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Wenxian Wang



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    JCSE01 - Perspectives for Lung Cancer Early Detection (ID 779)

    • Event: WCLC 2018
    • Type: Joint IASLC/CSCO/CAALC Session
    • Track: Screening and Early Detection
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/23/2018, 07:30 - 11:15, Room 202 BD
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      JCSE01.15 - Molecular Characteristics of ALK Primary Point Mutations Non-Small-Cell Lung Cancer in Chinese Patients (ID 14704)

      11:15 - 11:15  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background
      Anaplastic lymphoma kinase (ALK) gene rearrangements have been identified in lung cancer at 3-7% frequency, thus representing an important subset of genetic lesions that drive oncogenesis in this disease. While the genetic locus of ALK primary point mutations NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring ALK primary point mutations.

      A total of 339 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of ALK primary point mutation and other genes were detected by next generation sequencing.


      ALK gene primary point mutation rate was 8.55% (29/339) in non-small cell lung cancer, including V163L (3 patients), F921Gfs*16 (2 patients), K1416N (2 patients), A585T (2 patients), P1442Q (1 patient), A348T (1 patient), K1525E (1 patient), S737L (1 patient), P115L (1 patient), Q515E (1 patient), E314D (1 patient), R395H (1 patient), S1219F (1 patient), S341G (1 patient), P1543S (1 patient), G129V (1 patient), Q167H (1 patient), L550F (1 patient), T1012M (1 patient), D302Y (1 patient), H755Q (1 patient), H331Q (1 patient), G1474E (1 patient) and E119D (1 patient), and median overall survival (OS) for these patients was 20.0 months. Among them, 27 patients with co-occurring mutations had a median OS of 20.0 months, and median OS of the 2 patients without complex mutations was 8.5 months. Statistically significant difference was found between the two groups (P=0.02). Briefly, patients with (n=8) or without (n=21) co-occurring EGFR mutations had a median OS of 24.0 months and 20.0 months respectively (P=0.73); patients with (n=21) or without (n=8) co-occurring TP53 mutations had a median OS of 20.0 months and 17.0 months respectively (P=0.83).

      EGFR and TP53 gene accompanied may have less correlation with ALK primary point mutation in NSCLC patients. Results of ongoing studies will provide a platform for further research to offer individualized therapy with the purpose of improving outcomes. a9ded1e5ce5d75814730bb4caaf49419

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    P1.01 - Advanced NSCLC (Not CME Accredited Session) (ID 933)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 3
    • Now Available
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.01-113 - Analysis of Clinicopathological Features and Clinical Efficacy of Crizotinib in ROS1 Positive Non-Small Cell Lung Cancer (ID 11100)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      ROS1 gene-rearrangement in non-small-cell lung cancer (NSCLC) patients has recently been identified as a driver gene and benefited from crizotinib treatment. The aim of this study is to explore clinicopathological features and clinical efficacy of crizotinib in c-ros oncogene 1 receptor tyrosine kinase (ROS1) positive non-small cell lung cancer (NSCLC).

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A retrospective analysis of 2617 cases of NSCLC from January 2013 to December 2016, ROS1 fusion gene were detected by real-time reverse transcriptase-polymerase chain reaction (RT-PCR), fluorescent in situ hybridization (FISH) or next-generation sequencing (NGS) technique and part ROS1 fusion gene positive patients were received oral treatment with crizotinib.

      4c3880bb027f159e801041b1021e88e8 Result

      ROS1 fusion was found in 67 of 2167 cases (2.56%). 21 cases were male and 46 cases were female. The median age was 68 years old. Among these cases, 59 (88.05%) were adenocarcinoma and 8 were non-adenocarcinoma. According the TNM staging,4 cases were Ⅰ-Ⅲa and 63(94.02%) cases were Ⅲb-Ⅳ. EGFR gene status included 60 cases wild type, 1 case co-mutation and 6 cases unknown. There were statistical difference in sex, TNM staging and EGFR gene status between ROS1 fusion gene positive and negetive patients (P<0.001). 23 patients were received oral treatment with crizotinib and PR, SD, PD patients were 13 (56.52%), 5 (21.74%) and 5 (21.74%) respectively. The ORR was 56.52% and DCR was 78.26%. Of all the cases, median PFS was14.5 months and OS was 27.3 months. The one-year PFS was 50.4%.There were no difference of median PFS in age, sex, smoking history, PS score, pathology type, TNM staging ,TP53 gene status, EGFR gene status and the first line crizotinib treatment whether or not by single and multiple factor analysis. The 3/4 grade treatment-related adverse events were gastrointestinal disturbance, followed by increased transaminase.

      8eea62084ca7e541d918e823422bd82e Conclusion

      The rate of ROS1 fusion of NSCLC is lower. Crizotinib is an effective and safe drug for the treatment of ROS1 positive advanced NSCLC.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P1.01-27 - Influence of EGFR-TKIs Treatment Lines and PFS on the Emergence of T790M Mutation (Now Available) (ID 13584)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      For sensitizing EGFR mutation positive lung cancer patients, EGFR-TKIs can be used as the first-line or second-line (after chemotherapy) therapy according to NCCN guideline. However, whether different lines of EGFR-TKIs therapy or different PFS would affect the emergence of T790M, the leading cause of resistance to first and second generation of EGFR-TKIs was unknown.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We retrospectively analyzed 142 advance NSCLC patients with 93 patients received 1st-line EGFR-TKIs, and 49 patients received 2nd-line EGFR-TKIs after chemotherapy. EGFR sensitizing mutation and T790M mutation was detected simultaneously by hybridization capture-based NGS panel sequencing with tumor biopsy , ctDNA or pleural effusion samples.

      4c3880bb027f159e801041b1021e88e8 Result

      For the patients received 1st-line EGFR-TKIs, 47 carried L858R mutation and 46 carried EX19del mutation; while patients received 2nd-line EGFR-TKIs, 24 carried L858R mutation and 25 carried EX19del mutation. When those patients progressed on TKIs, T790M emerged in 25 of the 47 (53.19%) L858R carriers, and 23 of the 46 (50.00%) EX19del carriers with 1st-line EGFR-TKIs (p=0.76). However, only 6 of the 24 (25.00%) L858R carriers yet 16 of the 25 (64.00%) EX19del carriers with 2nd-line EGFR-TKIs had T790M detected (p=0.006). The incidence of T790M was significant lower in L858R carrier treated with 2nd-line compared with 1st-line EGFR-TKIs (25.00% vs 53.19%, p=0.023), however, there was no difference for EX19del carrier (50.00% vs 64.00%, p=0.26). To further analyzed whether different PFS affected the appearance of T790M, we divided patients into 3 groups as PFS≥13 months (n=48), PFS≤8 months (n=60) and the between (n=34). The incidence of T790M was significantly lower in the PFS≤8 months group compared with the PFS≥13 months (31.67% vs 62.5%, p=0.001). The difference was also significant if only counting the L858R carriers (18.52% vs 59.26%, p=0.002), but not significant in the EX19del carriers (42.42% vs 66.67%, p=0.082).

      8eea62084ca7e541d918e823422bd82e Conclusion

      1st-line or 2nd-line EGFR-TKIs generally did not significantly alter the emergence of T790M. But for the L858R mutation carriers, the incidence of T790M is significantly decreased if treated as a 2nd-line EGFR-TKIs therapy. In addition, patients with longer PFS were associated with higher incidence of T790M mutation.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P1.01-56 - Concurrent Mutations in Chinese Lung Cancer Patients Carrying HER2 Genomic Aberrations (ID 13756)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Although human epidermal growth factor receptor 2 (HER2, ERBB2) genomic aberration has been identified as therapeutic targets, clinical trials of HER2-directed therapies have disappointing results in lung cancer. We hypothesize that the concurrent alterations might be one of the reasons, thus the aim of this study was to describe frequent concurrent alterations in Chinese lung cancer patients harboring HER2 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 147 cancer patients with HER2 mutations were enrolled in the study. Tumor biopsy, ctDNA and pleural effusion samples were collected for detection alterations using hybridization capture based next-generation sequencing (NGS), which enables the simultaneous detection of single-nucleotide variants, insertions/deletions, rearrangements, and copy-number alterations of at least 59 genes (59-1021).

      4c3880bb027f159e801041b1021e88e8 Result

      Sixty-two of 147 patients with HER2 genomic aberrations were diagnosed as lung cancer. The HER2 gene was amplified in 11 (18%) patients, whereas HER2 mutations were detected in 48 patients, co-occurrence of HER2 amplification and mutations were in 3 patients. Thirty of the 62 patients (48.39%) had concurrent actionable mutations across 18 genes, which involved in RTK-PIK3CA-mTOR signaling pathways, cell-cycle pathway, DNA repair pathway, RAS-RAF-MAPK pathway and some others (details in table). Moreover, 7 patients had more than 2 concurrent mutations besides HER2 mutation/amplification.

