technology AssessmentProgramme Grants for Applied ResearchPublic Health , Mol BW, Whitaker LHR, et al. Gefitinib and methotrexate to resolve tubal ectopic pregnancy: the GEM3 RCT. Efficacy Mech Eval 2023;10(1)Report ContentFull ReportAbstractPlain Language SummaryScientific SummaryAbstractBackgroundTubal ectopic pregnancies can cause significant morbidity or even death. Current treatment is with methotrexate or surgery. However, methotrexate treatment can fail
                            2
                            2025PLoS ONE
                            Deubiquitination of epidermal growth factor receptor by ubiquitin-specific peptidase 54 enhances drug sensitivity to gefitinib in gefitinib-resistant non-small cell lung cancer cells. A precise balance between ubiquitination and deubiquitination is crucial for cellular regulation. Ubiquitin-specific peptidase 54 (USP54), an active deubiquitinase (DUB), modulates the ubiquitination of the epidermal growth factor receptor (EGFR). While the significance of USP54 in tumorigenesis is known, its specific function in cancer progression remains unclear. This study investigates the role of USP54 in gefitinib sensitivity in gefitinib-resistant non-small cell lung cancer (NSCLC) cells. Using western blotting and next-generation sequencing, we examined gene expression changes in ubiquitination
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                            3
                            2023EvidenceUpdates
                            Gefitinib Plus Chemotherapy vs Gefitinib Alone in Untreated EGFR-Mutant Non-Small Cell Lung Cancer in Patients With Brain Metastases: The GAP BRAIN Open-Label, Randomized, Multicenter, Phase 3 Study Use of tyrosine kinase inhibitors (TKIs) is the standard therapy for epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) with brain metastases. Several studies have shown that adding chemotherapy to EGFR-TKIs could improve progression-free survival (PFS) in patients with EGFR-mutant advanced NSCLC; however, the efficacy of these agents in patients with brain metastases remains unclear. To investigate the efficacy and safety of gefitinib plus chemotherapy (pemetrexed with platinum) compared with gefitinib alone in patients with untreated EGFR-mutant NSCLC brain
                            4
                            2025EvidenceUpdates
                            Rezivertinib versus gefitinib as first-line therapy for patients with EGFR-mutated locally advanced or metastatic non-small-cell lung cancer (REZOR): a multicentre, double-blind, randomised, phase 3 study This study aimed to compare the efficacy and safety of rezivertinib (BPI-7711) and gefitinib as first-line therapies in patients with EGFR-mutated locally advanced or metastatic non-small-cell lung cancer (NSCLC). This multicentre, double-blind, randomised, phase 3 study (REZOR) included eligible patients from 50 hospitals across China. Those who had been histologically or cytologically confirmed as having NSCLC with EGFR exon 19 deletion or exon 21 Leu858Arg mutation by central laboratory were randomly assigned (1:1) to receive once daily either rezivertinib 180 mg or gefitinib 250 mg
                            5
                            2024JAMA oncology
                            Gefitinib vs Gefitinib Plus Pemetrexed and Carboplatin Chemotherapy in EGFR-Variant Lung Cancer-Long-Term Results of a Randomized Clinical Trial. This randomized clinical trial examines whether adding chemotherapy with pemetrexed and carboplatin to gefitinib improves survival among patients with epidermal growth factor receptor (EGFR)–variant non–small cell lung cancer.
                            6
                            2022EvidenceUpdates
                            Updated Analysis of NEJ009: Gefitinib-Alone Versus Gefitinib Plus Chemotherapy for Non-Small-Cell Lung Cancer With Mutated EGFR JCO In a randomized, open-label, phase III NEJ009 study, gefitinib plus chemotherapy significantly improved progression-free survival (PFS) and overall survival (OS) compared with gefitinib-alone in patients with untreated non-small-cell lung cancer harboring mutations in epidermal growth factor receptor. Herein, we report the updated survival outcome and long-term tolerability. Patients were randomly assigned to gefitinib (gefitinib 250 mg orally, once daily) and gefitinib combined with carboplatin plus pemetrexed (GCP in a 3-week cycle for six cycles followed by concurrent gefitinib and pemetrexed maintenance) groups. At the data cutoff (May 22, 2020), GCP demonstrated
                            7
                            2025Lung Cancer
                            Long-term outcomes of neoadjuvant gefitinib in resectable stage II-IIIA non-small cell lung cancer: A phase II, prospective cohort study. Our previous study has showed the safety and efficacy of preoperative gefitinib in patients with stage II-IIIA resectable non-small cell lung cancer (NSCLC). This study aimed to report the long-term survival analysis and recurrent patterns. This was a single -arm, phase II clinical trial. Patients with resectable stage II-IIIA NSCLC harboring EGFR exon 19 deletion or exon 21 L858R mutations were enrolled. Patients were administrated with preoperative gefitinib (250 mg once daily for 42 days), followed by surgical resection. The primary endpoint was objective response rate (ORR); secondary endpoints included the rate of major pathologic response (MPR
                            8
                            2025Lung Cancer
                            Gefitinib for EGFR mutated lung adenocarcinoma during pregnancy: A case report with 5-Year Follow-Up. We report the case of a 37-year-old pregnant woman at 19 weeks of gestation who was diagnosed with a stage M1b EFGR lung adenocarcinoma, in 2019. After a right upper and middle bilobectomy (T3N1 and R0 pathological status) and a complete cerebellar metastasis resection, she was treated with gefitinib, which offered her a prolonged recurrence-free survival without any negative consequence for the fetal development or the future development of her now 5- year- old child.
