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K. Huang
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P2.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 234)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P2.04-018 - Whole Transcriptome Analysis of EGFR Wildtype Non-Small Cell Lung Cancer Patients with Clinical Benefit from Erlotinib (ID 2357)
09:30 - 09:30 | Author(s): K. Huang
- Abstract
Background:
Despite the success of targeted assays of EGFR mutations in defining the non-small cell lung cancer patients who benefit from EGFR-tyrosine kinase inhibition, there still remains a significant portion of patients whose tumors do not harbor EGFR mutations, yet achieve clinical benefit (progression-free survival > 6 months) from erlotinib treatment. We apply whole transcriptome sequencing (RNAseq) to discover expression and mutation changes associated with erlotinib response.
Methods:
We report the results of 108 stage IV non-small cell lung cancer patients treated with first line erlotinib. The primary endpoint assessed was progression-free survival (PFS), to which erlotinib has already shown to be beneficial when compared to placebo. Furthermore, RNAseq was performed on 73 tumors from 29 (40%) males and 44 (60%) females. The RNAseq samples were processed to obtain mutation and expression data.
Results:
108 patients were followed for PFS, 7 of which declined to be followed, 2 came off erlotinib due to toxicity, 3 died before completion of the first cycle of erlotinib, 5 were ineligible, and 2 have not had tumor recurrence to date. The remaining 92 patients had a mean PFS of 4.71 months (±1.03 months, 95% CI). No patients experienced a complete response, and 14 of 92 (15%) patients had a partial response. Of the tumors analyzed via RNAseq, 7 harbored EGFR mutations, including a complex exon 18 deletion in a patient with a partial response to erlotinib. 14 of 64 (22%) patients without EGFR mutations showed clinical benefit from erlotinib, none of which harbored other known actionable mutations. These EGFR wildtype tumors did not exhibit mutations in other known oncogenes in lung cancer. We hypothesize that they are addicted to EGFR signaling through other means than overactive kinase activity caused by activating mutations. Figure 1
Conclusion:
We present results from a clinical trial of first line erlotinib in stage IV non-small cell lung cancer. We show that there is a significant cohort of EGFR wildtype patients who receive clinical benefit from erlotinib and present preliminary data of their mutation status.
