^
    4years
    Phase 1 Study of the Efficacy and Safety of Ramucirumab in Combination with Osimertinib in Advanced T790M-Positive EGFR-Mutant Non-Small Cell Lung Cancer. (PubMed, Clin Cancer Res)
    Ramucirumab plus osimertinib demonstrated encouraging safety and antitumor activity in T790M-positive EGFR-mutant NSCLC.
    Clinical • P1 data • Journal • Combination therapy
    |
    EGFR (Epidermal growth factor receptor) • KDR (Kinase insert domain receptor)
    |
    EGFR mutation • EGFR L858R • EGFR exon 19 deletion • MET amplification • EGFR T790M • EGFR amplification • EGFR C797S • EGFR L858R + EGFR T790M • EGFR C797S + EGFR T790M + EGFR L858R • EGFR C797S + EGFR T790M + EGFR exon 19 deletion • EGFR positive • MET amplification + EGFR mutation • EGFR T790M + EGFR C797S • EGFR exon 2-7 deletion + EGFR amplification • EGFR mutation + EGFR T790M • EGFR exon 19 deletion + MET amplification • EGFR mutation + EGFR T790M + EGFR C797S • EGFR T790M + exon 19 deletion
    |
    Tagrisso (osimertinib)
    over4years
    EGFR mutation genotypes affect efficacy and resistance mechanisms of osimertinib in T790M-positive NSCLC patients. (PubMed, Transl Lung Cancer Res)
    Our findings indicate that the EGFR 19Del subtypes affect the clinical outcomes and resistance mechanisms to osimertinib in T790M-positive patients. Identifying patients with relatively worse treatment outcomes may be informative for establishing new therapies for these patients.
    Clinical • Journal
    |
    EGFR (Epidermal growth factor receptor)
    |
    EGFR mutation • EGFR L858R • EGFR exon 19 deletion • EGFR C797S • EGFR L858R + EGFR T790M • EGFR C797S + EGFR T790M + EGFR L858R • EGFR C797S + EGFR T790M + EGFR exon 19 deletion • EGFR L858R + EGFR exon 19 deletion • EGFR T790M + exon 19 deletion
    |
    Tagrisso (osimertinib)
    over4years
    [VIRTUAL] Progression after osimertinib in EGFR T790M-mutated non-small cell cancer patients (ERS 2020)
    Resistance mechanisms to osimertinib are diverse, therefore re-biopsy and Next Generation Sequencing are important to decide the subsequent strategy.
    Clinical
    |
    EGFR (Epidermal growth factor receptor) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
    |
    EGFR mutation • PIK3CA mutation • MET amplification • EGFR T790M • ALK fusion • EGFR C797S • PIK3CA amplification • EGFR C797S + EGFR T790M + EGFR exon 19 deletion • EGFR mutation + EGFR T790M • EGFR mutation + EGFR T790M + EGFR C797S • EGFR T790M + exon 19 deletion
    |
    Tagrisso (osimertinib)
    over4years
    Histological transformation of lung adenocarcinoma to small cell lung cancer with mutant C797S conferring acquired resistance to osimertinib. (PubMed, J Int Med Res)
    A man with recurrent lung adenocarcinoma harboring an EGFR exon 19 deletion received erlotinib for 10 months following curative surgery and adjuvant chemotherapy...The tumor was reduced after four cycles of etoposide and cisplatin and his respiratory symptoms improved...The patient received paclitaxel plus cisplatin for two cycles with partial response. Because heterogeneous genetic and phenotypic mechanisms of TKI-resistance may occur at different times and locations, histopathological and molecular testing both provide evidence to support appropriate treatment.
    Preclinical • Journal
    |
    EGFR (Epidermal growth factor receptor) • RB1 (RB Transcriptional Corepressor 1)
    |
    EGFR mutation • EGFR exon 19 deletion • EGFR T790M • EGFR C797S • RB1 deletion • RB1 mutation • EGFR C797S + EGFR T790M + EGFR exon 19 deletion • EGFR T790M + exon 19 deletion
    |
    cisplatin • Tagrisso (osimertinib) • erlotinib • paclitaxel • etoposide IV