PMC7537839_01
Therapeutic course timeline followed in the patient. (A) pemetrexed + carboplatin + radiotherapy + maintenance therapy of pemetrexed; (B) afatinib + radiotherapy; (C) pembrolizumab; (D) paclitaxel + carboplatin + bevacizumab; (E) T-DM1; (F) afatinib; (G) gemcitabine + intracavitary administration of Recombinant Human Endostatin Injection (ENDOSTAR); (H) pyrotinib.
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We summarized the therapeutic regimens received and major mutations detected in Figure 1.
Image scans revealed the clinical response to the treatment of pyrotinib.
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August 28, 2019, revealed progression of the lung, bone, and lymph node lesions with bulk pleural effusion (Figure 2). At the same time, the patient showed hypoproteinemia, cough, chest distress, and shortness of breath after activity. He achieved partial response according to the Response Evaluation Criteria in Solid Tumors 1.1 (Figure 2).
Molecular analysis of the patient before and after pyrotinib treatment. (A) NGS analysis based on pleural effusion showed ERBB2 exon 20 p.Y772_A775dup before pyrotinib treatment. (B) NGS analysis based on pleural effusion showed ERBB2 copy-number amplification is 4.5 before pyrotinib treatment. (C) NGS analysis based on pleural effusion showed ERBB2 exon 20 p.Y772_A775dup after pyrotinib treatment. (D) NGS analysis based on pleural effusion showed no copy number gain after pyrotinib treatment.
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NGS analysis (Burning Rock Biotech, Guangzhou, China) of pleural effusion ctDNA showed HER2 exon 20 p.Y772_A775dup (38.86%) and HER2 amplification (copy number: 4.5) (Figure 3). Dynamic monitoring of the pleural effusion ctDNA (Burning Rock Biotech, Guangzhou, China) showed that the HER2 mutation ratio had decreased significantly (7.99%) and the amplification had disappeared (Figure 3).
Fluctuation of CEA level in the blood. CEA, carcinoembryonic antigen.
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The levels of tumor CEA showed dynamic changes with different treatments (Figure 4).