Indication
EGFR T790M mutation-positive non-small cell lung cancer
EGFR T790M mutation-positive non-small cell lung cancer is a molecularly defined subtype of epithelial lung malignancy characterized by a specific threonine-to-methionine substitution at amino acid position 790 within exon 20 of the epidermal growth factor receptor gene. Read more about EGFR T790M mutation-positive non-small cell lung cancer
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Common EGFR T790M mutation-positive non-small cell lung cancer therapies.
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Coming soonEGFR T790M mutation-positive non-small cell lung cancer is a molecularly defined subtype of epithelial lung malignancy characterized by a specific threonine-to-methionine substitution at amino acid position 790 within exon 20 of the epidermal growth factor receptor gene.
This alteration primarily emerges in patients with advanced or metastatic non-small cell lung cancer as an acquired mechanism of secondary resistance following prior therapy with first- or second-generation EGFR tyrosine kinase inhibitors, though it rarely arises de novo.
Pathophysiologically, the mutation alters the ATP-binding pocket of the kinase domain via steric hindrance and increased affinity for ATP, restoring downstream oncogenic signaling and promoting tumor progression.
- cancer.gov
EGFR T790M mutation-positive non-small cell lung cancer is a molecularly defined subtype of epithelial lung malignancy characterized by a specific threonine-to-methionine substitution at amino acid position 790 within exon 20 of the epidermal growth factor receptor gene This alteration primarily emerges in patients with advanced or metastatic non-small cell lung cancer as an acquired mechanism of secondary resistance following prior therapy with first- or second-generation EGFR tyrosine kinase i...
- actaoncologicaturcica.com
EGFR T790M mutation-positive non-small cell lung cancer is a molecularly defined subtype of epithelial lung malignancy characterized by a specific threonine-to-methionine substitution at amino acid position 790 within exon 20 of the epidermal growth factor receptor gene
- fda.gov
This alteration primarily emerges in patients with advanced or metastatic non-small cell lung cancer as an acquired mechanism of secondary resistance following prior therapy with first- or second-generation EGFR tyrosine kinase inhibitors, though it rarely arises de novo
- mdpi.com
This alteration primarily emerges in patients with advanced or metastatic non-small cell lung cancer as an acquired mechanism of secondary resistance following prior therapy with first- or second-generation EGFR tyrosine kinase inhibitors, though it rarely arises de novo
- oncokb.org
Pathophysiologically, the mutation alters the ATP-binding pocket of the kinase domain via steric hindrance and increased affinity for ATP, restoring downstream oncogenic signaling and promoting tumor progression
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