      Table 1. concurrent genetic alterations in HER2-altered lung cancer patients

      Signaling pathway

      Concurrent

      actionable

      mutations

      Number of

      patients

      RTK-PIK3CA-mTOR

      EGFR 11
      PIK3CA 4
      STK11 2
      FBXW7 1
      TSC1 1
      FLCN 1
      C11orf30 1
      Cell-cycle CDKN2A 5
      CCND1 2
      RB1 1
      DNA repair BRCA2 1
      ATM 1
      RAS-RAF-MAPK BRAF 1
      KRAS 1
      Others MDM2 2
      JAK2 2
      SMARCA4 2
      PTCH1 1

      8eea62084ca7e541d918e823422bd82e Conclusion

      Concurrent of actionable genetic alterations in HER2-altered Chinese lung cancer patients was common. The complex molecular profiles elucidate the importance of comprehensive analysis of genetic mutations when considering anti-HER2 targeted therapy.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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    P1.03 - Biology (Not CME Accredited Session) (ID 935)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 16
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.03-01 - Association of APC Mutations with Chinese Patients Molecular Spectrum in Non-Small-Cell Lung Cancer (ID 11109)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The role of adenomatous polyposis coli (APC) gene in mitosis might be critical for regulation of genomic stability and chromosome segregation. APC gene mutations have been associated to have a role in colon cancer and since gastric and colon tumors share some common genetic lesions, it is relevant to investigate the role of APC tumor suppressor gene in gastric cancer. While the genetic sites of APC mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring APC mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 294 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of APC mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      APC gene mutation rate was 4.08% (12/294) in non-small cell lung cancer, including R232* (1 patient), Y159* (1 patient), R564* (1 patient), E984Dfs*21 (1 patient), K534Nfs*15 (1 patient), Q161* (1 patient), K1437* (1 patient), K792* (1 patient), T1556Nfs*3 (1 patient), N32S (1 patient), R259W (1 patient) and N372D (1 patient) , and median overall survival (OS) for these patients was 9.0 months. Among them, all patients were APC gene with co-occurring mutation. Briefly, patients with (n=8) or without (n=4) co-occurring EGFR mutations had a median OS of 9.0 months and 6.0 months respectively (P=0.01); patients with (n=6) or without (n=6) co-occurring TP53 mutations had a median OS of 6.5 months and 11.0 months respectively (P=0.04); patients with (n=4) or without (n=8) co-occurring KRAS mutations had a median OS of 16.5 months and 9.0 months respectively (P=0.27); patients with (n=2) or without (n=10) co-occurring CDKN2A mutations had a median OS of 6.5 months and 11.5 months respectively (P=0.68).

      8eea62084ca7e541d918e823422bd82e Conclusion

      The present study expanded the database on APC gene mutations in NSCLC and enriched the spectrum of known somatic mutations of the APC gene. Chemotherapy may be considered as a possible treatment for carriers of the mutation. EGFR mutated accompanied mutations might play a good prognosis in APC gene mutation NSCLC.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P1.03-02 - Analysis of SMAD4 Aberrations in Chinese Patients with Non-Small-Cell Lung Cancer (ID 11107)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Mothers against decapentaplegic homolog 4 (SMAD4) is an important protein in cancers. It plays pivotal roles in cellular pathways, including apoptosis. While the genetic locus of SMAD4 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring SMAD4 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 451 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of SMAD4 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      SMAD4 gene mutation rate was 1.77% (8/451) in non-small cell lung cancer, including R361H (3 patients), C324Y (1 patient), E526Q (1 patient), Q289* (1 patient), D493G (1 patient) and P522R (1 patient), and median overall survival (OS) for these patients was 13.0 months. Among them, all patients were SMAD4 gene with co-occurring mutation. Briefly, patients with (n=2) or without (n=6) co-occurring EGFR mutations had a median OS of 10.0 months and 15.0 months respectively (P=0.18); patients with (n=5) or without (n=3) co-occurring TP53 mutations had a median OS of 10.0 months and 19.5 months respectively (P=0.18); patients with (n=3) or without (n=5) co-occurring KRAS mutations had a median OS of 10.0 months and 15.0 months respectively (P=0.30); patients with (n=3) or without (n=5) co-occurring CDKN2A mutations had a median OS of 10.0 months and 15.0 months respectively (P=0.22).

      8eea62084ca7e541d918e823422bd82e Conclusion

      There are some significant difference of clinical features in SMAD4 gene mutations with smoking advance NSCLC. SMAD4 gene inactivation is associated with poorer prognosis in patients with NSCLC.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P1.03-03 - Molecular Characteristics of Chinese Patients with TSC2-Mutated Non-Small-Cell Lung Cancer: A Retrospective Study (ID 11118)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Tuberous sclerosis complex 2 (TSC2) is a rare autosomal dominant disorder causing benign tumors in the brain and other vital organs. There is some clinical evidence for the use of TSC2 mutations as prognostic and predictive biomarker. The aim of this study is to investigate mutations and prognosis of NSCLC harboring TSC2 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 554 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of TSC2 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      TSC2 gene mutation rate was 4.51% (25/554) in non-small cell lung cancer, including M286V (2 patients), R1743W (1 patient), V550G (1 patient), D1004Y (1 patient), E546K (1 patient), K1065E (1 patient), R1329P (1 patient), K1585R (1 patient), S1221L (1 patient), A678T (1 patient), F15V (1 patient), D1406N (1 patient), P237L (1 patient), V1144M (1 patient), V1034I (1 patient), D1406N (1 patient), N1224I (1 patient), Q371H (1 patient), P1770S (1 patient), R1268G), A1141T (1 patient), R537C (1 patient), M649I (1 patient) and A1294V (1 patient), and median overall survival (OS) for these patients was 20.0 months. Among them, 23 patients with co-occurring mutations had a median OS of 20.0 months, and median OS of the 2 patients without complex mutations was 7.0 months. No statistically significant difference was found between the two groups (P=0.15). Briefly, patients with (n=8) or without (n=17) co-occurring EGFR mutations had a median OS of 19.0 months and 20.0 months respectively (P=0.93); patients with (n=18) or without (n=7) co-occurring TP53 mutations had a median OS of 20.0 months and 27.5 months respectively (P=0.67).

      8eea62084ca7e541d918e823422bd82e Conclusion

      There is no significant difference of molecular features in TSC2 gene mutations in NSCLC. Patients with complex mutations benefited more from therapy than those with single mutations. Next generation sequencing provides a simplified strategy and reasonably high detection rate for TSC2 mutation, which suggested application of the strategies into clinical molecular diagnostics.

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      P1.03-04 - Molecular Characteristics of ALK Primary Point Mutations Non-Small-Cell Lung Cancer in Chinese Patients (ID 11103)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Anaplastic lymphoma kinase (ALK) gene rearrangements have been identified in lung cancer at 3-7% frequency, thus representing an important subset of genetic lesions that drive oncogenesis in this disease. While the genetic locus of ALK primary point mutations NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring ALK primary point mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 339 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of ALK primary point mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      ALK gene primary point mutation rate was 8.55% (29/339) in non-small cell lung cancer, including V163L (3 patients), F921Gfs*16 (2 patients), K1416N (2 patients), A585T (2 patients), P1442Q (1 patient), A348T (1 patient), K1525E (1 patient), S737L (1 patient), P115L (1 patient), Q515E (1 patient), E314D (1 patient), R395H (1 patient), S1219F (1 patient), S341G (1 patient), P1543S (1 patient), G129V (1 patient), Q167H (1 patient), L550F (1 patient), T1012M (1 patient), D302Y (1 patient), H755Q (1 patient), H331Q (1 patient), G1474E (1 patient) and E119D (1 patient), and median overall survival (OS) for these patients was 20.0 months. Among them, 27 patients with co-occurring mutations had a median OS of 20.0 months, and median OS of the 2 patients without complex mutations was 8.5 months. Statistically significant difference was found between the two groups (P=0.02). Briefly, patients with (n=8) or without (n=21) co-occurring EGFR mutations had a median OS of 24.0 months and 20.0 months respectively (P=0.73); patients with (n=21) or without (n=8) co-occurring TP53 mutations had a median OS of 20.0 months and 17.0 months respectively (P=0.83).

      8eea62084ca7e541d918e823422bd82e Conclusion

      EGFR and TP53 gene accompanied may have less correlation with ALK primary point mutation in NSCLC patients. Results of ongoing studies will provide a platform for further research to offer individualized therapy with the purpose of improving outcomes.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P1.03-06 - Molecular Landscape of FGFR1 Point Mutations in Chinese Non-Small-Cell Lung Cancer Patients: A Retrospective Study (ID 11119)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Mutations of the fibroblast growth factor receptor 1 (FGFR1) is believed to predict response to FGFR inhibitors, but the genetic spectrum of FGFR1 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring FGFR1 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 469 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of FGFR1 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      FGFR1 gene mutation rate was 2.99% (14/469) in non-small cell lung cancer, including S99L (3 patients), S107L (2 patients), N546K (1 patient), R756H (1 patient), G70R (1 patient), R661Q (1 patient), V94I (1 patient), R50Q (1 patient), D312V (1 patient), R6Q (1 patient) and M427V (1 patient), and median overall survival (OS) for these patients was 11.4 months. Among them, all patients were FGFR1 gene with co-occurring mutation. Briefly, patients with (n=3) or without (n=11) co-occurring EGFR mutations had a median OS of 16.7 months and 11.0 months respectively (P=0.56); patients with (n=11) or without (n=3) co-occurring TP53 mutations had a median OS of 11.4 months and 20.7 months respectively (P=0.48); patients with (n=2) or without (n=12) co-occurring STK11 mutations had a median OS of 5.0 months and 11.4 months respectively (P=0.57); patients with (n=3) or without (n=11) co-occurring PTCH1 mutations had a median OS of 5.7 months and 11.4 months respectively (P=0.11).

      8eea62084ca7e541d918e823422bd82e Conclusion

      It demonstrated that FGFR1 mutation was an infrequent genetic alteration, and for firstly, and we found FGFR1 mutation also was an independent delayed adverse prognostic factor only in early stage NSCLC patients, suggesting that FGFR1 mutation may be a viable prognostic factor in these patients.