                            9
                            2023Lancet
                            Combination of gefitinib and methotrexate to treat tubal ectopic pregnancy (GEM3): a multicentre, randomised, double-blind, placebo-controlled trial. Tubal ectopic pregnancies can cause substantial morbidity or even death. Current treatment is with methotrexate or surgery. Methotrexate treatment fails in approximately 30% of women who subsequently require rescue surgery. Gefitinib, an epidermal growth factor receptor inhibitor, might improve the effects of methotrexate. We assessed the efficacy of oral gefitinib with methotrexate, versus methotrexate alone, to treat tubal ectopic pregnancy. We performed a multicentre, randomised, double-blind, placebo-controlled trial across 50 UK hospitals. Participants diagnosed with tubal ectopic pregnancy were administered a single dose of intramuscular
                            10
                            Lazertinib versus Gefitinib as First-Line Treatment for EGFR-mutated Locally Advanced or Metastatic NSCLC: LASER301 Korean Subset. This subgroup analysis of the Korean subset of patients in the phase 3 LASER301 trial evaluated the efficacy and safety of lazertinib versus gefitinib as first-line therapy for epidermal growth factor receptor mutated (EGFRm) non-small cell lung cancer (NSCLC ). Patients with locally advanced or metastatic EGFRm NSCLC were randomized 1:1 to lazertinib (240 mg/day) or gefitinib (250 mg/day). The primary endpoint was investigator-assessed progression-free survival (PFS). In total, 172 Korean patients were enrolled (lazertinib, n=87; gefitinib, n=85). Baseline characteristics were balanced between the treatment groups. One-third of patients had brain metastases (BM
                            11
                            2024Lung Cancer
                            Ningetinib plus gefitinib in EGFR-mutant non-small-cell lung cancer with MET and AXL dysregulations: A phase 1b clinical trial and biomarker analysis. MET and AXL dysregulations are implicated in acquired resistance to EGFR-TKIs in NSCLC. But consensus on the optimal definition for MET/AXL dysregulations in EGFR-mutant NSCLC is lacking. Here, we investigated the efficacy and tolerability of ningetinib (a MET/AXL inhibitor) plus gefitinib in EGFR-mutant NSCLC, and evaluated the clinical relevance of MET/AXL dysregulations by different definitions. Patients in this phase 1b dose-escalation/dose-expansion trial received ningetinib 30 mg/40 mg/60 mg plus gefitinib 250 mg once daily. Primary endpoints were tolerability (dose-escalation) and objective response rate (dose-expansion). MET/AXL status
                            12
                            2024Journal of Clinical Oncology
                            Overall Survival From the EORTC LCG-163 APPLE Trial of Osimertinib Versus Gefitinib Followed by Osimertinib in Advanced EGFR-Mutant Non-Small-Cell Lung Cancer. JCO Osimertinib has been established as a standard of care for patients with common sensitizing -mutant advanced non-small-cell lung cancer (NSCLC) although the sequential approach (first-generation inhibitor gefitinib followed by osimertinib) has not been formally compared. The phase II APPLE trial (ClinicalTrials.gov identifier: NCT02856893) enrolled 156 treatment-naïve patients, and two treatment strategies were evaluated: osimertinib up front or the sequential treatment approach with gefitinib up front followed by osimertinib at the time of progression, either molecular progression (detection of plasma T790M resistance mutation
                            13
                            2024Molecular Therapy
                            CRISPR-mediated ablation of TP53 and EGFR mutations enhances gefitinib sensitivity and anti-tumor efficacy in a mouse model of lung cancer. Multiple pathogenic single-nucleotide polymorphism (SNP)s have been identified as contributing factors in the aggravation of cancer prognosis and emergence of drug resistance in various cancers. Here we targeted a mutated EGFR and TP53 oncogene harboring a single-nucleotide missense mutation (EGFR-T790M and TP53-R273H), that associated with gefitinib resistance. Co-delivery of adenine base editor and EGFR and TP53 SNP-specific single-guide RNA via adenovirus resulted in precise correction at the oncogenic mutation site with high accuracy and efficiency in vitro and in vivo. Importantly, compared to a control group treated only with a gefitinib, an EGFR
                            14
                            The Impact of Baseline Vitamin D Level in Patients Receiving Gefitinib-Directed Therapy for EGFR-Mutant Non-Small-Cell Lung Cancer. There is contradicting evidence on vitamin D levels and cancer mortality rates. In this study, we aimed to evaluate the impact of baseline vitamin D level on the outcome in patients with estimated glomerular filtration rate (EGFR)-mutant advanced non-small-cell lung cancer (NSCLC) who received either gefitinib or gefitinib with chemotherapy (pemetrexed and carboplatin) as first-line therapy in a prospective randomized study. This was a post hoc analysis of a phase III randomized trial comparing gefitinib with gefitinib with carboplatin and pemetrexed in patients with advanced NSCLC with activating EGFR mutations in the first-line setting. As a part of regular
