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Yanping Chen



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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): Yanping Chen

      • 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.

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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: 1
    • 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): Yanping Chen

      • 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).

      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.

      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.

      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.

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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): Yanping Chen

      • 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.

      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.

      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).

      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.

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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): Yanping Chen

      • 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.

      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.

      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).

      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.

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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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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.

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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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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.

      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.

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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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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).

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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.

      Conclusion

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

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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: 4
    • 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): Yanping Chen

      • 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.

      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.

      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).

      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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      P2.03-10 - 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): Yanping Chen

      • 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.

      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.

      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.

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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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    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): Yanping Chen

      • 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.

      Method

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

      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.

      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): Yanping Chen

      • 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.

      Method

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

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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).

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

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 5
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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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): Yanping Chen

      • 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.

      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).

      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.

      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): Yanping Chen

      • 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.

      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.

      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.

      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): Yanping Chen

      • 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.

      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.

      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.

      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): Yanping Chen

      • 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.

      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.

      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).

      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): Yanping Chen

      • 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.

      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.

      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.

      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.

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