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Yue Zeng



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    FP01 - Early Stage/Localized Disease (ID 111)

    • Event: WCLC 2020
    • Type: Posters (Featured)
    • Track: Early Stage/Localized Disease
    • Presentations: 1
    • Moderators:
    • Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall
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      FP01.02 - The Efficacy of Postoperative Radiotherapy in IIIA-N2 Non-Squamous NSCLC with Different EGFR Mutation Status: A Retrospective Analysis (ID 3680)

      00:00 - 00:00  |  Author(s): Yue Zeng

      • Abstract
      • Slides

      Introduction

      The effect of postoperative radiotherapy (PORT) on completely resected IIIA-N2 non-squamous non-small cell lung cancer (NSCLC) remains controversial. Growing postoperative therapies for epidermal growth factor receptor (EGFR)-mutant patients make the role of PORT ambiguous. Previous in-vitro studies have indicated that the status of EGFR mutation status can influence the radio-sensitivity of lung cancer, which needs more clinical investigation to verify. In this retrospective study, we aim to assess the efficacy of PORT in IIIA-N2 non-squamous NSCLC with different EGFR mutation status.

      Methods

      We enrolled patients who were diagnosed with completely resected stage IIIA-N2 non-squamous NSCLC, receiving postoperative radiotherapy or not, between April 2011 and May 2017 from the Second Xiangya Hospital and Hunan Cancer Hospital. And we analyzed the influence of PORT on disease-free survival (DFS) and overall survival (OS) in NSCLC patients with different EGFR mutation status.

      Results

      In total, 124 patients were eligible. The median follow-up time was 43.2 months (range 6-103 months). In multivariate analysis, age (>60 years old), cycles of chemotherapy (<4) and multiple-station N2 metastasis were correlated with shorter DFS. Multiple-station N2 metastasis,wild-type EGFR and no PORT were independent risk factors for OS. PORT significantly improved OS (46.40 months vs. 34.17 months, P = 0.021) but not DFS (19.02 months vs. 17.23 months, P = 0.266). In the EGFR wild-type group, PORT prolong OS (43.20 months vs. 28.67 months, P = 0.007), especially in EGFR wild-type group with multiple-station N2 metastasis (39.73 months vs. 24.9 months, P = 0.006) rather than DFS (18.43 months vs. 17.77 months, P = 0.775). There was a trend that PORT improved OS (69.30 months vs. 49.97 months, P = 0.057) and DFS (21.17 months vs. 17.17 months, P = 0.075) in the EGFR-mutant group, although there was no significant difference. In EGFR-mutant patients with multiple-station N2 metastasis, the DFS was significantly prolonged (23.13 months vs. 14.10 months, P = 0.021) in the PORT group. Nevertheless, the OS (72.5 months vs. 60.63 months, P = 0.189) and DFS (13.7 months vs. 24.33 months, P = 0.664) were not improved in EGFR-mutant patients with single-station N2 metastasis(Figure 1).figure 1.jpg

      Comparison of overall survivall (A,C,E) and disease-free survival (B,D,F) between the PORT and the non-PORT group. PORT=postoperative radiotherapy.

      Conclusion

      It is necessary for stage IIIA-N2 non-squamous NSCLC patients to receive PORT,especially for EGFR wild-type patients. Meanwhile, PORT can reduce local recurrence and metastasis in EGFR-mutant group, particularly in EGFR-mutant patients with multiple-station N2 metastasis. More prospective studies are needed to clarify the role of PORT in the EGFR-mutant IIIA-N2 non-squamous NSCLC patients.

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    P84 - Targeted Therapy - Clinically Focused - ALK (ID 261)

    • 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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      P84.04 - HIP1-ALK Positive Non-Small-Cell Lung Cancer: Clinicopathological Characteristics and Prognosis (ID 2947)

      00:00 - 00:00  |  Author(s): Yue Zeng

      • Abstract
      • Slides

      Introduction

      Anaplastic lymphoma kinase (ALK) fusions were identified in 2-7% of non-small cell lung cancer (NSCLC), and the most frequently occurring ALK fusion partner was EML4. Huntingtin interacting protein 1 (HIP1)-ALK fusion was rarely reported in NSCLC cases. This study is aimed to summarize clinicopathological characteristics and prognosis and to describe the efficacy and safety of ALK inhibitors in HIP1-ALK positive NSCLC.

      Methods

      We queried cases of NSCLC from multi-center and screened for patients who harbored HIP1-ALK. Meanwhile, adequate document retrieval was performed to identify published cases of HIP1-ALK positive NSCLC. Then we reviewed medical records or case descriptions of all patients retrospectively. Moreover, efficacy and safety of ALK inhibitors were evaluated based on RECIST v1.1 and CTCAE v5.0, respectively.

      Results

      A total of 9 patients (6 from multi-center and 3 from published cases) with HIP1-ALK were identified by next-generation sequencing (NGS). Female accounted for 77.8% with a median age of 56 years (range, 33-73 years). The median follow-up period was 13 months (range, 4 months-34 months). In addition, all patients were non-smokers with histological types of adenocarcinoma. Stage distribution included 22.2% stage I, 22.2% stage Ⅲ, and 55.6% stage IV (Table 1). In all cases, HIP1-ALK fusion did not incorporate other common driver genetic alterations. 8 cases received crizotinib or alectinib and all responded. 2 patients (25%) had a complete remission to crizotinib or alectinib with progression-free survival (PFS) beyond 9 months. Furthermore, 3 patients (37.5%) got a partial response to crizotinib or alectinib. 2 patients (25%) treated with crizotinib showed stable disease for at least 13 months. 1 patient (12.5%) was treated with adjuvant crizotinib after complete surgical resection with disease-free survival beyond 15 months. Among 8 patients, 2 patients switched to alectinib after crizotinib resistance, and both showed remarkable response. None died during the follow-up. Adverse events included grade-Ⅰ constipation, grade-Ⅰ localized edema, grade-Ⅰ alanine aminotransferase and aspartate aminotransferase elevation.

      table 1.jpg

      Conclusion

      We firstly report a case series of HIP1-ALK positive NSCLC, whose clinicopathological characteristics are similar to EML4-ALK fusion NSCLC. Secondly, HIP1-ALK fusion may be mutually exclusive of other driver alterations. NGS is essential for detecting HIP1-ALK. Thirdly, ALK inhibitors should be recommended for advanced NSCLC harboring HIP1-ALK, and crizotinib-resistant patients could benefit from alectinib. Long follow-up and large-sample study are needed to determine the long-term prognosis.

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