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Rongrong Chen



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    P1.01 - Advanced NSCLC (ID 158)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.01-126 - The Co-Occurring Genomic Landscape of ERBB2 Exon 20 Insertion in Non-Small Cell Lung Cancer (NSCLC) and the Potential Indicator of Response to Afatinib (Now Available) (ID 1284)

      09:45 - 18:00  |  Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      Human epidermal growth factor receptor 2 (ERBB2, HER-2) 20 exon insertion (ERBB2ex20ins) has been identified as an oncogenic driver in lung cancer, for which no valid therapy is currently approved. Concurrent alterations may elucidate its refractory features. Previous studies on Afatinib, a pan-ERBB inhibitor, have revealed an inconsistent clinical activity of it for this group of patients.

      Method

      Plasma or tissue samples of 112 patients with ERBB2ex20ins were performed next generation sequencing (NGS) for 59 or 1021 cancer-related genes in a Clinical Laboratory Improvement Amendments-certified Laboratory from July 2016 to December 2018. The sequencing data of MSKCC Cohort was downloaded from the public Cancer Genome Atlas Database. The clinical outcomes of 18 patients receiving Afatinib treatment were collected by each contributing doctor in charge and pooled for analysis.

      Result

      Among the 112 patients, most of cases were female (54%, 60/112) and adenocarcinoma (68%, 76/112). Considering the insertions sites, three subtypes were A775ins (71%; 79/112), G776indel (17%; 19/112) and P780ins (12%; 14/112) in the order of frequency. 80.4% (90/112) of patients had at least one additional alteration. The most frequent co-occurring genes were TP53 (66.1%, 74/112), LRP1B (18.2%, 10/55), EPHA5 (9.1%, 5/55), MLL3 (9.1%, 5/55) and RB1 (8.0%; 9/112). Putative other driver aberrations were mutually exclusive from ERBB2ex20ins. Furthermore, cell cycle pathway was the most commonly involved pathway (84.0%; 94/112) of all the concurrent genes. No substantial differences of concurrence in genomic or pathway level were observed among the three ERBB2 insertion subtypes. The co-occurring genomic feature of ERBB2ex20ins in Our Cohort of Chinese people had an overall strong concordance with the MSKCC Cohort from the United States (R2=0.74, P<0.01). For the prognosis, patients had a worse OS when co-occurring mutation in TP53 [median OS:14.5m (95%CI: 12.7m-16.3m) vs 30.3m (95% CI: not reached)], while the OS was not significantly different among three subtypes. The median duration time for patients with disease control of Afatinib was 4.5 months (95%CI: 3.6m-5.4m; range: 2.5m-13.4m). Of note, ERBB2ex20ins in subclonal status was a significantly independent factor relating to shorter PFS of Afatinib [median PFS: 1.2m (95%CI: 0.8-1.6m) vs 4.3m (95%CI: 3.3m-5.3m), P<0.05]. Dynamic detection in two patients found ERBB2 amplification may be a resistance mechanism for Afatinib.

      Conclusion

      Concurrence of genetic alterations in NSCLC patients with ERBB2ex20ins was common. The complex genomic characteristic should be fully considered by stratifying patients according to potentially relevant co-mutations other than ERBB2 insertion sites in the designing regimens for them. In addition, the therapeutic effect of Afatinib on patient with ERBB2ex20ins is limited, the clonal status of ERBB2ex20ins may be an important factor with prognosis value.

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    P1.04 - Immuno-oncology (ID 164)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Immuno-oncology
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.04-74 - Characteristics of T Cell Receptor Repertoire of Lung Cancer Patients (Now Available) (ID 1554)

      09:45 - 18:00  |  Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      As the importance of T cell receptor (TCR) repertoire gains appreciation, particularly given their potential utility for cancer immunotherapeutic prognostication, the characteristics of TCR repertoire are needed. We detected the complementarity determining region 3 (CDR3) by TCR sequence to describe diversity and changes in human’s immune system with age and difference clinical stage .

      Method

      The TCRβ repertoire of 19 stage IV lung cancer patients and 77 stage I/II/III lung cancers patients was analyzed. Genomic DNA was extracted from peripheral blood and used to amplified and sequenced the CDR3 region of rearranged TCRβ genes. Finally, we got the relative frequencies of patients T cell clones. Shannon index was calculated on the clonal abundance of all productive TCR sequences. The normalized Shannon index was determined by dividing Shannon index by the natural logarithm of the number of unique productive TCR sequences.

      Result

      Diversity of the TCR repertoire can be measured using the Shannon index. Analysis had been made to test the diversity relationship among a cluster of clinical features, such as stages, age and gender. Diversity were significantli decreasing with clinical stages(p=0.0482). Comparison of the diversity between stage IV and stage I/II/III patients, we found stage IV lung cancer has more lower diversity(p=0.0048). In these patients, diversity had showed a significantli correlation with age(r=-0.3036, p=0.0026). Diversity was significantly lower in patients 55 years of age or older compared to younger patients (p=0.0083).