                            15
                            FTO promotes gefitinib-resistance by enhancing PELI3 expression and autophagy in non-small cell lung cancer. The established recognition of N6-methyladenosine (m6A) modification as an indispensable regulatory agent in human cancer is widely accepted. However, the understanding of m6A's role and the mechanisms underlying its contribution to gefitinib resistance is notably limited. Herein, using RT -qPCR, Western blot, Cell proliferation and apoptosis, as well as RNA m6A modification assays, we substantiated that heightened FTO (Fat Mass and Obesity-associated protein) expression substantially underpins the emergence of gefitinib resistance in NSCLC cells. This FTO-driven gefitinib resistance is hinged upon the co-occurrence of PELI3 (Pellino E3 Ubiquitin Protein Ligase Family Member 3
                            16
                            2024Journal of Ethnopharmacology
                            Mechanistic Insights into Yifei Sanjie Pill's Regulation of EMT to Enhance Gefitinib Treatment effect in NSCLC by in silico analysis and experimental validation. The Yi-Fei San-Jie pill (YFSJ) is a well-known Chinese medicine that has been used to treat non-small cell lung cancer in China for decades. Previous studies have shown that YFSJ combined with gefitinib can effectively inhibit the proliferation of gefitinib-resistant non-small cell lung cancer (NSCLC) cell lines by promoting apoptosis and autophagy, but the molecular biological mechanisms involved and whether YFSJ combined with gefitinib can have synergistic effects still need to be further explored. Thus, the present study aimed to establish an in silico and experimental framework to decipher the underlying mechanism by which YFSJ
                            17
                            Gefitinib (an EGFR tyrosine kinase inhibitor) plus anlotinib (an multikinase inhibitor) for untreated, EGFR-mutated, advanced non-small cell lung cancer (FL-ALTER): a multicenter phase III trial. Dual inhibition of vascular endothelial growth factor and epidermal growth factor receptor (EGFR) signaling pathways offers the prospect of improving the effectiveness of EFGR-targeted therapy . In this phase 3 study (ClinicalTrial.gov: NCT04028778), 315 patients with treatment-naïve, EGFR-mutated, advanced non-small cell lung cancer (NSCLC) were randomized (1:1) to receive anlotinib or placebo plus gefitinib once daily on days 1-14 per a 3-week cycle. At the prespecified final analysis of progression-free survival (PFS), a significant improvement in PFS was observed for the anlotinib arm over
                            18
                            2024BMC Cancer
                            FTO/m6A mediates miR-138-5p maturation and regulates gefitinib resistance of lung adenocarcinoma cells by miR-138-5p/LCN2 axis. Lung cancer (LC) occupies an important position in the lethality of cancer patients. Acquired resistance to gefitinib in lung adenocarcinoma (LUAD) seriously affects the therapeutic efficacy of LC. Thus, it is of major scientific and clinical significance to probe the mechanism of gefitinib resistance in LUAD for ameliorating the prognosis of patients. The expression of miRNAs in gefitinib-resistant LUAD cells was validated using qRT-PCR. Cell viability was assessed through CCK-8, whereas cell death was examined through PI staining. Changes in the ferroptosis process were evaluated by detecting the intracellular Glutathione (GSH), Malondialdehyde (MDA), and Reactive
                            19
                            2024BMC Cancer
                            First-line treatment with gefitinib in combination with bevacizumab and chemotherapy in advanced non-squamous NSCLC with EGFR-mutation. The safety and efficacy of combination of gefitinib with chemotherapy and bevacizumab in treatment patients with epidermal growth factor receptor (EGFR) mutations are currently unknown. This study was designed to evaluate the safety and preliminary efficacy of a combination therapy consisting of gefitinib, bevacizumab, pemetrexed, and carboplatin in patients with advanced non-squamous non-small cell lung cancer (NSCLC) harboring EGFR mutations. Eligible patients with EGFR-mutated advanced non-squamous NSCLC were recruited and received gefitinib combination with bevacizumab plus pemetrexed and carboplatin treatment. The primary endpoints were safety and progression
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                            2018European Medicines Agency - EPARs
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