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Danielle Collons
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P33 - Pathology - Immunotherapy Biomarker (ID 101)
- Event: WCLC 2020
- Type: Posters
- Track: Pathology, Molecular Pathology and Diagnostic Biomarkers
- Presentations: 1
- Moderators:
- Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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P33.11 - Immunotherapy Outcomes in KRAS Mutated vs KRAS Wild-Type Advanced Lung Adenocarcinoma (ID 2006)
00:00 - 00:00 | Presenting Author(s): Danielle Collons
- Abstract
Introduction
KRAS is the most frequent oncogene driver mutation found in NSCLC in Western countries with the majority of KRAS mutations occurring in lung adenocarcinoma. Patients with KRAS-mutated NSCLC generally have poorer outcomes with chemotherapy and tyrosine kinase inhibitors. However, the predictive role of KRAS status in patients with NSCLC receiving immune checkpoint inhibitors (ICI) remains unclear. We sought to compare outcomes of advanced lung adenocarcinoma treated with ICI based on KRAS status.
Methods
From a single institution database of patients diagnosed with NSCLC from January 2016 to December 2018, we conducted a retrospective analysis of cases of stage IV lung adenocarcinoma who received treatment with ICI. A standard form was used to extract clinical characteristics including age, sex, race, treatment type, mutation status, PDL1 expression, disease control rate (DCR), partial response (PR), progression-free survival (PFS), and overall survival (OS).
Results
We identified 41 cases of stage IV lung adenocarcinoma treated with ICI, 8 were excluded due to insufficient data, 33 were included for analysis. The median age was 63 years, 19 (58%) of the patients were female, and 20 (61%) of the patients were black. 19 (58%) of the patients were treated with pembrolizumab, 7 (21%) with nivolumab, 5 (15%) with atezolizumab, and 2 (6%) with durvalumab. 16 patients (43%) had KRAS mutations, of which 3 (19%) had a concurrent MET mutation and 1 (6%) had a concurrent ALK mutation. The most common KRAS mutation was G12C with 7 (44%) cases. In the KRAS wild-type population, 10 (59%) patients had PDL1 expression >1% and DCR was 65% with 47% PR. In the KRAS mutated population, 14 (88%) of patients had PDL1 expression >1% and DCR was 75% with 63% PR. There was no difference in PFS (13.2mo vs 15.2mo, p = 0.47) or OS (16mo vs 16.7mo, p = 0.85) between KRAS wild-type vs KRAS mutated populations treated with ICI.
Conclusion
KRAS mutated advanced lung adenocarcinoma had similar PFS and OS compared with KRAS-wild type advanced lung adenocarcinoma treated with ICI despite numerically higher DCR and PDL1 expression in KRAS-mutants. Larger studies are needed to clarify the predictive role of KRAS mutational status in advanced lung adenocarcinoma treated with ICI.