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      P1.03-07 - A Comparison of Consistency of Detecting HER2 Gene Mutations in Peripheral Blood and Tumor Tissue of Non-Small-Cell Lung Cancer Patients (ID 11114)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      HER2 is expressed in solid carcinomas including cancers of the breast, stomach, lung and pancreas. Preclinical and clinical studies have confirmed that HER2 is a driver gene in non-small-cell lung cancer (NSCLC). Three principal mechanisms of HER2 alteration include: protein overexpression, gene amplification and gene mutations. In NSCLC, HER2 mutations were identified to represent a distinct subset of driver genes that usually excluded with other common driver genes like EGFR, KRAS and ALK, based on published studies. The aim is to detect the consistency of the HER2 gene mutation in peripheral blood and tumor tissue of patients with NSCLC and discuss the clinical application value of HER2 gene mutation in peripheral blood.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Real-time fluorescent quantitative PCR was used to determine the HER2 gene mutation of peripheral blood and tumor tissue specimens collected from 185 cases of NSCLC. A comparison of HER2 gene mutation consistency of peripheral blood and tumor tissue specimens was conducted. The correlation between HER2 gene mutations and clinical characteristics of the patients was analyzed.

      4c3880bb027f159e801041b1021e88e8 Result

      The HER2 gene mutation rate was 3.78% in peripheral blood of 7 patients with NSCLC, and was 2.16% in 4 cancer tissues, the mutation consistency was 75.00% in peripheral blood tumor tissue matched samples. The consistency was statistically significant (κ=0.553, P<0.001). The incidence of HER2 gene mutation in peripheral blood correlate with smoking history (P<0.05),but did not correlate with age,gender and pathological type (P>0.05).The incidence of HER2 gene mutation in tumor tissue correlated with gender and smoking history (P<0.05),but did not correlate with age and pathological type.

      8eea62084ca7e541d918e823422bd82e Conclusion

      The consistency of the HER2 gene mutation in peripheral blood and tissue is high. HER2 gene mutations of peripheral blood could be used for clinical diagnosis and treatment in cases when tissue specimen is hard to get.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P1.03-08 - Detection of PTCH1 Gene Variants in Non-Small Cell Lung Cancer Patients from China (ID 11116)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Recently, the Patched homolog 1 gene (PTCH1) gene mutations are identified in non-small-cell lung cancer (NSCLC). While the genetic spectrum of PTCH1 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring PTCH1 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 269 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of PTCH1 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      PTCH1 gene mutation rate was 6.32% (17/269) in non-small cell lung cancer, including S827G (2 patients), G445S (1 patient), A1130T (1 patient), L1036F (1 patient), E173D (1 patient), P1210L (1 patient), Y820* (1 patient), D710E (1 patient), C37W (1 patient), N258I (1 patient), F614Y (1 patient), P681S (1 patient), V1381G (1 patient), G37R (1 patient), A741V (1 patient) and P1282L plus R893H (1 patient), and median overall survival (OS) for these patients was 18.0 months. Among them, all patients were PTCH1 gene with co-occurring mutation. Briefly, patients with (n=5) or without (n=12) co-occurring EGFR mutations had a median OS of 22.0 months and 18.0 months respectively (P=0.25); patients with (n=11) or without (n=6) co-occurring TP53 mutations had a median OS of 18.0 months and 14.0 months respectively (P=0.28); patients with (n=2) or without (n=15) co-occurring BRAF mutations had a median OS of 4.0 months and 18.0 months respectively (P=0.14); patients with (n=2) or without (n=8) co-occurring PIK3CA mutations had a median OS of 17.0 months and 18.0 months respectively (P=0.96).

      8eea62084ca7e541d918e823422bd82e Conclusion

      PTCH1 gene mutation coexists with other gene mutation in NSCLC. EGFR, TP53, BRAF and PIK3CA gene accompanied may have less correlation with PTCH1 mutation in NSCLC patients. Analysis of PTCH1 mutations shows promise as a way to refine individual patients with NSCLC, and provides more insight into effective treatment strategies for patients with PTCH1 mutations.

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      P1.03-09 - ROS1 Rearrangement in Pulmonary Sarcomatoid Carcinoma: A Retrospective Study of the Real World (ID 11206)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Pulmonary sarcomatoid carcinoma (PSC) is a recognized category of highly aggressive and poorly differentiated non-small-cell lung carcinoma (NSCLC), with five different subtypes: pleomorphic, spindle, giant cell, carcinosarcoma, and pulmonary blastoma. Although uncommon (0.1% to 0.4% of all pulmonary malignancies), their clinical importance is underscored by poorer prognosis and higher rate of resistance to conventional chemotherapy than other NSCLCs. And the incidence of c-ros oncogene 1, receptor tyrosine kinase (ROS1) rearrangement in PSC is controversial. The aim of this study was to reveal the reliable frequency and the clinical-pathologic characteristics of PSC with ROS1 rearrangement in Chinese population.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 35 patients with PSC were recruited between September 2007 and December 2017. The status of ROS1 rearrangement was detected by reverse transcription polymerase chain reaction (RT-PCR).

      4c3880bb027f159e801041b1021e88e8 Result

      Of this study, three patients were identified with ROS1 rearrangement in Chinese PSC population (2.86%, 1/35). The patient was a pulmonary pleomorphic carcinoma (PPC).

      8eea62084ca7e541d918e823422bd82e Conclusion

      The incidence rates of ROS1 rearrangement in PSC in the Chinese population are more than those of other subtypes of NSCLC. Crizotinib may serve as an effective treatment for ROS1-rearranged PSC.

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      P1.03-10 - The Molecular Spectrum of NF1 Variants in Chinese Non-Small-Cell Lung Cancer Patients (ID 11111)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Activation of the RAS/MAPK pathway is critical in non-small-cell lung cancer. Non-small-cell lung cancer can be grouped into four molecular subtypes based on their main genetic driver: EGFR-mutant, ALK-fusion, ROS1-fusion, and triple wild-type tumors. The NF1 protein, neurofibromin 1, negatively regulates RAS proteins through GTPase activity. Somatic mutations in NF1 cause neurofibromatosis type I, a common genetic tumor syndrome caused by dysregulation of the RAS/MAPK pathway, ie, RAS pathy. While the genetic sites of NF1 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring NF1 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 337 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of NF1 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      NF1 gene mutation rate was 6.23% (21/337) in non-small cell lung cancer, including M645V (3 patients), A1998V (1 patient), Q83E (1 patient), P654T (1 patient), Q912* (1 patient), C324* (1 patient), C1032S (1 patient), I1628M (1 patient), L43V (1 patient), A861Qfs*17 (1 patient), Q239E (1 patient), D1623N (1 patient), T586Vfs*18 (1 patient), R2328C (1 patient), E41* (1 patient), V437Nfs*35 (1 patient), P2046L plus G1219* (1 patient), D2055Mfs*6 plus T2133Sfs*45 (1 patient) and C1288F plus K2252* (1 patient), and median overall survival (OS) for these patients was 10.0 months. Among them, all patients were NF1 gene with co-occurring mutation. Briefly, patients with (n=3) or without (n=18) co-occurring EGFR mutations had a median OS of 15.5 months and 10.0 months respectively (P=0.69); patients with (n=18) or without (n=3) co-occurring TP53 mutations had a median OS of 10.0 months and 6.0 months respectively (P=0.21); patients with (n=3) or without (n=18) co-occurring RB1 mutations had a median OS of 19.5 months and 9.0 months respectively (P=0.27); patients with (n=3) or without (n=18) co-occurring SMARCA4 mutations had a median OS of 20.5 months and 9.0 months respectively (P=0.19).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Patients with complex mutations benefited more from therapy than those with single mutations. NF1 genetic alter occurs in a subset of NSCLC, and improved understanding of the implications of NF1 aberrations is critical for the identification of therapeutic target candidates.

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      P1.03-23 - The Molecular Landscape and Outcome of Chinese Patients with Non-Small Cell Lung Cancer Harboring NTRK1 Point Mutations: A Retrospective Study (ID 11224)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The identification and clinical validation of cancer driver genes are essential to accelerate the translational transition of cancer genomics, as well as to find clinically confident targets for the therapeutic intervention of cancers. While the genetic variability of neurotrophic receptor tyrosine kinase 1 (NTRK1) mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring NTRK1 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 389 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of NTRK1 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      NTRK1 gene mutation rate was 4.11% (16/389) in non-small cell lung cancer, including H268Q (1 patient), V181M (1 patient), Q459R (1 patient), G726C (1 patient), R89H (1 patient), M635I (1 patient), L126Q (1 patient), G138R (1 patient), E245A (1 patient), M530T (1 patient), L549Cfs*73 (1 patient), N293S (1 patient), E245A (1 patient), W236C (1 patient), E456K (1 patient) and F297L (1 patient), and median overall survival (OS) for these patients was 11.0 months. Among them, all patients were NTRK1 gene with co-occurring mutation. Briefly, patients with (n=5) or without (n=11) co-occurring EGFR mutations had a median OS of 14.0 months and 11.0 months respectively (P=0.90); patients with (n=12) or without (n=4) co-occurring TP53 mutations had a median OS of 11.0 months and 6.0 months respectively (P=0.67); patients with (n=3) or without (n=13) co-occurring BRAF mutations had a median OS of 14.0 months and 11.0 months respectively (P=0.43); patients with (n=4) or without (n=16) co-occurring CDKN2A mutations had a median OS of 3.5 months and 14.0 months respectively (P<0.01).

      8eea62084ca7e541d918e823422bd82e Conclusion

      NTRK1 oncogenic activation through gene fusion defines a novel and distinct subset of NSCLC. EGFR, TP53 and BRAF gene accompanied may have less correlation with KIT mutation in NSCLC patients. CDKN2A accompanied mutations might play a worse prognosis in NTRK1 gene mutation non-small cell lung cancer.

