Changes in cross-sectional area of pulmonary vessels on chest computed tomography after chemotherapy in patients with advanced non-squamous non-small-cell lung cancer

2016 ◽  
Vol 77 (5) ◽  
pp. 1011-1018 ◽  
Author(s):  
Masato Karayama ◽  
Naoki Inui ◽  
Hideki Kusagaya ◽  
Seiichiro Suzuki ◽  
Yusuke Inoue ◽  
...  
2021 ◽  
Vol 16 (3) ◽  
pp. S280
Author(s):  
H. Onozawa ◽  
D. Nemoto ◽  
J. Miura ◽  
D. Eriguchi ◽  
H. Adachi ◽  
...  

2021 ◽  
Vol 59 (2) ◽  
pp. 240-246
Author(s):  
Hirohisa Kano ◽  
Toshio Kubo ◽  
Kiichiro Ninomiya ◽  
Eiki Ichihara ◽  
Kadoaki Ohashi ◽  
...  

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052092791 ◽  
Author(s):  
Xiaohui Ren ◽  
Xinfeng Cai ◽  
Jing Li ◽  
Xia Zhang ◽  
Jianfei Yu ◽  
...  

Epidermal growth factor receptor (EGFR) gene-mutated non-small cell lung cancer may initially respond to EGFR tyrosine kinase inhibitors (TKIs), but may subsequently become resistant; however, the resistance mechanisms remain unclear. We report a rare case of acquired resistance to osimertinib associated with transformation to small cell lung cancer (SCLC) with cis-C797S mutation. A man with recurrent lung adenocarcinoma harboring an EGFR exon 19 deletion received erlotinib for 10 months following curative surgery and adjuvant chemotherapy. However, he switched to osimertinib after repeat biopsy showed EGFR exon 19 deletion and T790M mutation leading to erlotinib resistance. His disease progressed after 15 months and repeat biopsy showed SCLC. Next-generation sequencing of peripheral blood detected EGFR exon 19 deletion, T790M mutation, cis-C797S mutation, and RB1 inactivation. The tumor was reduced after four cycles of etoposide and cisplatin and his respiratory symptoms improved. However, computed tomography after six cycles of chemotherapy showed multiple bilateral lung lesions, and single-photon emission computed tomography showed bone metastasis. 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.


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