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BIOMARKER:

EGFR C797S + T790M + exon 19 deletion

i
Other names: EGFR, ERBB, ERBB1, Epidermal growth factor receptor
Entrez ID:
8ms
Ramucirumab plus osimertinib demonstrated encouraging safety and antitumor activity in T790M-positive EGFR-mutant NSCLC.
Clinical • P1 data • Journal • Combination therapy
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EGFR (Epidermal growth factor receptor) • KDR (Kinase insert domain receptor)
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EGFR mutation • EGFR L858R • MET amplification • EGFR T790M • EGFR exon 19 deletion • EGFR amplification • EGFR C797S • EGFR L858R + T790M • EGFR T790M + exon 19 deletion • EGFR T790M + C797S • MET amplification + EGFR mutation • EGFR C797S + T790M + L858R • EGFR C797S + T790M + exon 19 deletion • EGFR exon 19 deletion + MET amplification • EGFR mutation + EGFR T790M • EGFR mutation + EGFR T790M + EGFR C797S • EGFR mutation + EGFR amplification • EGFR positive
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Tagrisso (osimertinib)
11ms
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
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EGFR (Epidermal growth factor receptor)
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EGFR mutation • EGFR L858R • EGFR exon 19 deletion • EGFR C797S • EGFR L858R + T790M • EGFR T790M + exon 19 deletion • EGFR C797S + T790M + L858R • EGFR C797S + T790M + exon 19 deletion • EGFR L858R + EGFR exon 19 deletion
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Tagrisso (osimertinib)
11ms
Resistance mechanisms to osimertinib are diverse, therefore re-biopsy and Next Generation Sequencing are important to decide the subsequent strategy.
Clinical
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EGFR (Epidermal growth factor receptor) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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EGFR mutation • PIK3CA mutation • MET amplification • EGFR T790M • ALK fusion • EGFR C797S • PIK3CA amplification • EGFR T790M + exon 19 deletion • EGFR C797S + T790M + exon 19 deletion • EGFR mutation + EGFR T790M • EGFR mutation + EGFR T790M + EGFR C797S
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Tagrisso (osimertinib)
12ms
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
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EGFR (Epidermal growth factor receptor) • RB1 (RB Transcriptional Corepressor 1)
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EGFR mutation • EGFR T790M • EGFR exon 19 deletion • EGFR C797S • RB1 mutation • EGFR T790M + exon 19 deletion • RB1 deletion • EGFR C797S + T790M + exon 19 deletion
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cisplatin • erlotinib • Tagrisso (osimertinib) • paclitaxel • etoposide IV
1year
Current approved treatment for EGFR mutation-positive NSCLC has been revolutionized with three generations of EGFR tyrosine kinase inhibitors (TKIs): the first- and second-generation TKIs, such as gefitinib, erlotinib and afatinib, selectively targeting EGFR activating mutations existing in exon 19 and 21; and the third-generation EGFR-wild-type sparing, irreversible activating mutations/T790M inhibitor, osimertinib. Further phenotypic analysis demonstrated that the triple-mutation cell line was resistant to the third generation inhibitors in contrast to the parental double-mutation cell line. This newly developed triple-mutation lung cancer cell line provided a very useful tool for oncology drug discovery for NSCLC.
EGFR (Epidermal growth factor receptor)
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EGFR mutation • EGFR L858R • EGFR overexpression • EGFR C797S • EGFR L858R + T790M • EGFR C797S + T790M + L858R • EGFR C797S + T790M + exon 19 deletion • EGFR H1975
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erlotinib • Gilotrif (afatinib) • gefitinib • Tagrisso (osimertinib)
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