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      P1.03-25 - The Frequency and Prognosis of ATM Mutations in Chinese Non-Small-Cell Lung Cancer Patients (ID 11113)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The ataxia-telangiectasia mutated kinase protein (ATM) plays a critical role in the cellular response to double strand DNA damage. While the genetic locus of ATM mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring ATM mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 389 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of ATM mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      ATM gene mutation rate was 6.17% (24/389) in non-small cell lung cancer, including L229V (1 patient), V2298E (1 patient), M2041V (1 patient), D126N (1 patient), S2123N (1 patient), Q95L (1 patient), R337H (1 patient), H1474R (1 patient), R772Sfs*25 (1 patient), W488L (1 patient), M1064T (1 patient), E347A (1 patient), K1192R (1 patient), P1374S (1 patient) R248* (1 patient), M1321I (1 patient), I346N (1 patient), H2430R (1 patient), G494D (1 patient), N2282S (1 patient), A1945S (1 patient), E518* plus D1616V (1 patient), Q161* plus E699Q (1 patient) and D2448G plus L2261Tfs*12 (1 patient), and median overall survival (OS) for these patients was 18.0 months. Among them, all patients were ATM gene with co-occurring mutation. Briefly, patients with (n=8) or without (n=16) co-occurring EGFR mutations had a median OS of 21.0 months and 11.0 months respectively (P=0.19); patients with (n=13) or without (n=11) co-occurring TP53 mutations had a median OS of 21.0 months and 14.0 months respectively (P=0.44).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Although EGFR and TP53 gene accompanied may have less correlation with ATM mutation in NSCLC patients, predict which patients may harbor ATM mutations, could have implications in triaging toward ATM variant identification for potential future targeted therapy. These data have implications for the identification of therapeutic target candidates .

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      P1.03-26 - Analysis of DDR2 Gene Aberrations in Chinese Non-Small-Cell Lung Cancer Patients and Evaluation of Their Prognosis (ID 11105)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Recently, Mutations in discoidin domain receptor 2 (DDR2) gene were recently identified as promising molecular targets in non-small-cell lung cancer. While the genetic spectrum of DDR2 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring DDR2 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 283 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of DDR2 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      DDR2 gene mutation rate was 3.18% (9/283) in non-small cell lung cancer, including S311N (3 patients), E44K (1 patient), R709Q (1 patient), T564I (1 patient), R742Q (1 patient), G206* (1 patient) and M117I (1 patient), and median overall survival (OS) for these patients was 20.0 months. Among them, all patients were DDR2 gene with co-occurring mutation. Briefly, patients with (n=6) or without (n=3) co-occurring EGFR mutations had a median OS of 20.0 months and 9.0 months respectively (P=0.29); patients with (n=4) or without (n=5) co-occurring TP53 mutations had a median OS of 17.0 months and 21.5 months respectively (P=0.63); patients with (n=2) or without (n=7) co-occurring KRAS mutations had a median OS of 13.5 months and 20.0 months respectively (P=0.82); patients with (n=2) or without (n=7) co-occurring PTPRD mutations had a median OS of 15.0 months and 20.0 months respectively (P=0.96).

      8eea62084ca7e541d918e823422bd82e Conclusion

      DDR2 mutations were observed in 3.18 % of cases of NSCLC. DDR2-mutated NSCLC can exhibit other driver gene alterations. No clinical characteristics were significantly associated with DDR2 mutation.

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      P1.03-27 - Somatic Mutations in BRCA2 Genes Are Associated with Prognosis in Chinese Non-Small-Cell Lung Cancer Patients (ID 11115)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The role of BRCA2 gene somatic mutations are mainly to maintain genome integrity in response to DNA damage through different mechanisms. Deregulation of BRCA2 is associated with the development of tumor and altered sensitivity to chemotherapeutic agents, but the genetic variability of BRCA2 somatic mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring BRCA2 somatic mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 362 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of BRCA2 somatic mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      BRCA2 gene somatic mutation rate was 4.97% (18/362) in non-small cell lung cancer, including S547P (2 patients), G1433W (2 patients), I488V (1 patient), C315S (1 patient), T2007S (1 patient), I1929V (1 patient), H3117Y (1 patient), G1370V (1 patient), T768S (1 patient), E2260Q (1 patient), R2087K (1 patient), E3167Q (1 patient), S163T (1 patient), T152I (1 patient), E2275Q (1 patient) and S163T (1 patient) , and median overall survival (OS) for these patients was 18.0 months. Among them, all patients were BRCA2 gene with co-occurring somatic mutation. Briefly, patients with (n=3) or without (n=15) co-occurring EGFR mutations had a median OS of 21.0 months and 18.0 months respectively (P=0.22); patients with (n=11) or without (n=7) co-occurring TP53 mutations had a median OS of 7.5 months and 18.0 months respectively (P=0.15); patients with (n=2) or without (n=16) co-occurring HER2 mutations had a median OS of 11.0 months and 20.0 months respectively (P=0.24).

      8eea62084ca7e541d918e823422bd82e Conclusion

      BRCA2 mutations represent a distinct subset of NSCLC. NGS might be useful for evaluation of BRCA2 unclassified variants. Our results show that BRCA2 mutations delineate an aggressive subtype of lung cancer for which a targeted treatment through BRCA2 inhibition might offer new opportunities.

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      P1.03-28 - Association Between Molecular Characteristics of CTNNB1 Mutations and Prognosis in Patients with Nsclc in Chinese Patients (ID 11097)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Recently, CTNNB1, encoding beta-catenin, is a well-known tumor-related gene in the wnt signaling pathway. While the genetic variability of CTNNB1 mutation NSCLC patients is unclear.The aim of this study is to investigate mutations and prognosis of NSCLC harboring CTNNB1 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 677 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of CTNNB1 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      CTNNB1 gene mutation rate was 1.92% (13/677) in non-small cell lung cancer, including S33F (4 patients), S33C (1 patient), D32H (1 patient), G34R (1 patient), G34V (1 patient), G34del (1 patient), D11G (1 patient), S45P (1 patient), S45F (1 patient) and S45del plus S33Y (1 patient), and median overall survival (OS) for these patients was 12.0 months. Among them, all patients were CTNNB1 gene with co-occurring mutations. Briefly, patients with (n=7) or without (n=6) co-occurring EGFR mutations had a median OS of 25.8 months and 8.5 months respectively (P=0.18); patients with (n=10) or without (n=3) co-occurring TP53 mutations had a median OS of 10.0 months and 17.5 months respectively (P=0.35); patients with (n=2) or without (n=11) co-occurring BRAF mutations had a median OS of 7.5 months and 13.0 months respectively (P=0.14); patients with (n=2) or without (n=11) co-occurring ATM mutations had a median OS of 17.5 months and 11.0 months respectively (P=0.53).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Accompanied gene has not well been connected with CTNNB1 gene mutations. Our finding expands the mutant spectrum of CTNNB1 gene and adds new understanding of the phenotype.

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      P1.03-32 - Molecular Characteristics and Prognosis FBXW7 Mutations in Chinese Non-Small-Cell Lung Cancer Patients (ID 11209)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      FBXW7 (F-box and WD repeat domain containing-7) is a tumor suppressor protein that regulates the degradation of various oncoproteins in several malignancies. However, limited information is available regarding FBXW7 mutations in non-small-cell lung cancer. While the genetic variability of FBXW7 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring FBXW7 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 229 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of FBXW7 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      FBXW7 gene mutation rate was 3.06% (7/229) in non-small cell lung cancer, including G66Efs*55 (1 patient), I487Sfs*23 (1 patient), S668Vfs*39 (1 patient), G493E (1 patient), R49W(1 patient), S550Efs*26 (1 patient) and R505L (1 patient), and median overall survival (OS) for these patients was 10.0 months. Among them, all patients were FBXW7 gene with co-occurring mutation. Briefly, patients with (n=2) or without (n=5) co-occurring EGFR mutations had a median OS of 13.5 months and 10.0 months respectively (P=0.56); patients with (n=5) or without (n=2) co-occurring TP53 mutations had a median OS of 6.0 months and 17.5 months respectively (P=0.27); patients with (n=2) or without (n=5) co-occurring PIK3CA mutations had a median OS of 8.0 months and 14.0 months respectively (P=0.43); patients with (n=3) or without (n=4) co-occurring STK11 mutations had a median OS of 4.0 months and 17.5 months respectively (P=0.06).

      8eea62084ca7e541d918e823422bd82e Conclusion

      FBXW7, normally a tumor suppressor, can act as an oncogene when mutated and may play an important role in the pathogenesis of NSCLC. EGFR, TP53 and PIK3CA gene accompanied may have less correlation with FBXW7 mutation in NSCLC patients. Everolimus may displayed moderated efficacy in patients with FBXW7 mutation. STK11 accompanied mutations might play a worse prognosis in FBXW7 gene mutation NSCLC.

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      P1.03-33 - Mutational Spectrum and Prognosis of Non-Small-Cell Lung Cancer Harboring MTOR Mutations in Chinese Population (ID 11220)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Mammalian Target of Rapamycin (mTOR) is a validated target in cancer. It remains to be determined whether non-small-cell lung cancer patients bearing mTOR mutation could be selected for treatment with PI3K-AKT-mTOR pathway inhibitors. While the genetic spectrum of MTOR mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring MTOR mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 639 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of MTOR mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      MTOR gene mutation rate was 3.60% (23/639) in non-small cell lung cancer, including T1830_T1833[2>1] (3 patients), S221N (1 patient), C1483F (1 patient), D1527H (1 patient), I1964V (1 patient), E1799K (1 patient), L88F (1 patient), P2273L (1 patient), E97K (1 patient), L565Q (1 patient), M1038I (1 patient), A1792V (1 patient), R1896Q (1 patient), G1678E (1 patient), M2327I (1 patient), E2419K (1 patient), A2248S (1 patient), T1870S (1 patient), V2198A (1 patient), R1482P (1 patient) and E1362K (1 patient), and median overall survival (OS) for these patients was 13.0 months. Among them, all patients were MTOR gene with co-occurring mutation. Briefly, patients with (n=5) or without (n=18) co-occurring EGFR mutations had a median OS of 17.0 months and 11.0 months respectively (P=0.33); patients with (n=15) or without (n=8) co-occurring TP53 mutations had a median OS of 11.0 months and 13.0 months respectively (P=0.42).

