Publication-only abstracts (abstract number preceded by an "e"), published in conjunction with the 2019 ASCO Annual Meeting but not presented at the Meeting, can be found online only.
Phase (Ph) I/II study of pembrolizumab (P) with gemcitabine (G) in patients (pts) with previously-treated advanced (Adv) non-small cell lung cancer (NSCLC).
Metastatic Non-Small Cell Lung Cancer
Lung Cancer—Non-Small Cell Metastatic
2019 ASCO Annual Meeting
J Clin Oncol 37, 2019 (suppl; abstr e20652)
Author(s): Rachel E. Sanborn, Regan M. Duffy, Brenda K Fisher, Kelly Shea Perlewitz, Herschel D. Wallen, Rui Li, William L Redmond, Yoshinobu Koguchi, Bernard A. Fox; Earle A. Chiles Research Institute, Providence Cancer Institute, Portland, OR; Providence Cancer Center, Portland, OR; Earle A. Chiles Research Institute at Robert W. Franz Cancer Center, Providence Cancer Institute, Portland, OR; Providence Oncology and Hematology Care Clinic, Newberg, OR; Providence Cancer Institute, Portland, OR; Earle A. Chiles Research Institute at the Robert W. Franz Cancer Center, Portland, OR
Background: P has demonstrated improved survival alone or with chemotherapy in untreated adv NSCLC. G may increase antigen cross-presentation and prime CD8 T cell response via tumor apoptosis. This study evaluated P + G in pts with previously-treated adv NSCLC naïve to anti-PD1. Methods: The study included ph 1 (previously reported), then single arm ph II, 1-3 prior therapies, regardless of PD-L1 status. Treatment: G, 1250 mg/m2, Days (D) 1 & 8 + P 200 mg D 1; 21-day cycles. G given max 6 cycles, P max 2 years. Tumor tissue was collected for PD-L1 (22C3). Immune response via whole blood immunophenotyping and ProtoArray was conducted. Results: 16 pts enrolled. Male/Female: 8/8; Age 53-75 (Median 64.5); ECOG 0/1: 2/14 pts, respectively. Median prior therapies: 1 (Range (R) 1-3). Median cycles: 4 (R 1-24). Primary reason for discontinuation: progression. Toxicity was primarily attributed to G, including Gr 3: neutropenia (5), leukopenia (3), anemia (2); lymphopenia, URI, hyponatremia (1 each). Gr 4: 1 hypoxia attributed to intrapulmonary hemorrhage from G. Other toxicities attributed to both G and P included dyspnea (2), pneumonitis (2) (Gr 3). Progression free survival (PFS): 3.2 months (m) (R 0.6-18.5 m). Overall survival (OS) is not yet mature (4 pts in follow up). 14/16 pts were evaluable for response. Stable disease (SD): 9 (56%); partial response (PR): 2 (13%); progression (PD): 3 (19%). 2 pts discontinued prior to first evaluation (1 pulmonary hemorrhage; 1 clinical progression). 1 pt had SD as best response for 18.5 m before PD. Disease control rate (DCR; CR + PR + SD): 56%. 12 pts were PD-L1 evaluable (central). 2 pts had PD-L1 testing through alternate source (22C3). Of the 14 pts with PD-L1 result: PD-L1 0%: 8 (50%); PD-L1 10-40%: 3; ≥50%: 3 (19% each) PFS of 0% PD-L1: 3.75 m (1 PR, 6 SD; DCR 88%). PFS ≥50% PD-L1: 3 m (1 SD, 0 PR). Exploratory immune profiling showed late peripheral immune activation in 3 of 6 pts with Cycle 6 samples (all SD; PFS 5.8 m). ProtoArray analysis is pending. Conclusions: P+G was a feasible combination, without unexpected toxicity. The majority of pts had 0% PD-L1 expression. PFS was not associated with PD-L1 level. PFS did not differ from G or P alone. OS pending. Clinical trial information: NCT02422381