Virtual Library
Start Your Search
C. Park
Author of
-
+
P2.01 - Poster Session/ Treatment of Advanced Diseases – NSCLC (ID 207)
- Event: WCLC 2015
- Type: Poster
- Track: Treatment of Advanced Diseases - NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
-
+
P2.01-044 - EGFR-TKIs as Second-Line Treatment of Patients with NSCLC with or without Activating EGFR Mutation as Assessed by Sensitive PNA Clamping Method (ID 1099)
09:30 - 09:30 | Author(s): C. Park
- Abstract
Background:
Although TAILOR phase 3 trial showed superiority of docetaxel versus erlotinib as second line treatment in NSCLC with wild type EGFR as assessed by direct sequencing, second-line treatment of patients with wild-type status is controversial and EGFR-TKIs are still used as second line treatment.
Methods:
We retrospectively analyzed the results of 2[nd] line treatment with EGFR-TKIs in 25 patients with activating EGFR mutations and 68 patients with wild-type EGFR as assessed by PNA clamping (Panagene®, South Korea), which is more sensitive than direct sequencing.
Results:
There was no significant difference in age, sex, smoking history and histologic subtypes of NSCLC between the two groups. Erlotinib was more frequently used in EGFR wild group (48/68, 71%), while use of gefitinib was significantly higher in EGFR mutation group (15/25, 60%, p=0.003). Progression-free survival (PFS) was significantly longer in EGFR mutation group than EGFR wild group: median PFS was 11.6 months (95% CI 6.2~17.1) in mutation group versus 1.8 months (1.5~2.1) in wild group (log rank p<0.001). PFS was numerically shorter than the 2.4 months (2.1~2.6) of TAILOR trial. Figure 1
Conclusion:
This results show that possibility of survival benefit using second-line EGFR-TKI is very low in patients with NSCLC with wild-type EGFR status, when tested with sensitive EGFR mutation detection technique. Thus chemotherapy should be favored for the second line treatment of patients with NSCLC with wild-type EGFR status.
-
+
P3.01 - Poster Session/ Treatment of Advanced Diseases – NSCLC (ID 208)
- Event: WCLC 2015
- Type: Poster
- Track: Treatment of Advanced Diseases - NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
-
+
P3.01-015 - Efficacy, Safety and Dosage of Afatinib in Patients with NSCLC after Failure of Prior EGFR-TKI (ID 1110)
09:30 - 09:30 | Author(s): C. Park
- Abstract
Background:
Afatinib is an irreversible ErbB family blocker that inhibits EGFR with activating mutations as well as the T790M resistance mutations. In Non-Small Cell lung cancer (NSCLC), afatinib has been evaluated in the LUX-Lung trials, with improvement in progression-free survival (PFS) in patients with acquired resistance to prior EGFR tyrosine kinase inhibitor (EGFR-TKI) treatment. This study investigated efficacy, safety and dosage of afatinib under a Named Patient Use (NPU) program in a single institution.
Methods:
We analyzed 60 patients with stage IV NSCLC that had been treated with ≥ 1 platinum based chemotherapy, and with activating EGFR mutation or disease control for ≥ 6 months with prior EGFR-TKIs (gefitinib or erlotinib). The daily dose of afatinib was started with 50mg, which was decreased to 40mg and 30mg according to adverse events and tolerability of patients. Of 60 analyzed patients, 2 received afatinib as 3rd line treatment, 27 as 4th line, 19 as 5th line and 12 as ≥ 6th line. Activating EGFR mutations were detected in 11 (exon 19 deletion) and 7 (L858R) cases. No activating mutation was found in 19 cases, and EGFR status was not studied in 23 cases.
Results:
Thirteen patients achieved partial remission, 33 stable disease, and 12 progression, and 2 not-evaluable resulting in a response rate of 21.7% and a disease control rate of 76.7%. Median PFS was 5.2 months (95% CI, 4.1 to 6.4 months) and median OS was 13.4m (95% CI, 12.6 to 14.2) since the commencement of afatinib. Toxicities leading to drug discontinuation were experienced by 4 patients (6.7%). Grade 3 diarrhea occurred in 10 patients (16.7%), and dosage reductions of afatinib were required in 35 patients, to 40mg in 25 and to 30mg in 10 cases. Patients were grouped by final dosage of afatinib (50mg in 25 cases, 40/30mg in 35 cases). The PFS and OS were significantly longer for patients whose dosage of afatinib were reduced to 40 or 30 mg, compared to patients without dosage reduction (7.5 vs 3.1m and 18.0 vs 9.1m, respectively, p<0.05). Figure 1
Conclusion:
Afatinib showed PFS of 5.2 months and OS of 13.4 months in selected patients after failure of prior EGFR-TKIs. Aggressive dosage reduction should be considered in the course of treatment with afatinib.