      8eea62084ca7e541d918e823422bd82e Conclusion

      MTOR mutation may predict a worse prognosis of NSCLC. MTOR pathway inhibitors everolimus may be beneficial for NSCLC patients with specific MTOR mutations. EGFR and TP53 gene accompanied may have less correlation with MTOR mutation in NSCLC patients. The findings of this study could facilitate both clinical trial design and therapeutic strategies.

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    P1.09 - Pathology (Not CME Accredited Session) (ID 941)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.09-18 - 15 Cases of Clinical and Molecular Features Analysis in Pulmonary Adenoid Cystic Carcinoma (ID 11108)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Pulmonary adenoid cystic carcinoma (PACC) of the lung is a malignant tumor arising in the tracheobronchial glands distributed in the airway submucosa. The aim of this study is to investigate the molecular characteristics of PACC.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      From July 2013 to December 2016, 15 PACC patients received treatment. All the patients were diagnosed by pathology. We retrospectively reviewed the clinical data and genetic state.

      4c3880bb027f159e801041b1021e88e8 Result

      EGFR mutation rate was 6.67% (1/15), and it was 19del, the relationship between EGFR gene status and gender (P=1.000), age (P=1.000), smoking status (P=1.000) and stage (P=1.000) were no significant, and ALK fusion and ROS1 fusion gene was not detected.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Gene change exists PACC, and the gene detection cannot be ignored in PACC.

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    P1.13 - Targeted Therapy (Not CME Accredited Session) (ID 945)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.13-08 - Distribution, Differences in Clinical Characteristics and Resistance Mechanism of ALK Variants in Chinese Lung Cancer Patients. (ID 13678)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      ALK rearrangements are established targetable drivers in NSCLC. Recent reports indicate differential progression-free survival to ALK inhibitors according to specific EML4-ALK variant.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 172 unique Chinese lung cancer patients with tumors harboring ALK rearrangements (ALK+) were enrolled in the study from 2016 to 2018. ALK+ were detected by Ventana, FISH, or next-generation sequencing based ER-Seq method, which enables simultaneously assess single-nucleotide variants, insertions/deletions, rearrangements, and somatic copy-number alterations across at least 59 genes (59-1021). Tissue biopsy was the first choice for NGS mutation profiling, and ctDNA or pleural effusion testing was used as an alternative.

      4c3880bb027f159e801041b1021e88e8 Result

      Of these 172 cases, the median diagnosis age was 50 (range 24-78), 58% were female, 90% was NSCLC. Of the 147 ALK+ cases detected by NGS, we identified 65 (44%) EML4-ALK v1 (E13; A20), 18 (12%) EML4-ALK v2 (E20; A20), 43 (29%) EML4-ALK v3 (E6; A20), 13 (9%) other EML4-ALK, and 8 (5%) non-EML4-ALK rearrangements. 2 new fusion genes were found in non EML4-ALK rearrangements (SRBD1-ALK (EX20; EX20) and CLIP4-ALK (EX9; EX20)), and the CLIP4-ALK patient’s tissue was also ALK positive by Ventana. V1 found a higher proportion of pleural effusion at baseline than non-v1 (12% v.s.5%). Mutation profiling by NGS were performed after disease progression in 55 patients treated with crizotinib. mPFS was 8.1 months, no significant difference existed between v1 and v3 (P=0.69). But the presence of known ALK resistance mechanisms was significantly higher in v3 as compared to non-v3 (67% v.s. 27%, P=0.038).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Next generation sequencing allows for detection of the specific ALK fusion partner and variants, increases the understanding of the biology of ALK+ NSCLC, and may have value to foretell potential mechanisms of resistance.

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    P2.01 - Advanced NSCLC (Not CME Accredited Session) (ID 950)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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      P2.01-117 - Concurrent Gene Alterations in Treatment-Naïve EGFR-Mutant Advanced Non-Small Cell Lung Cancer (ID 13102)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      EGFR-TKIs is the standard first line treatment for EGFR-mutant advanced non-small-cell lung cancer (NSCLC). However, 20% to 30% of patients who receive EGFR-TKIs exhibit primary resistance. The gene alterations in treatment-naïve EGFR-mutant advanced NSCLC should be better explored.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We retrospectively reviewed gene test results of 980 treatment-naïve advanced NSCLC samples in our institute. Tumor biopsy, ctDNA, pleural effusion or cerebrospinal fluid samples were analyzed using hybridization capture-based NGS ER-seq method, white blood cells as control, which enables simultaneously assess single-nucleotide variants (SNV), insertions/deletions (indel), rearrangements and somatic copy-number(CNV) variation at least 59 genes (range 59-1021 genes).

      4c3880bb027f159e801041b1021e88e8 Result

      Three hundreds and eighty one cases with EGFR sensitive mutation were identified, 358 adenocarcinoma, 7 squamous cell carcinoma, 1 adenosquamous carcinoma and 15 NSCLC. Among the patients, 88 patients (23.1%) harbored concurrent actionable mutations with EGFR, which 43 were exon 19 deletion, 37 were L858R and 8 were uncommon EGFR mutations. One patient had co-occurring L858R, T790M and CDKN2A frameshift mutation. The actionable mutations were from 23 genes, which involved in cellular signaling pathways, and some genes had been reported associated with EGFR-TKIs resistance (details in table). Except the actionable mutations, TP53 mutations were detected in 225 samples (59.1%, 225/381), which 35.1% (79/225) in exon8. Bcl-2–like 11(BIM) deletion were detected in 31 (8.1%, 31/381) white blood cells.

      Signaling Pathways

      Concurrent gene alterations

      Frequency(N=88)

      Cell cycle*

      CDKN2A

      3.9%

      CDK4

      2.1%

      CCNE1

      0.8%

      CCND1

      0.8%

      CCND3

      0.3%

      PI3K/AKT/mTOR*

      PIK3CA

      2.9%

      PTEN

      1.3%

      TSC1/2

      1.0%

      AKT2

      0.3%

      NF1

      0.3%

      RTKs*

      MET

      0.8%

      HER2

      0.8%

      FGFR2

      0.3%

      FGFR3-TACC3

      0.3%

      Ras/Raf/MAPK*

      KRAS

      0.8%

      Homologous Recombination Repair pathway

      BRCA2(sc+gm)

      0.8%

      BRCA1(sc)

      0.5%

      ATM

      0.5%

      PALB2

      0.3%

      Others

      CTNNB1

      2.9%

      MDM2

      2.4%

      SMARCA4

      0.8%

      JAK2

      0.5%

      sc, somatic mutation;

      gm, germline mutation;

      *, genes had been reported associated with EGFR-TKIs resistance

      8eea62084ca7e541d918e823422bd82e Conclusion

      Concurrent gene alterations in treatment-naïve EGFR-mutant advanced NSCLC is common, and mutiple genes are involved. This maybe contribute to the primary resistance to EGFR-TKIs in EGFR-mutant advanced NSCLC. Indicate the importance of multiplex molecular test and further researches of target therapies.

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    P2.03 - Biology (Not CME Accredited Session) (ID 952)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 5
    • Moderators:
    • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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      P2.03-08 - Molecular Spectrum of Patients with MSH2 Mutations in Chinese Non-Small Cell Lung Cancer (ID 11236)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Although inactivation of MutS Homolog 2 (MSH2) genes may predict sensitivity to immunotherapy in non-small cell lung cancer. little is known about their etiology and prognosis in non-small-cell lung cancer (NSCLC). The aim of this study is to investigate mutations and prognosis of NSCLC harboring MSH2 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 326 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of MSH2 mutation or other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      MSH2 gene mutation rate was 9.51% (31/326) in non-small cell lung cancer, including H839R (5 patients), L390F (4 patients), E809K (3 patients), I169V (3 patients), I544M (1 patient), R217C (1 patient), T8M (1 patient), T552S (1 patient), A189S (1 patient), Q493P (1 patient), I735V (1 patient), A45T (1 patient), A573T (1 patient), R534L (1 patient), V712Sfs*5 (1 patient), F58L (1 patient), S676L (1 patient), N583S (1 patient), I766V plus A2V (1 patient) and Q419K plus Q629R (1 patient), and median overall survival (OS) for these patients was 16.0 months. Among them, all patients were MSH2 gene with co-occurring mutation. Briefly, patients with (n=6) or without (n=25) co-occurring EGFR mutations had a median OS of 6.5 months and 17.0 months respectively (P=0.02); patients with (n=20) or without (n=11) co-occurring TP53 mutations had a median OS of 14.0 months and 17.0 months respectively (P=0.85).

      8eea62084ca7e541d918e823422bd82e Conclusion

      MSH2 is involved in MMR, controlling several aspects of genome stability. Immunotherapy may displayed moderated efficacy in patients with MSH2 mutation. EGFR accompanied mutations might play a good prognosis in MSH2 gene mutation NSCLC.

