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Peng-Bo Deng



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    P48 - Small Cell Lung Cancer/NET - Chemo - IO (ID 236)

    • Event: WCLC 2020
    • Type: Posters
    • Track: Small Cell Lung Cancer/NET
    • Presentations: 1
    • Moderators:
    • Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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      P48.05 - Anlotinib Plus Platinum-Etoposide in 1st-Line Treatment of Extensive-Stage Small-Cell Lung Cancer: A Single-Arm Phase II Trial (ID 1479)

      00:00 - 00:00  |  Presenting Author(s): Peng-Bo Deng

      • Abstract
      • Slides

      Introduction

      Most patients with small-cell lung cancer(SCLC) have extensive-stage disease, and poor prognosis. The most commonly initial chemotherapy regiment in extensive-stage SCLC is combination of etoposide and cisplatin or carboplatin( platinum-etoposide). The single-arm phase II trial assessed anlotinib, an oral VEGFR, FGFR, PDGFR and c-Kit tyrosine kinase inhibitor, in combination platinum-etoposide in treatment-naïve extensive-stage small-cell lung cancer (ES-SCLC) patients.

      Methods

      This single-arm phase II trial enrolled ES-SCLC patients without prior systematic chemotherapy or immunity checkpoint inhibitors therapy. Platinum-etoposide regiment consisted of etoposide 100mg/m2, d1~3 of 21-day cycle, with investigators’ choice of either cisplatin(75-80mg/m2, Q3W) or carboplatin ( AUC=5~6, Q3W). Anlotinib treated of 12mg Qd from day 1 to 14 of a 21-day cycle. Eligible patients received anlotinib plus platinum-etoposide for 4~6 cycles, and followed by maintenance therapy with anlotinib. The efficacy was evaluated every 6-weeks(2 cycles) through treatment. The dual-primary endpoints were progression free survival(PFS) and objective response rate(ORR). The secondary endpoints were overall survival(OS), disease control rate(DCR) and safety.

      Results

      Of 37 patients enrolled between Aug 10, 2018 and Aug 21, 2020, 36 patients were available for efficacy analysis(n=36, demographics in Table 1 ). The median PFS was 9.41 months (95%Cl: 7.91-10.91) and the median OS is 13.87 months( 95%Cl: 7.12-20.62) with event rate of 47.2%. ORR and DCR were 88.89% and 97.22%, respectively. Seventeen (47%) of pts. experienced total of 69 grade 1-2 adverse events, possibly or definitely related to therapy. The most common adverse events was hypertriglyceridemia( 56%) and the most common≥grade 3 adverse events included: hypertriglyceridemia( 44%), hypercholesteremia( 33%), oral mucositis( 22%), granulocytopenia( 17%).

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      Conclusion

      This trial met its dual-primary endpoints of PFS and ORR for anlotinib plus platinum-etoposide at the interim analysis. The safety profile was comparable with previous reports of platinum-etoposide. These results providing the flexibility of combining anlotinib with different platinum-based regimens in ES-SCLC.

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    P76 - Targeted Therapy - Clinically Focused - EGFR (ID 253)

    • Event: WCLC 2020
    • Type: Posters
    • Track: Targeted Therapy - Clinically Focused
    • Presentations: 1
    • Moderators:
    • Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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      P76.20 - The Predictive Values of Non-Resistant Nncommon EGFR Mutations in Advanced Non-Small Cell Lung Cancer Patients (ID 1303)

      00:00 - 00:00  |  Presenting Author(s): Peng-Bo Deng

      • Abstract
      • Slides

      Introduction

      The efficacy of EGFR-TKIs in patients with non-resistant uncommon EGFR mutations is controversial. The predictive values of mutation patterns, the presence of concurrent mutations and the choice of different generations of EGFR-TKIs have not been well elucidated.

      Methods

      A total of 2095 patients underwent NGS for EGFR mutation testing were screened. We enrolled NSCLC patients harbouring non-resistant uncommon EGFR mutations, defined as mutations other than single L858R, 19del, T790M, 20ins, and synonymous mutation. Among them, 72 patients with advanced/recurrent disease who received 1st (n=55) or 2nd generation (n=17) EGFR-TKIs as first-line therapy and with retrievable PFS data were enrolled for subsequent survival analyses. In addition, we also included a cohort of 83 patients harbouring only sensitizing EGFR mutations treated with EGFR-TKIs as first-line therapy for comparison.

      Results

      A total of 934 (934/2095,44.6%) EGFR mutated patients were identified. In this cohort, the most frequently occurring concurrent alterations were TP53 (34.5%) followed by RB1 (6.1%), and PIK3CA (4.6%). Amplifications frequently occurred in EGFR (20.4%), CDK4 (3.5%), and MYC (3.2%). Non-resistant uncommon EGFR mutations were detected in 144 (15.42%) patients. Among them,72 were included for survival analyses, who were categorized according to mutation patterns: group1 patients harbouring EGFR uncommon mutation in combination with EGFR 19 Del/L858R (n=45); group 2 patients harbouring single or complex EGFR uncommon mutations (n=27). Our analyses revealed that patients with only sensitizing mutations and patients in group 1 had a significantly longer median PFS (mPFS) than those in groups 2 (13.01months vs 8.05months, p=0.048;14.65months vs 8.05 months; p=0.004). While no significant difference was found in mPFS between patients with only sensitizing mutations and patients in group 1 (p=0.165). The mPFS between 1st and 2nd generation EGFR-TKIs cohort was 12.42months versus 12.39months, respectively (p=0.7). Similarly, there was also no significant difference existed in mPFS between the two treatment cohorts in each subgroup of non-resistant uncommon mutations.Next, we investigated whether the presence of concurrent mutations in tumour-suppressor genes or oncogenes would affect PFS of patients with uncommon EGFR mutations. The mPFS of patients with no concurrent mutation (n=41), patients with concurrent tumour-suppressor genes mutations (n=26) and patients with concurrent oncogenic driver mutations (n=5) were 13.80months, 8.05months and 16.92months, respectively (p=0.04). Furthermore, patients with no concurrent mutation had a significantly longer mPFS than patients with concurrent tumour-suppressor genes mutations (p=0.011). Collectively, multivariate analysis showed that patients with coexisting 19del/L858R (p=0.006, HR: 0.435,95% CI:0.242-0.784) were independently associated with favourable PFS; Non-adenocarcinoma, poor ECOG performance score and the presence of concurrent tumour-suppressor genes mutations were independent risk factors for PFS. (p=0.024, HR: 3.575,95% CI: 1.185-10.788; p=0.018, HR: 2.069,95% CI: 1.133-3.779; p=0.002, HR: 2.623,95% CI: 1.434-4.800, respectively).

      Conclusion

      Our study revealed that NSCLC patients harbouring non-resistant uncommon EGFR mutations in combination with 19del/L858R are associated with favourable PFS. The presence of concurrent tumour-suppressor gene mutations is associated with a worse prognosis. Patients receiving 2nd generation EGFR-TKI share a comparable PFS to those treated with 1st generation EGFR-TKIs.

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