scholarly journals Squamous cell transformation as a mechanism of acquired resistance to tyrosine kinase inhibitor in EGFR‐mutated lung adenocarcinoma: a report of two cases

2020 ◽  
Vol 8 (2) ◽  
Author(s):  
Hironori Uruga ◽  
Takeshi Fujii ◽  
Nobuyuki Nakamura ◽  
Shuhei Moriguchi ◽  
Kazuma Kishi ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Tyrosine Kinase Inhibitor ◽  
Squamous Cell ◽  
Kinase Inhibitor ◽  
Cell Transformation ◽  
Acquired Resistance ◽  
Egfr Mutated

scholarly journals Acquired Resistance of EGFR-Mutated Lung Cancer to Tyrosine Kinase Inhibitor Treatment Promotes PARP Inhibitor Sensitivity

Cell Reports ◽  
2019 ◽  
Vol 27 (12) ◽  
pp. 3422-3432.e4 ◽  
Author(s):  
Lynnette Marcar ◽  
Kankana Bardhan ◽  
Liliana Gheorghiu ◽  
Patrick Dinkelborg ◽  
Heike Pfäffle ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Parp Inhibitor ◽  
Acquired Resistance ◽  
Egfr Mutated ◽  
Inhibitor Treatment

scholarly journals The mechanism of acquired resistance to irreversible EGFR tyrosine kinase inhibitor-afatinib in lung adenocarcinoma patients

Oncotarget ◽  
2016 ◽  
Vol 7 (11) ◽  
pp. 12404-12413 ◽  
Author(s):  
Shang-Gin Wu ◽  
Yi-Nan Liu ◽  
Meng-Feng Tsai ◽  
Yih-Leong Chang ◽  
Chong-Jen Yu ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Acquired Resistance ◽  
Egfr Tyrosine Kinase Inhibitor ◽  
Egfr Tyrosine Kinase

scholarly journals Dual EGFR and ABL Tyrosine Kinase Inhibitor Treatment in a Patient with Concomitant EGFR-Mutated Lung Adenocarcinoma and BCR-ABL1-Positive CML

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Kousuke Watanabe ◽  
Hidenori Kage ◽  
Saki Nagoshi ◽  
Kazuhiro Toyama ◽  
Yoshiyuki Ohno ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Present Report ◽  
Oral Drug ◽  
Molecular Response ◽  
Double Primary Cancers ◽  
Tki Treatment ◽  
Egfr Mutated

Tyrosine kinase inhibitor (TKI) combination is expected to increase in the era of precision medicine. TKI combination may be required to treat double primary cancers, each having a targetable gene, or to treat a single malignancy with multiple targetable genes. Here, we demonstrate the first report of dual EGFR and ABL TKI treatment in a patient with concomitant EGFR-mutated lung adenocarcinoma and BCR-ABL1-positive chronic myeloid leukemia (CML). A 60-year-old man with an 8-year history of CML was diagnosed as advanced EGFR-mutated lung adenocarcinoma. Complete molecular response of CML had been achieved by imatinib, and ABL-TKI had been switched to nilotinib four years previously due to muscle cramps. We discontinued nilotinib and started afatinib. Although partial response of lung adenocarcinoma was achieved, cytogenetic relapse of CML was observed following nilotinib discontinuation. We applied the previously described framework of cytochrome P450 3A4-mediated oral drug-drug interactions and selected gefitinib and nilotinib to treat both malignancies. We effectively and safely administered this combination for seven months. The present report is the first to demonstrate the safety and efficacy of dual EGFR and ABL TKI treatment in a patient with concomitant EGFR-mutated lung adenocarcinoma and CML.

scholarly journals A case with small-cell transformation after treatment with EGFR tyrosine kinase inhibitor for lung adenocarcinoma

2015 ◽  
Vol 26 ◽  
pp. vii138
Author(s):  
Atsushi Osoegawa ◽  
Takafumi Hashimoto ◽  
Takumi Yohei ◽  
Abe Miyuki ◽  
Suehiro Shuji ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Cell Transformation ◽  
Small Cell ◽  
Egfr Tyrosine Kinase Inhibitor ◽  
Egfr Tyrosine Kinase
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