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X. Zhang
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P3.01 - Advanced NSCLC (ID 621)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Advanced NSCLC
- Presentations: 2
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.01-018 - Mutation Abundance Affects the Therapeutic Efficacy of EGFR-TKI in Patients with Advanced Lung Adenocarcinoma: A Retrospective Analysis (ID 8850)
09:30 - 09:30 | Author(s): X. Zhang
- Abstract
Background:
To detect the mutation abundance and sites of epidermal growth factor receptor (EGFR), and to investigate their influence on the therapeutic efficacy of EGFR-tyrosine kinase inhibitors (EGFR-TKIs) in patients with advanced non-small cell lung cancer (NSCLC).
Method:
A total of 2,417 NSCLC patients with EGFR gene mutations were retrospectively analyzed using an amplification refractory mutation system (ARMS). Of 861 patients, 407 patients had exon 19 deletions and 454 patients had exon 21 (L858R) site mutations of the EGFR gene. Next we analyzed the mutation abundance of lung adenocarcinoma patients who received EGFR-TKI therapy and complete follow up. 194 patients diagnosed with stage IIIB or stage IV lung adenocarcinoma with an ECOG score of 0-3 were enrolled. The primary endpoint was to determine associations between progression-free survival (PFS) and mutation abundance or mutation sites after EGFR-TKI therapy. The secondary endpoint was to evaluate the objective response rate and effects when EGFR-TKI was administered as the first-line treatment, as well as risk factor analysis for PFS.
Result:
Of the 194 enrolled patients, the median PFS was 9.3 months (95% CI, 8.2–10.8 months). The PFS was significantly different with EGFR gene mutation abundance after EGFR-TKI therapy (P = 0.014). The median PFS was significantly longer when the cut-off value of EGFR mutation abundance of exon 19 or exon 21, exon19 was > 26.7% and 61.8%, respectively. For patients who received EGFR-TKI as first-line treatment, the median PFS was significantly longer in the high mutation abundance group than in the low mutation abundance group (12.7 m vs 8.7 m, P = 0.002). However, there was no significant correlation with gender, age or smoking status and PFS.
Conclusion:
The PFS benefits were greater in patients with a higher abundance of exon 19 mutations in the EGFR gene after EGFR-TKI treatment.
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P3.01-061 - Endostar Combined with Re-Challenged Gefitinib in Previous Treatment Failed NSCLC: A Retrospective Study (ID 9950)
09:30 - 09:30 | Author(s): X. Zhang
- Abstract
Background:
To investigate the efficacy of gefitinib combined with recombinant human endostatin (endostar) as a salvage therapy in patients who failure to benefit from gefitinib in previous treatment of advanced non‐small cell lung cancer (NSCLC) due to resistance with T790M mutant negative or unknown.
Method:
Patients with pathologically confirmed stage IV NSCLC who had failed of disease control by gefitinib were retrospectively reviewed. In total, twenty patients were enrolled incluing two patients with squamous disease, eighteen patients were adenocarcinoma. The median age was 61.6, ranging from 43 to 75. After acquired gefitnib treatment resistance, six patients were tested their tumor samples by re‐biopsy and confirmed T790M negative. Fourteen patients refused to re-biopsy, therefore the T790M status were unknow among them. In our analysis, from September 2009 to May 2014, all patients met the selection standards above received endostar (15 mg/day, i.v. day 1‐7, 21 days per cycle) additionally and keep taking gefitinib after preious treatment failure. The efficacy and toxicities of the combined treatment were observed.
Result:
Two patient achieved partial response (PR) (10%) , twelve patients had stable disease (SD) (60%) , six of those patient had progressive disease (PD) (30%) . The objective response rate (ORR) was 10% and the disease control rate (DCR) was 70%. Median progression free survival was 4.2 months (95% CI, 3.21 ‐ 5.19 months) , whereas median OS time was 8.0 months (95% CI, 4.96 ‐ 11.04 months). The results of efficacy accessed in terms of DCR, PFS and OS were not correlated with the sex, age, performance status (PS) score, histologic types or the treatment duration of gefitinib.
Conclusion:
After the failed attempting of gefitnib treatment, the combination of Endostar with gefitinib treatment could stabilize disease in T790M negative or unknown patients, and prolonged their survival time with tolerable toxicities.