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      P2.03-09 - The Real World of NTRK Fusion Data in the Chinese Lung Cancer Populations: A Multicenter Study (ID 11307)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      NTRK fusions have been recently identified as a therapeutic target in a rare fraction of Caucasian patients with lung cancer (3.3%). The aim of this study was to evaluate the prevalence of NTRK fusions in Chinese lung cancer populations, which had not been reported earlier, and to describe targeting potential in Chinese lung cancer populations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A multicenter study in China was initiated from February 2014, and lung cancer patients have been enrolled as of December 2017. Capture-based comprehensive genomic profiling was performed on 2719 lung cancer FFPE samples (non-squamous/squamous/small=2061/349/309) sequenced to a mean coverage depth of > 650X for up to 381 cancer-related genes. Genomic alterations (GA) included short variant (SV) base subs and insertions/deletions, copy number alterations, and rearrangements/fusions. Tumor mutational burden (TMB; mut/Mb) was calculated on up to 1.2 Mb of sequenced DNA.

      4c3880bb027f159e801041b1021e88e8 Result

      Of this entire cohort, just one (0.04%) patient was identified with a TPM3-NTRK1 fusion. The patient was diagnosed with SCLC. TPM3-NTRK1 fusion was found by biopsy using NGS, the genes co-altered with NTRK fusion was no concurrent with KRAS, EGFR, ALK, ROS1, or other known drivers were identified in the study cohort cases.

      8eea62084ca7e541d918e823422bd82e Conclusion

      NTRK fusions are a rare molecular subtype in Chinese lung cancer populations. Given clinical evidence for the activity of targeted therapy approaches, molecular eligibility for clinical trials of larotrectinib or entrectinib should include these fusion subtypes. The clinical evidence for responsiveness of NTRK fusions driven lung cancer provides an opportunity to personalize treatments and improve clinical outcomes for patients.

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      P2.03-10 - Gene Mutational Profiling Of Chinese TKI-Sensitizing EGFR Mutations NSCLC Patients Required Resistance to Icotinib Using NGS (ID 11235)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Icotinib is an oral first-generation epidermal receptor 1/epidermal growth factor receptor (HER1/EGFR) tyrosine kinase inhibitor (TKI). Identification of actionable genetic alterations conferring drug-resistance can be helpful for guiding the subsequent treatment decision. One of the major resistant mechanisms is EGFR-T790M mutation. Other mechanisms, such as MET amplifications, BRAF mutations and PIK3CA mutations, were also reported. In this study, we performed gene mutational profiling in a cohort of 162 TKI-sensitizing EGFR mutations NSCLC patients and acquired resistance to icotinib using targeted NGS.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 162 patients with stage IIIb-IV TKI-sensitizing EGFR mutations NSCLC were undergoing tumor biopsies, blood or serous effusions withdrawing by the time of acquiring resistance to icotinib. We used targeted NGS to detect genes status of patients.

      4c3880bb027f159e801041b1021e88e8 Result

      In total, we identified 373 genetic alterations with a median of 2.3 mutations per patient. 64.20% (104/162) of patients still exhibit TKI-sensitizing EGFR mutations, and 46.30% (75/162) of patients acquired EGFR-T790M mutations. Besides other known resistance mechanisms, we identified MET amplification 6.17% (10/162) of patients, BRAF mutations in 3.09% (5/162) of patients, and PIK3CA mutations in 2.47% (4/162) of patients. Interestingly, we also observed RBM10, ASXL1 and BMX mutations in EGFR-T790M wild patients, which are restricted to icotinib treatment resistance.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our study uncovered mutational profiles of TKI-sensitizing EGFR mutations NSCLC patients with icotinib resistance with potential therapeutic implications. Our analysis strongly suggests that MET amplification, BRAF mutations and PIK3CA mutations may serve as bypass resistance mechanisms in patients who are EGFR T790M wild type.

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      P2.03-11 - PDGFRA Defines a Unique Molecular Subtypes of Chinese Non-Small Cell Lung Cancer Patients (ID 11238)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Activation of the platelet-derived growth factor (PDGF) signaling system has been implicated in the development and malignant progression of non-small-cell lung cancer. Recently, the platelet-derived growth factor receptor A (PDGFRA) gene mutations are identified in non-small-cell lung cancer (NSCLC). While the genetic locus of PDGFRA mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring PDGFRA mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 467 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of PDGFRA mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      PDGFRA gene mutation rate was 2.14% (10/467) in non-small cell lung cancer, including S716R (1 patient), L615* (1 patient), A916T (1 patient), H104R (1 patient), V536M (1 patient), N505K (1 patient), V421I (1 patient), V538M (1 patient), M578K (1 patient) and V544A (1 patient), and median overall survival (OS) for these patients was 24.0 months. Among them, all patients were PDGFRA gene with co-occurring mutation. Briefly, patients with (n=2) or without (n=8) co-occurring EGFR mutations had a median OS of 19.0 months and 24.0 months respectively (P=0.96); patients with (n=6) or without (n=4) co-occurring TP53 mutations had a median OS of 24.0 months and 19.0 months respectively (P=0.99); patients with (n=2) or without (n=8) co-occurring BRCA2 mutations had a median OS of 25.0 months and 19.0 months respectively (P=0.17); patients with (n=2) or without (n=8) co-occurring IDH2 mutations had a median OS of 15.0 months and 24.0 months respectively (P=0.22).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Mutation type of PDGFRA has a potential for predicting the course of the disease and might contribute to management individualization of NSCLC patients. EGFR, TP53, BRCA2 and IDH2 gene accompanied may have less correlation with PDGFRA mutation in NSCLC patients. Imatinib may displayed moderated efficacy in patients with PDGFRA mutation.

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      P2.03-35 - Non-Small-Cell Lung Cancer with SMO Gene Variants of Uncertain Significance Share Distinct Molecular Features (ID 11207)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Recently, alterations of the Smoothened (SMO) gene (mutation, amplification, mRNA overexpression) were found in 12.2% of tumors of The Cancer Genome Atlas (TCGA) lung adenocarcinomas by whole-exome sequencing. While the genetic locus of SMO mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring SMO mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 423 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of SMO mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      SMO gene mutation rate was 2.60% (11/423) in non-small cell lung cancer, including T179M (4 patients), S566R (1 patient), P694Lfs*82 (1 patient), S590T (1 patient), P693S (1 patient), P60L (1 patient), E211D plus G212C (1 patient) and M230I plus A289T (1 patient), and median overall survival (OS) for these patients was 24.0 months. Among them, all patients were SMO gene with co-occurring mutation. Briefly, patients with (n=6) or without (n=5) co-occurring EGFR mutations had a median OS of 19.0 months and 25.0 months respectively (P=0.23); patients with (n=2) or without (n=9) co-occurring TP53 mutations had a median OS of 19.0 months and 25.0 months respectively (P=0.36); patients with (n=3) or without (n=8) co-occurring KRAS mutations had a median OS of 23.0 months and 24.0 months respectively (P=0.75); patients with (n=4) or without (n=7) co-occurring BRCA2 mutations had a median OS of 16.0 months and 24.0 months respectively (P=0.01).

      8eea62084ca7e541d918e823422bd82e Conclusion

      SMO mutations may be a potential novel mechanism of acquired resistance in EGFR-mutated NSCLC patients. EGFR, TP53 and KRAS gene accompanied may have less correlation with SMO mutation in NSCLC patients. BRCA2 accompanied mutations might play a worse prognosis in SMO gene mutation NSCLC. Screening of SMO alteration by the role of the Hh pathway suggests new opportunities to design new treatment strategies in NSCLC.

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    P2.06 - Mesothelioma (Not CME Accredited Session) (ID 955)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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      P2.06-39 - Next Generation Sequencing Reveals Genetic Landscape of Malignant Mesothelioma (ID 12702)

      16:45 - 18:00  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Malignant mesothelioma (MM) is a rare form of cancer affecting the mesothelium lining. The 5-year survival rate of advanced patients is less than 1% due to the lack of effective medical therapies. To investigate the possibility of targeted therapy for MM patients, a deeper understanding of the genetic basis is required.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We reviewed 26 samples taken from 22 MM patients who underwent genetic testing at our institute from 2016 to the present. Somatic mutation profiles were analyzed using hybridization capture based next-generation sequencing (NGS), which enables the simultaneous detection of single-nucleotide variants, insertions/deletions, rearrangements, and copy-number alterations of at least 59 genes (range 59 – 1021 genes).

      4c3880bb027f159e801041b1021e88e8 Result

      The 26 samples included 8 tumor tissue samples, 17 blood samples and 1 ascetic fluid sample. The most frequently mutated genes were TP53 (11/21), followed by NF2 (6), RB1 (4), NF1 (3), FLT1 (3), BAP1 (2), EGFR (2), FAT2 (2), FGFR4 (2), KIT (2), MAP3K1 (2), MLL4 (2), STK11 (2), APC, ATR, BRAF, BRCA2, CDKN2A, ERBB3, FBXW7, MET, KRAS, PIK3CA and so on. Among these mutations, 5 of NF2 mutations and 2 of NF1 mutations were loss-of-function mutations, which suggests the possible sensitivity of mTOR inhibitors administration. Besides, patients with the active or inactive mutations of KRAS, BRAF, CDKN2A, ERBB3, MET and PIK3CA gene might be sensitive to corresponding targeted drugs. MET exon 14 skipping mutation, commonly identified in non-small-cell cancer (NSCLC) patients, had never been reported in MM patients before. c-Met inhibitors such as crizotinib and cabozantinib may be of efficacy for this patient. Apart from predicting therapeutic effectiveness of MEK inhibitors, the detection of KRAS activating mutation may also provide prognostic information.

