Amivantamab (JNJ-61186372) induces clinical, biochemical, molecular, and radiographic response in a treatment-refractory NSCLC patient harboring amplified triple EGFR mutations (L858R/ T790M/G796S) in cis

Amivantamab (JNJ-61186372) induces clinical, biochemical, molecular, and radiographic response in a treatment-refractory NSCLC patient harboring amplified triple EGFR mutations (L858R/ T790M/G796S) in cis

The sequential use of 1st-/2nd-generation to 3rd-generation epidermal growth factor (EGFR) tyrosine kinase inhibitors (TKIs) has led to the emergence of triple EGFR mutations generally consisting of the founder mutation (del 19 or L858R), gatekeeper mutation (T790M) and mutation (C797S) that abolish...

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Bibliographic Details
Main Authors: Balmanoukian, A.S (Author), Klempner, S.J (Author), Madison, R. (Author), Nagasaka, M. (Author), Ou, S.-H.I (Author), Zhang, S.S (Author)
Format: Article
Language:English
Published: Elsevier Ireland Ltd 2022
Subjects:
amivantamab
Amivantamab
Antibodies, Bispecific
bispecific antibody
bi-specific antibody
drug resistance
Drug Resistance, Neoplasm
EGFR amplification
EGFR protein, human
EGFR triple mutation
EGFR/MET dual inhibition
epidermal growth factor
Epidermal Growth Factor
epidermal growth factor receptor
ErbB Receptors
genetics
human
Humans
L858R/T790M/G796S
Lung Neoplasms
lung tumor
mutation
Mutation
Osimertinib esistance
protein kinase inhibitor
Protein Kinase Inhibitors
Trogocytosis
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