PMC7727031_01
Representative clinical images, carcinoembryonic antigen (CEA), and cancer antigen 125 (CA-125) monitoring during the course of treatment. (A) Computed tomography (CT) scans showed the patient's tumor mass (arrows) during alectinib treatment. The levels of (B) CEA and (C) CA-125 (purple arrows) show that the disease was controlled under alectinib treatment. PR, partial response; NGS, next-generation sequencing.
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Chinese male with no history of smoking or alcohol consumption visited our hospital in October 2018 with the chief complaint of dyspnea and pain in his right leg and left chest. Computed tomography (CT) revealed a massive shadow in the upper lobe of the left lung, as well as pleural effusion, and metastases in both lungs and mediastinal lymph nodes (Figure 1A). Two weeks post-treatment, chest-CT showed a decreased tumor mass (Figure 1A), and the clinical ECOG PS was 1. Three months later, the patient achieved a partial response (PR), which was demonstrated by CT reexamination (Figure 1A), and a sustained response was ongoing as of April 2020. Throughout the course of alectinib treatment, the levels of circulating CEA and CA-125 dramatically decreased and was maintained at a relatively low level compared to pre-treatment levels (Figure 1B and C).
Identification of the STRN-ALK fusion by targeted next-generation sequencing. (A) Paired-end sequencing data indicated the somatic intrachromosomal STRN-ALK fusion, as demonstrated by the Integrative Genomics Viewer. (B) The schematic structure of the genomic DNA sequence shows the STRN-ALK fusion points.
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The circulating tumor DNA (ctDNA) from plasma and pleural effusion revealed an STRN: exon3-ALK: exon20 fusion (Figure 2), with a high mutant allele frequency (8.7% and 15.9%, respectively).