Abstract 1426P
Background
Comprehensive genomic profiling (CGP) assays have been utilized with advanced solid tumor patients who have completed standard chemotherapy in Japan. These assays are expected to investigate the driver oncogenes comprehensively, especially for patients with advanced non-small cell lung cancer (NSCLC) whose driver oncogenes have not been detected at initial diagnosis. However, there are few reports on the proportion of advanced NSCLC patients with undetected driver oncogenes at initial diagnosis who have newly identified driver oncogenes using CGP assays.
Methods
We retrospectively analyzed patients with advanced NSCLC who received CGP assays between August 2019 and March 2022. Patients under the age of 20 years were excluded. We used the Center for Cancer Genomics and Advanced Therapeutics database. The driver oncogenes were defined as EGFR, ALK, ROS1, BRAF V600E, KRAS, HER2, MET exon 14 skipping, RET and NTRK. We investigated the proportion of driver oncogenes in patients with NSCLC and which were newly identified using CGP assays.
Results
A total of 986 NSCLC patients who received CGP assays were enrolled. The adenocarcinoma, squamous cell carcinoma, not other specified, other types of patients were 764 (77.5%), 128 (13.0%), 86 (8.7%), and 8 (0.8%) cases, respectively. Among all patients, 451 (45.7%) patients were detected driver oncogenes. Among 330 NSCLC patients with undetected EGFR, ALK, ROS1, and BRAF V600E at initial diagnosis, 121 (36.7%) patients had newly identified driver oncogenes. EGFR mutation was 4 (1.2%) patients of exon 19 deletion, 1 (0.3%) patient of exon 21 L858R, 12 (3.6%) patients of exon 20 insertion, and 1 (0.3%) patient of G719A. ALK and BRAF V600E were 1 (0.3%) patient, respectively. The other driver oncogenes detected using CGP assays were 23 (7.0%) patients of KRAS G12C, 40 (12.1%) patients of KRAS non-G12C, 20 (6.1%) patients of HER2 mutation, 14 (4.2%) patients of MET exon 14 skipping, and 4 (1.2%) patients of RET.
Conclusions
CGP assays are useful for identifying driver oncogenes in patients with advanced NSCLC, especially for patients whose driver oncogenes were not identified at initial diagnosis.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Graduate School of Medical Science, Kyoto Prefectural University of Medicine.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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