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K. Kanazawa
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P3.02b - Poster Session with Presenters Present (ID 494)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 2
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.02b-067 - A Single-Institution Experience of Afatinib in Patients with EGFR-Mutated Advanced Non-Small Cell Lung Cancer (ID 5148)
14:30 - 14:30 | Author(s): K. Kanazawa
- Abstract
Background:
Afatinib, an irreversible ErbB family blocker, inhibits EGFR, HER2, and HER4. LUX-Lung 1 and 4 showed that afatinib was effective for patients with EGFR-mutated non-small cell lung cancer (NSCLC) who experienced progression after chemotherapy and gefitinib/erlotinib therapy. LUX-Lung 3 and 6 showed that afatinib had a significantly better response rate and prolonged progression free survival (PFS) compared with pemetrexed plus cisplatin or gemcitabine plus cisplatin in a first-line setting. However, those trials recruited only patients who met inclusion criteria. Thus, the relevance of the outcomes needs to be examined in a clinical setting. Moreover, diarrhea and skin rash are frequently observed in patients receiving afatinib. Establishing optimal management of adverse events is essential to improve clinical outcomes and quality of life in patients receiving afatinib.
Methods:
We retrospectively reviewed chart records of 15 EGFR-mutated NSCLC patients who had received afatinib from July 2014 to August 2015 at our institution.
Results:
Median age was 68 years (range, 53–72 years). Fourteen patients had adenocarcinoma. Nine and 4 patients had an Eastern Cooperative Oncology Group performance status (ECOG PS) of 0 and 1, respectively. Three and 6 patients were treated as first- and third-line therapies, respectively. Thirteen patients had exon 19 deletion. One patient harbored both an L858R mutation in exon 21 and a de novo T790M mutation in exon 20. PFS of the 3 patients who were treated with afatinib as first-line therapy was 0.9, 6.8, and 16.4 months. Median PFS of 12 patients who had previous EGFR-TKI therapy was 4.0 months (95% confidential interval 2.1–5.9 months). The de novo T790M NSCLC patient experienced disease progression at 1.3 months. The response rate of pretreated patients was 16%. Fourteen patients were treated with afatinib 40 mg/day. One patient began afatinib 20 mg/day because of ECOG PS 2. Dose reduction was required in 8 (53%) patients. Grade 3 or 4 adverse events occurred in 3 (20%) patients. One patient had grade 3 paronychia and another patient had grade 3 diarrhea. Both patients could continue afatinib with dose reduction. Five patients had reduction of afatinib to 30 mg/day and 2 patients required reduction by 10-mg decrements down to 20 mg/day.
Conclusion:
Clinical outcomes in terms of PFS and objective response rate of afatinib in our EGFR-mutated NSCLC patients with prior therapy were comparable to LUX-Lung 1 and 4. Adverse events were tolerable and manageable with careful dose reduction.
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P3.02b-113 - Clinical Course of NSCLC Patients with EGFR Mutation Undergoing Rebiopsy and Osimertinib Therapy (ID 5272)
14:30 - 14:30 | Author(s): K. Kanazawa
- Abstract
Background:
Osimertinib, a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI), was approved in May 2016 in Japan. Its administration requires a tumor rebiopsy to detect the EGFR T790M mutation. AURA and AURA2 studies with 411 patients demonstrated a remarkable clinical outcome with an overall response rate (ORR) of around 65% and progression-free survival (PFS) of 9.7 months. Several authors reported that the detection rate of T790M by tumor rebiopsy in these patients was approximately 52 to 68%. However, thorough accumulation of data is required to establish the clinical relevance of T790M detection and osimertinib response.
Methods:
We retrospectively reviewed the clinical courses of NSCLC patients with the EGFR mutation, who had undergone rebiopsies and osimertinib therapy.
Results:
Eleven patients with the EGFR mutation (exon19del [n=10] and L858R [n=1]) were included. Average age was 67 years old (range 53–79). The following EGFR-TKIs were administered to the 11 patients before rebiopsy; elrotinib (n=6), afatinib (n=5) and gefitinib (n=2). The patients received rebiopsy in the 2nd line treatment (n=3), 3rd line (n=2), 5th line (n=2), 6th line (n=2) and 7th line (n=2). Rebiopsy sites were primary lung tumors (n=8), supraclavicular lymph node (n=1), liver metastasis (n=1) and pleural effusion (1). Among them, T790M was detected in four, zero, one, and one, respectively (detection rate: 54.5%). Rebiopsy was successfully performed in all patients, among whom one required a second attempt. ASP8273, another third-generation EGFR-TKI, and osimertinib were administered in one and two patients, respectively. The remaining two patients are to be treated with osimertinib. Both patients who received osimertinib achieved partial response, and their ECOG performance status (PS) was remarkably improved from 4 to 1, and 3 to 1. One of the two patients experienced grade 4 neutropenia; thus, the osimertinib dose was reduced from 80 mg to 40 mg daily. The remaining patient suffered from erythema; however, it was improved after ten-day cessation of medication. Osimertinib was then resumed at 80 mg daily with no severe side effects experienced thereafter.
Conclusion:
The detection rate of T790M by rebiopsy was consistent with previous reports. Osimertinib was feasible and effective for our patients with poor PS; however, a prospective study is required to confirm osimertinib’s validity for such patients. In WCLC 2016, we will increase the number of patients who undergo rebiopsy and osimertinib therapy, and we hope to demonstrate detailed detection patterns of T790M, as well as ORR and PFS.