      8eea62084ca7e541d918e823422bd82e Conclusion

      NGS can identify genetic mutations comprehensively and provide predictive and prognostic implications for MM patients. It is a cost-effective tool to describe the genetic landscape of MM, which will facilitate the development of novel therapeutics for the treatment of MM patients.

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    P3.01 - Advanced NSCLC (Not CME Accredited Session) (ID 967)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 2
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.01-104 - EGFR-RAD51 Fusion Variant in Lung Adenocarcinoma and Response to Erlotinib: A Case Report (ID 11102)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The most frequent epidermal growth factor receptor (EGFR) mutations of lung cancer include exon 19 in deletion and the exon 21 L858R mutation. And EGFR-tyrosine kinase inhibitor (TKI) as the standard first line treatment show good response to classical/sensitizing EGFR mutations. With the development of detection methods, some uncommon genomic mutation events such as exon 18-25 kinase domain duplications (KDD) and EGFR rearrangements (EGFR-RAD51 or EGFR-PURB) are found. We reported a case of EGFR-RAD51 fusion in non-small-cell lung cancer(NSCLC) and the efficacy of erlotinib to this type fusion of NSCLC patients.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 48-year-old male diagnosed with adenocarcinoma (IV, T1N2M1), who was shown to have EGFR fusion by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      The patient with right lung tumor and multiple brain metastases NSCLC. Histological examination of surgical specimens from the brain tumor showed lung adenocarcinoma metastasis. By using next generation sequencing assay, we found that tumor had EGFR-RAD51 fusion rather than the most common kind of EGFR mutations. Then the patient experienced a remarkable tumor response to erlotinib. Considering this rare EGFR fusion and remarkable response to TKI treatment, we conclude that the incidence of EGFR fusions in NSCLC patients should be attentive. NSCLC patients with EGFR-RAD51 fusion gene response to treatment with EGFR inhibitor.

      8eea62084ca7e541d918e823422bd82e Conclusion

      With the guidance of precise diagnosis, it is important that we should realize other rare EGFR gene mutations and novel diagnostic method.

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      P3.01-39 - Analysis of Acquired EGFR T790M Mutation in Patients with Non-Small Cell Lung Cancer Who Received Icotinib Progress (ID 11110)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      As the first epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) in China, icotinib shows promising anticancer activity in vitro and vivo. The phase III clinical study (ICOGEN) showed that icotinib has a good efficacy and tolerability in Chinese patients with advanced non-small cell lung cancer (NSCLC) compared with gefitinib. The aim of this study is to investigate the acquired EGFR T790M situation of the non-small cell lung cancer patients who received icotinib treatment progress.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      The ARMS method was used to detect the samples in 209 cases of EGFR 19del or L858R mutation non-small cell lung cancer.

      4c3880bb027f159e801041b1021e88e8 Result

      There were 123 cases accompanied 19del and 86 cases accompanied L858R in 209 cases non-small cell lung cancer samples who received icotinib treatment progress, the acquired T790M mutation type patients was 45.93% (96/209), icotinib treatment. resistance after the acquired T790M mutation with 19 del/L858R group had statistical difference (P<0.034).

      8eea62084ca7e541d918e823422bd82e Conclusion

      19 del patients who received treatment for icotinib are more likely to appear acquired T790M mutation than L858R patients from NSCLC, and we should attach importance to it.

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    P3.03 - Biology (Not CME Accredited Session) (ID 969)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 2
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.03-08 - Analysis of ESR1 Mutation Spectrum from Non-Small-Cell Lung Cancer in Chinese Patients (ID 11205)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      A number of studies have documented that estrogen receptor alpha (ESR1) may play an important role in the development and progression of breast cancer. While the genetic variability of ESR1 mutation NSCLC patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring ESR1 mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 501 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of ESR1 mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      ESR1 gene mutation rate was 1.60% (8/501) in non-small cell lung cancer, including V392I (1 patient), H373Y (1 patient), E22K (1 patient), E589Q (1 patient), Q375R (1 patient), N304S (1 patient), G457V (1 patient) and M437I plus M421I (1 patient), and median overall survival (OS) for these patients was 14.0 months. Among them, all patients were ESR1 gene with co-occurring mutation. Briefly, patients with (n=3) or without (n=5) co-occurring EGFR mutations had a median OS of 19.0 months and 6.0 months respectively (P=0.36); patients with (n=4) or without (n=4) co-occurring TP53 mutations had a median OS of 11.0 months and 14.0 months respectively (P=0.45); patients with (n=2) or without (n=6) co-occurring BCRA2 mutations had a median OS of 4.0 months and 19.0 months respectively (P=0.03); patients with (n=3) or without (n=5) co-occurring RB1 mutations had a median OS of 19.0 months and 9.0 months respectively (P=0.47).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our results demonstrated that decreased ESR1 gene mutation correlated with poor overall survival in non-small-cell lung cancer patients. ESR1 gene mutation may define a subset of patients with lung cancer appropriate for investigational therapeutic strategies.

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      P3.03-09 - Molecular Spectrum of KIT Mutations Detection in Chinese Non-Small Cell Lung Cancer Patients (ID 11213)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The KIT gene activation of the gene depends on ligand binding with stem cell factor, which enables the phosphorylation of substrate proteins. Subsequently, certain signal transduction pathways are activated, which stimulate important cellular functions, such as proliferation and apoptosis. Mutations in KIT that cause autophosphoryla­tion without the presence of the ligand lead to uncontrolled cell proliferation, which eventually induces tumor develop­ment. The aim of this study is to investigate mutations and prognosis of NSCLC harboring KIT mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A total of 402 patients with non-small-cell lung cancer were recruited between July 2012 and December 2015. The status of KIT mutation and other genes were detected by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      KIT gene mutation rate was 3.48% (14/402) in non-small cell lung cancer, including T84M (3 patients), K918Nfs*6 (1 patient), E849Q (1 patient), G961S (1 patient), I748T (1 patient), S741Y (1 patient), S712F (1 patient), D816Y (1 patient), T304A (1 patient), H180N (1 patient), R19C (1 patient) and A736D plus T734N (1 patient), and median overall survival (OS) for these patients was 23.0 months. Among them, all patients were KIT gene with co-occurring mutation. Briefly, patients with (n=4) or without (n=10) co-occurring EGFR mutations had a median OS of 23.5 months and 23.0 months respectively (P=0.63); patients with (n=6) or without (n=8) co-occurring TP53 mutations had a median OS of 15.0 months and 23.0 months respectively (P=0.47); patients with (n=2) or without (n=12) co-occurring HER2 mutations had a median OS of 4.5 months and 23.0 months respectively (P=0.01); patients with (n=2) or without (n=12) co-occurring RB1 mutations had a median OS of 14.5 months and 23.0 months respectively (P=0.26).

      8eea62084ca7e541d918e823422bd82e Conclusion

      HER2 accompanied mutations might play a worse prognosis in KIT gene mutation NSCLC. We report different mutations than those previously reported, which emphasizes the importance of personalized medicine that could be empowered by the use of bioinformatics tools in the diagnostic process and therapeutic approaches.

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    P3.13 - Targeted Therapy (Not CME Accredited Session) (ID 979)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.13-06 - Analysis of ALK Rearrangement Non-Small Cell Lung Cancer Cell Blocks from Pleural Effusion (ID 11112)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Anaplastic lymphoma kinase (ALK) rearrangements occur in 1% to 7% of non-small-cell lung cancers (NSCLCs). Crizotinib, an ALK inhibitor, has been demonstrated to provide dramatic clinical benefits in ALK rearrangement advanced NSCLC. The aim of this study is to investigate the clinical value of ALK rearrangement NSCLC blocks cell from pleural effusion.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Two hundred and fifteen cases of ALK rearrangement non-small cell lung cancer (NSCLC) blocks cell from pleural effusion, Four hundred and four cases of tissues were detected by reverse transcription polymerase chain reaction (RT-PCR) method. The consistency of ALK rearrangement was examined in 74 cases of patients with tissues and cell blocks.

      4c3880bb027f159e801041b1021e88e8 Result

      ALK rearrangement was found in 26 of 215 cell blocks (positive detection rate of 12.09 %). ALK rearrangement was detected in 25 of 404 tissue blocks (positive detection rate of 6.19%). There were 67 cases in the 74 (90.54%) cases had the same consistency as tissue block. ALK rearrangement was detected in 11 of 74 (14.86%) cell blocks, and 14 of 74 (18.92%) tissue blocks.

      8eea62084ca7e541d918e823422bd82e Conclusion

      The rate of ALK rearrangement in cell blocks of NSCLC is higher than in matched tissue blocks. The patients with malignant pleural effusion are likely to tend ALK rearrangement.

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    P3.15 - Treatment in the Real World - Support, Survivorship, Systems Research (Not CME Accredited Session) (ID 981)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.15-06 - Capillary Leak Syndrome in a Primary Lung Adenocarcinoma Patient with Thrombocytopenia from Interleukin-11 Treatment (ID 11104)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Capillary leak syndrome (CLS) is an uncommon complication characterized by generalized edema and hypotension. We report a 62-year-old male patient with lung and liver metastasis who had underwent liver radiofrequency ablation.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      He was treated with interleukin (IL)-11 (3 mg per day) because of chemotherapy induced thrombocytopenia.

      4c3880bb027f159e801041b1021e88e8 Result

      After 9 days of therapy, the patient complained of abdominal distension and with bilateral edema of all four extemities. Chest computed tomography and B ultrasound of the abdomen showed pleural effusions and ascites. IL-11 was then discontinued, fluid resuscitation was performed, fresh frozen plasma and packed red blood cells were transfused, and methylprednisolone therapy was administered. The patient had recovered after 12 days of treatment.

