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S. Ahn
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P1.06 - Poster Session/ Screening and Early Detection (ID 218)
- Event: WCLC 2015
- Type: Poster
- Track: Screening and Early Detection
- Presentations: 1
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.06-029 - Serum Glutathione Peroxidase 3 as a Biomarker of Postoperative Relapse in Patients with Lung Cancer (ID 892)
09:30 - 09:30 | Author(s): S. Ahn
- Abstract
Background:
Glutathione peroxidase 3 (GPx3) which is an extracellular secretory protein is down regulated in patients with early stage lung cancer. We examined the usefulness of serum GPx3 as a biomarker for monitoring of relapse after surgery.
Methods:
We prospectively collected serial serum samples at baseline, 3 months (3m), 6 months (6m), and 12 months (12m) after operation from the patients who underwent surgery during the year 2013. GPx3 levels were measured three times per sample using the enzyme-linked immunosorbent assay, and the mean values were analyzed by repeated measure analysis of variance.
Results:
A total of 126 (73 adenocarcinoma, 31 squamous cell carcinoma, 22 others) patients were analyzed in this study. Median age of patients was 66 years old (range, 39-80) and 19 (15.4%) out of 123 lung cancer patients were confirmed relapse during the follow-up period of 2 years. In squamous cell carcinoma, the changes of mean serum GPx3 were significantly different between relapse (baseline: 13.3 ± 1.1 μg/mL, 3m: 17.1 ± 4.6 μg/mL, 6m: 14.8 ± 2.7 μg/mL, 12m: 17.9 ± 1.7 μg/mL) and control group (baseline: 10.8 ± 2.3 μg/mL, 3m: 13.4 ± 3.4 μg/mL, 6m: 12.4 ± 2.6 μg/mL, 12m: 13.5 ± 4.7 μg/mL, p=0.043). The changes of mean serum GPx3 levels were not different between two groups in all histology (p=0.258) and adenocarcinoma (p=0.701).
Conclusion:
Postoperative serum GPx3 levels were significantly elevated only in relapsed squamous cell histology, not in adenocarcinoma. More large scaled validation studies are warranted.
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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)
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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): S. Ahn
- 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.
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P2.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 234)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P2.04-089 - Detection of Epidermal Growth Factor Receptor (EGFR) Mutations in Circulating Tumor DNA During EGFR-Tyrosine Kinase Inhibitor Treatment (ID 575)
09:30 - 09:30 | Author(s): S. Ahn
- Abstract
Background:
Epidermal growth factor receptor (EGFR) mutations are predictive marker of EGFR-tyrosine kinase inhibitor (TKI) therapy. We compared the sensitivity of EGFR mutation detection techniques between tumor tissue and peripheral blood sample in patients with EGFR-TKI treatment.
Methods:
We collected plasma and serum sample before EGFR-TKI and after acquired resistance in 11 patients with EGFR mutations (5 cases of 19 deletion and 5 cases of L858R) from paraffin-embedded tissues using PNAClamp[TM]EGFR Mutation Detection kit. DNA extraction from plasma and serum was performed using the QIAamp MinElute virus spin kit. EGFR mutation analysis for blood was done by pyrosequencing and PANAMutyper[TM]R EGFR kit. The degree of agreement was evaluated by Cohen's kappa value.
Results:
The median EGFR-TKI duration of total 11 (7 male, 4 female) cases was 6 months (range 4-24). The sensitivity of plasma EGFR mutations were 33.3% in pyrosequencing. The sensitivities of PANAMutyper[TM]R were 72.7% in plasma and 45.5% in serum sample. The degree of agreements between tissue and blood sample were better in plasma PANAMutyper[TM]R (k=0.429, p=0.033) and serum PANAMutyper[TM]R (k=0.290, p=0.026) than plasma pyrosequencing (k=0.194, p=0.087). After the development of acquired resistance, plasma EGFR mutations were still detected in 4 cases by PANAMutyper[TM]R. One of them showed 19 deletion and T790M mutation at the same time.
Conclusion:
The sensitivity and the strength of agreement of PANAMutyper[TM]R test were better than pyrosequencing. So this technique can be useful to detect EGFR mutation in peripheral blood.
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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)
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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): S. Ahn
- 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.
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P3.03 - Poster Session/ Treatment of Locoregional Disease – NSCLC (ID 214)
- Event: WCLC 2015
- Type: Poster
- Track: Treatment of Locoregional Disease – NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P3.03-023 - Phase III Study of Accelerated Hypofraction in CCRT of Unresectable Stage III NSCLC: Interim Analysis of KROG 0903 (ID 866)
09:30 - 09:30 | Author(s): S. Ahn
- Abstract
Background:
KROG 0301 prospective phase I & II study of the modified hypofractionation using concomitant boost to the gross tumor volume (GTV) simultaneously in the patients with unresectable NSCLC showed outstanding results comparing to the previous ones. So, we designed phase III prospective clinical trial comparing it with the standard 2 Gy fractionation.
Methods:
Eligibility criteria were histologically proven unresectable stage III NSCLC determined by thoracic surgeon and more than one lesion measurable with CT scan according to the criteria of RECIST (version 1.1). Exclusion criteria were supraclavicular nodal metastasis, superior vena cava syndrome, atelectasia obscuring GTV contouring, and disease suspected to extend the major vessels and bronchus and to be at the risk of hemorrhage after concurrent chemoradiation (CCRT). In conventional fractionated RT group (Arm-1), a dose of 2Gy was delivered daily to the PTV and total cumulative dose was 44Gy to the PTV in 22 fractions and field was reduced and 2Gy was delivered to GTV and proceeded to 60Gy to the GTV in 30 fractions. In hypofractionated RT group (Arm-2), a dose of 1.8Gy was delivered daily to the PTV with a synchronous boost of 0.6Gy to the GTV to bring its daily dose to 2.4Gy per fraction. Total cumulative doses were 60Gy to the GTV and 45Gy to PTV in 25 fractions over 5 weeks. All patients received concurrent weekly chemotherapy consisting of paclitaxel first (50mg/m[2] intravenously over 1 hour) and cisplatin (20mg/m[2] intravenously over 1 hour) on days 1,8,15,22,29, and (36). Chemotherapy was performed before radiotherapy in a day. Dose modification of chemotherapy was guided according to the severity of toxicity.
Results:
One-hundred twelve patients who were followed more than 6 months after completion of planned treatment were included in this analysis. Median F-U was 14 months. Median age was 67 years(45-75) and male to female was 112/8. Stage IIIA was 81(72%) and IIIB 31(28%). Sixty and fifty-two patients were allocated in Arm-1 and 2, respectively. Patient’s characteristics were evenly distributed between two groups. Overall survival, local progression free, and disease progression free survival of all patients was median 30 months, 15months, and 12 months, respectively. Two- and 3-year survival rates were 53.6% vs. 54.1% and 50.4% vs. 44.6% in Arm-1 and Arm-2 (p=0.95), respectively. Two-year local tumor control rates were 58.3% and 50.0% (p=0.977) and 2-year progression free survival rates were 41.4% and 34.2% (p=0.704) in Arm-1 and Arm-2, respectively. Radiation esophagitis (≥ grade 2) was 15(25%) and 10(20%) and radiation pneumonitis (≥ grade 2) was 8(13.3%) and 7(13.5%) in Arm-1 and Arm-2, respectively.
Conclusion:
Interim analysis did not show any statistically significant toxicity or survival differences between two groups. This on-going clinical study needs to continue for the confirmative results.
