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M. Maemondo
Author of
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OA 05 - Next Generation TKI (ID 657)
- Event: WCLC 2017
- Type: Oral
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:James Chih-Hsin Yang, Fiona Blackhall
- Coordinates: 10/16/2017, 15:45 - 17:30, Room 301 + 302
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OA 05.08 - Final Result of Phase I/II Study (AF-001JP) of Alectinib, a Selective CNS-Active ALK Inhibitor, in ALK+ NSCLC Patients (Pts) (ID 9732)
17:00 - 17:10 | Author(s): M. Maemondo
- Abstract
- Presentation
Background:
Alectinib (ALC) is a selective, CNS-active ALK tyrosine kinase inhibitor. In two Phase 3 studies (J-ALEX and ALEX), ALC proved superior efficacy and tolerability compared to crizotinib (CRZ). Here we report the final efficacy and safety results of the 46 pts enrolled in the phase II part of study AF-001JP with a longer follow-up period than that observed in J-ALEX and ALEX studies.
Method:
ALC 300 mg b.i.d was given to ALK+ NSCLC pts who were ALK inhibitor-naive and had disease progression after at least one line of chemotherapy to investigate the efficacy and safety until the investigator confirmed no further clinical benefits.
Result:
This study was completed in December 2016. The median treatment duration was 46.1 months (range: 1-62). 20 of 46 pts were on treatment with alectinib at the study termination. Progressive disease (PD) was confirmed in 20 pts (43%). Median PFS was not reached and 4-year PFS rate was 52% (95% CI: 36-66). 14 of 46 pts had CNS metastasis at baseline. Median PFS was 38 months (95% CI: 9-NE) in pts with CNS metastases and was not reached in pts without CNS metastases. Four pts had CNS progression and the 4-year cumulative incidence rate of CNS progression was 9.5%. Median OS was not reached and the 4-year OS rate was 70% (95% CI: 54-81). Safety profile was similar to that reported previously and there were no treatment-related Grade 4 or 5 adverse events for this long administration period.
Conclusion:
Regardless of CNS metastases at baseline, ALC have demonstrated excellent efficacy in ALK+ NSCLC pts without prior ALK inhibitor treatment. ALC was well tolerated over a prolonged administration period.
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P1.03 - Chemotherapy/Targeted Therapy (ID 689)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Chemotherapy/Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 10/16/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P1.03-005 - Phase 2 Study of Ceritinib in Patients with ALK+ NSCLC with Prior Alectinib Treatment in Japan: ASCEND-9 (ID 8417)
09:30 - 09:30 | Author(s): M. Maemondo
- Abstract
Background:
ALK inhibitors are a standard of care for ALK-positive metastatic NSCLC and several ALK inhibitors are currently available. Alectinib is one of the recommended therapies as 1[st] line treatment for ALK-positive metastatic NSCLC in Japan based on robust progression-free survival (PFS) prolongation and favorable safety profile. However, even with treatment with alectinib, these cancers eventually progress after acquiring resistance against alectinib. Therefore, which drug should be chosen after alectinib is relevant clinical question. Recently, ceritinib, which is a highly selective oral ALK inhibitor, has demonstrated superior activity compared to chemotherapy in the 1[st] line setting for patients with ALK-positive metastatic NSCLC (ASCEND-4, Soria et al. Lancet 2017). It also showed clinically meaningful benefit in patients who failed to prior ALK inhibitor treatment including alectinib (Nishio et al. J Thorac Oncol 2015). In this study, we tried to evaluate efficacy and safety of ceritinib in ALK-positive metastatic NSCLC patients who progressed on alectinib treatment.
Method:
ASCEND-9 (NCT02450903) is a single-arm, open-label, multicenter, phase 2 study of ceritinib 750 mg/day (fasted) in adult patients with ALK+ (Vysis ALK Break Apart FISH Probe kit test), stage IIIB/IV NSCLC previously treated with alectinib and had subsequent disease progression. Other key inclusion criteria are ≥ 1 measurable lesion per RECIST 1.1 and WHO PS 0-1. Patients must have received previous treatment with alectinib, but prior crizotinib and/or up to 1 chemotherapy regimen are allowed. Patients with asymptomatic CNS metastases are eligible. Ceritinib may be continued beyond RECIST-defined PD. Primary endpoint is investigator assessed-overall response rate (ORR) per RECIST 1.1. Secondary endpoints include disease control rate (DCR), time to response (TTR), duration of response (DOR), PFS and safety. Biomarkers are evaluated for exploratory purpose.
Result:
Twenty patients were enrolled at 10 centers in Japan from Aug 2015 to Feb 2017. At present, the study is underway, and the results including ORR, DCR, TTR, DOR, PFS, safety and exploratory biomarker data will be presented at the 2017 WCLC.
Conclusion:
Section not applicable.
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P2.06 - Epidemiology/Primary Prevention/Tobacco Control and Cessation (ID 707)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Epidemiology/Primary Prevention/Tobacco Control and Cessation
- Presentations: 1
- Moderators:
- Coordinates: 10/17/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P2.06-009 - Trace Elements Affect Lung Cancer Subtypes (ID 10282)
09:30 - 09:30 | Author(s): M. Maemondo
- Abstract
Background:
The cause and mechanism of lung cancer in “never smokers” are still unclear. Additionally, the onset of driver mutations (e.g., EGFR, ALK, KRAS, and RET) and the mechanism of their ethnic difference are unclear. Several studies have suggested that some trace elements may affect the onset of lung cancer. However, the effect of trace elements on lung cancer carcinogenesis is poorly understood. The aim of this study was to assess if trace elements may be the cause of carcinogenesis in lung cancer tissues of patients with lung cancer with a non-smoking history, driver mutations, or histology.
Method:
The study included patients with non-small cell lung cancer who had undergone surgical resection. For the measurement of trace elements, surgically resected formalin-fixed paraffin-embedded lung cancer samples were studied using particle induced X-ray emission analysis. In total, 54 elements were investigated in each sample. EGFR mutation, KRAS mutation, and ALK rearrangement were assessed using commercially available CLIA testing. Based on the pathology and driver mutation status, samples were classified into the following groups: lung adenocarcinoma (LADC) with EGFR mutation (LADC EGFRm+); LADC with KRAS mutation (LADC KRASm+); LADC without EGFR mutation, KRAS mutation, and ALK rearrangement (LADC wt); and lung squamous cell carcinoma (SCC). Tissues from 20 patients with a non-malignant disease (e.g., pneumothorax) were also analyzed for trace elements as controls.
Result:
In total, 80 patients with non-small cell lung cancer were included. The median patient age was 70years. Of the 80 patients, 30 (37.5%) were males and 72 (90%) had stage I/II disease. The levels of 6 trace elements were increased in the LADC wt group. Copper was increased in the LADC EGFRm+ group. Cobalt and zinc were increased in the LADC KRASm+ group. There were no differences in trace element levels between the SCC group and the control group.
Conclusion:
Trace elements may play a role in the pathology and molecular signature of lung cancer.