      8eea62084ca7e541d918e823422bd82e Conclusion

      This case report demonstrates that patients with lung cancer can develop this rare form of CLS after treatment with IL-11. The manifestation of IL-11-induced CLS indicates that it may be a severe side effect of IL-11 treatment in cancer.

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    P3.CR - Case Reports (Not CME Accredited Session) (ID 984)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 7
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.CR-04 - Lung Cancer with Concurrent ROS1 Rearrangement and KRAS Mutation: A Case Report (ID 11106)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      ROS1 rearrangement has recently emerged as a new molecular subtype in non-small cell lung cancer (NSCLC), and is predominantly found in lung adenocarcinomas compared with other oncogenes such as EGFR, KRAS, or ALK. Patients who have both mutations are extremely rare.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 42-year-old female diagnosed with adenocarcinoma (IIIB, T2N3M0), who was shown to have ROS1 and KRAS mutations by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      The patient was prescribed oral crizotinib and a CT scan show a partial response in the pulmonary lesions after one month. Unfortunately, a CT scan show progression of the pulmonary lesion after three months. And the patient was treated with the MEK inhibitor, selumetinib (AZD6244), combined with pemetrexed. The patient was alive at now.

      8eea62084ca7e541d918e823422bd82e Conclusion

      We reviewed the related literature to determine the frequency of gene mutations in NSCLC patients. A better understanding of the molecular biology of NSCLC with multiple driver genomic aberrations will assist in determining optimal treatment.

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      P3.CR-08 - Clonally Related Primary ALK Rearrangement Adenocarcinoma and Associated Metastatic Lesions: A Case Report (ID 11208)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Anaplastic lymphoma kinase (ALK) rearrangement is a driver gene in non-small cell lung cancer (NSCLC). ALK-positive tumors are sensitive to ALK tyrosine kinase inhibitors (TKIs). Detecting key driver genes is crucial to personalized treatment. Different histomorphological patterns have different driver genes.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 42-year-old male diagnosed with adenocarcinoma (III), who was shown to have ALK fusion by reverse transcription polymerase chain reaction (RT-PCR).

      4c3880bb027f159e801041b1021e88e8 Result

      The patient diagnosed with adenocarcinoma, who had different histomorphologies in the primary lung site (mucinous type) and lymph node metastasis (solid type), but had the same genotype, which both presented with an ALK rearrangement, while negative for an EGFR mutation.This histological heterogeneity did not necessarily indicate a genomic difference.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Genomic analysis may be a supplement of the histological feature of ALK-rearranged tumors. These gene alterations could help patients to choose an appropriate TKI and its impact on the therapeutic responses.

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      P3.CR-09 - MET-UBE2H fusion as a novel mechanism of acquired EGFR resistance in<br /> lung adenocarcinoma" with  "MET fusion as a novel mechanism of acquired EGFR resistance in<br /> lung adenocarcinoma (ID 11219)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      As we all known, the most common mechanism of acquired resistance to EGFR-TKIs treatment is the development of the EGFR T790M mutation, which occurs almost one half of cases of acquired resistance. Other previously described resistance mechanisms include HER2 amplification, MET amplification, PIK3CA mutation, epithelialmesenchymal transition (EMT), and small cell transformation.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 43-year-old female diagnosed with adenocarcinoma including brain and bone metastases, who was shown to have MET fusion after erlotinib acquired resistance by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      The patient with left lung tumor. Cytological examination of sepecimens from primary focus show adenocarcinoma." with "A bronchoscopic biopsy sepecimens from primary foucus show adenocacrcinoma. By next generation sequencing we found EGFR 19 exon E746_S752delinsV and MET-UBE2H fusion after erlotinib acquired resistance, and the patient experienced a remarkable tumor response to crizotinib remains at 6 months on therapy.

      8eea62084ca7e541d918e823422bd82e Conclusion

      We report the occurrence of MET-UBE2H fusion along with EGFR 19del at disease progression after treatment with erlotinib. Hence we attribute the emergence of MET-UBE2H fusion as a possible mechanism of acquired resistance to first generation EGFR-TKI in EGFR mutated NSCLC.

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      P3.CR-10 - HIP1-ALK Fusion Variant in Non-Small-Cell Lung Cancer and Response to Crizotinib (ID 11274)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Several fusion partners of ALK have been reported in patients with non-small cell lung cancer (NSCLC). And huntingtin interacting protein 1 (HIP1)-ALK is one kind of ALK fusion types.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We reported a case of HIP1-ALK fusion variant in non-small-cell lung cancer and further reviewed the clinical characteristic and the efficacy of crizotinib to this type fusion of NSCLC patients.

      4c3880bb027f159e801041b1021e88e8 Result

      A 56-year-old Chinese woman with multiple lung metastases NSCLC(T1N0M1, stage Ⅳ). Histological examination of the tumor showed lung adenocarcinoma. Ventana (D5F3) ALK IHC assay (Ventana Medical Systems, Roche, Inc) analysis of the left lung tissue revealed the presence of an ALK rearrangement. Then the patient experienced a remarkable tumor response to crizotinib. By using next generation sequencing assay, we found that tumor had HIP1-ALK (H21; A20) rather than the most common kind of Echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK). Considering this rare ALK fusion and remarkable response to crizotinib treatment, we conclude that the incidence of HIP1-ALK in NSCLC patients with ALK rearrangement should be attentive. NSCLC patients with HIP1-ALK fusion gene response to treatment with ALK inhibitors.

      8eea62084ca7e541d918e823422bd82e Conclusion

      With the guidance of precise diagnosis, it is important that we should realize other rare ALK fusions and novel diagnostic method.

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      P3.CR-11 - ROS1 Fusion and MET Amplification Dual Drive Coexistence in Lung Adenocarcinoma and Response to Crizotinib: A Case Report (ID 11212)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      The c-ros oncogene 1 (ROS1) fusion is almost mutually exclusive to MET amplication in non-small cell lung cancer (NSCLC), and it is not seen in the literature for patients to exhibitthree mutations.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 66-year-old female diagnosed with IV stage adenocarcinoma, who was shown to have ROS1 fusion and MET amplication by fluorescence in situ hybridization (FISH), and verified by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      The patient with right lung tumor and brain metastases NSCLC. Histological examination of surgical sepecimens from primary focus show adenocarcinoma. By fluorescence in situ hybridization (FISH), we found ROS1 fusion and MET amplication. Then we verified a novel ROS1fusion: ZCCHC8-ROS1, and the patient experienced a remarkable tumor response to crizotinib for 6 months (PFS).

      8eea62084ca7e541d918e823422bd82e Conclusion

      To the best of to our knowledge, this is the first case report of a patient with concurrent ROS1 fusion and MET amplication, and ZCCHC8-ROS1. This patient had an excellent response to crizotinib, suggesting that concurrent ROS1 fusion and MET amplication response to crizotinib was less than ROS1 fusion single driver.

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      P3.CR-12 - A Novel Oncogenic Driver in a Lung Adenocarcinoma Patient Harboring an EGFR-KDD and Response to Afatinib (ID 11273)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Oncogenic mutations in the epidermal growth factor receptor (EGFR) are found in a subset of patients with non-small cell lung cancer (NSCLC) and serve as important predictive biomarkers in this disease. EGFR exon 18-25 kinase domain duplication (EGFR-KDD) mutations has rencently emerged as a new EGFR gene molecular subtype in non-small cell lung cancer(NSCLC) is extremely rare.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 59-year-old male diagnosed with adenocarcinoma, who was shown to have gene detected by the next generation sequencing (NGS)and treatment with afatinib.

      4c3880bb027f159e801041b1021e88e8 Result

      Histopathological observations with hematoxylin and eosin staining was shown adenocarcinoma, immunohistochemical staining for the expression of TTF-1, NapsinA and CK7. The gene detected by NGS that found an EGFR-KDD, CTNNB1 p.S37Y and TP53 p.R282W. Our case is the second report EGFR-KDD in Chinese populations. The patient was treated with afatinib therapy. And afatinib therapy showed a good response.

      8eea62084ca7e541d918e823422bd82e Conclusion

      The cases presented here highlight that adjusting our strategy and using newly available tools, such as comprehensive NGS tests, could prove useful in detecting alternative ways in which the EGFR pathway is altered (and can be targeted) in tumors.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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      P3.CR-13 - Dual Drive Coexistence of EML4-ALK Fusion and TPM3-ROS1 Fusion Lung Adenocarcinoma: A Case Report (ID 11092)

      12:00 - 13:30  |  Author(s): Wenxian Wang

      • Abstract
      • Slides

      Background

      Recent reports of overlap between ROS1 fusions and other oncogenic driver alterations have still been controversial. We reported a case of concomitant EML4-ALK fusion and TPM3-ROS1 in non-small-cell lung cancer (NSCLC) and further reviewed the clinical characteristic in this type double fusion of NSCLC patients.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      A 47-year-old male diagnosed with adenocarcinoma (IA, T1aN0M0), who was shown to have ALK and ROS1 fusion by next generation sequencing.

      4c3880bb027f159e801041b1021e88e8 Result

      The patient presented with a locally tumor of the left upper lobe with physical examination. He received lung cancer surgery with thoracoscopic. by using next generation sequencing assay, we found that tumor had concomitant EML4-ALK fusion and TPM3-ROS1. No recurrence was observed from a follow-up of 7 months in the case. Considering this rare ALK fusion and ROS1 double rearranged, we conclude that the incidence of this double mutation in NSCLC patients should be attentive.

      8eea62084ca7e541d918e823422bd82e Conclusion

      With the guidance of precise diagnosis, it is important that we should realize the incidence of concomitant ROS1 fusion and other driver genes including ALK or EGFR. And it should further explore treatment model and provides additional therapeutic options.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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