      Conclusion

      These results suggest that patients with advanced cancer exhibit limited TCR repertoire diversity and that this diversity is further limited in patients with advanced clinical stage and older age. Interestingly, these factors are often associated with a poor immune status.

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    P1.12 - Small Cell Lung Cancer/NET (ID 179)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Small Cell Lung Cancer/NET
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.12-10 - The Genomic Profiles of Small Cell Lung Cancer in East Asian (Now Available) (ID 1608)

      09:45 - 18:00  |  Presenting Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      Small cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy with poor survival, which is initially effective treated by chemotherapy and relapses rapidly. Comprehensive genomic analysis of SCLC contribute to the understanding of drug resistance mechanisms and discerning patients who respond to treatments, especially immunotherapy that has been proved to be efficient in SCLCs harboring high tumor mutational burden (TMB). This study was initiated to investigate the genomic profiles of SCLC in Chinese.

      Method

      SCLC specimens were obtained by surgery or biopsy from 64 patients. Whole-exome sequencing (WES) was performed on tumor samples without paired PBMCs. Alterations were confirmed with VAF between 5% and 90%, subsequently filtered by mutated genes above 5% in J.Geroge’s and LY. Jiang’s researches. Tumor mutational burden was calculated by the number of non-synonymous mutations. The mutations of highly mutated driver genes in SCLC was also determined based on MH. Bailey’s study.

      Result

      TP53 and RB1 were the most frequently mutated genes in SCLCs, occurred in 87.5% (56/64) tumors, and furthermore related to a higher mutational burden (P = 0.0008 and 0.0274, respectively). Tumor mutational burden after filtered by highly mutated genes in SCLC was 333 non-synonymous mutations per tumor, with high mutation rates exhibited in advanced stage of SCLCs, while the smoking history did not correlate with the number of mutations. Driver genes mutation in high frequency was detected almost in all tumors (63/64), with 17.4 mutations on average (0-144). Tumors with POLE mutation tended to harbor a higher driver genes mutation rates, as well as a higher TMB. Pathway analysis using altered driver genes showed enrichment of PI3K-Akt (adj. P = 8.38e-07), MAPK (adj. P = 1.63e-05), mismatch repair (adj. P = 4.55e-05), cell cycle (adj. P= 0.0016), and Wnt (adj. P= 0.0047) signaling pathways. We did not observe significant correlation of mutations in Wnt signaling pathway with survival, though it has proved to be a mechanism of chemoresistance in SCLCs.

      fig.1.jpg

      Conclusion

      SCLCs exhibited complex genomic features with extensive mutational burden and high numbers of altered driver genes. Various sorts of cancer-related pathways were enriched, highlighted the complicacy of SCLCs.

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    P1.14 - Targeted Therapy (ID 182)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Targeted Therapy
    • Presentations: 3
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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      P1.14-11 - A Prospective Multicenter Study of Target-Capture Deep Sequencing in Paired Tissue and ctDNA to Guide EGFR-Mutated Lung Cancer Treatment (Now Available) (ID 1542)

      09:45 - 18:00  |  Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      TKIs have significantly improved the survival of NSCLC pts carrying sensitive mutations. However, heterozygous responses were observed. We conducted a prospective multicenter clinical trial to explore factors associated with the efficacy of EGFR-TKI, and assess the mutation and TMB concordance between plasma and tissue NGS.

      Method

      Paired tumor and plasma samples were obtained from treatment naïve advanced NSCLC pts whenever applicable. DNA was sequenced by target-capture deep sequencing of 1021 tumor-related genes (pan-cancer panel). PFS was estimated using Kaplan-Meier method and compared using log-rank test. Tissue TMB (tTMB) and plasma TMB (bTMB) analysis interrogated SNVs/Indels with VAF ≥3 % and ≥0.5 %, respectively. TMB-H pts were identified with ≥9 muts/Mb.

      Result

      From Feb. 2017 to Jan. 2019, 262 advanced NSCLC pts were enrolled from 12 centers. In 224 pts with paired tumor and plasma samples, 144 had EGFR sensitive mutations in tumor samples (L858R, 46%; Ex19Indel, 42%), of whom, 106 (74%) had the identical mutations detected in plasma. The detection rate of tissue EGFR mutations in paired plasma was significantly higher in pts with extrathoracic metastasis (81% vs. 61%, p = 0.03). In 38 pts lacking paired samples, 20 pts had EGFR sensitive mutations detected. Thus, 164 pts were identified as EGFR positive by either plasma or tissue NGS. One hundred of them were treated EGFR TKIs (ORR: 70%, mPFS: 20 mo). The ORR was affected by EGFR subtypes (Ex19Indel vs. L858R: 72% vs. 45%, p = 0.02), concomitant CNV/fusion (with vs. without: 11% vs. 68%, p = 0.002) and CDKN2A mutations (with vs. without: 0% vs. 66%, p = 0.007). Mutations in p53 pathway (p = 0.02), CDK12/13 (p = 0.0002), concomitant CNV/fusion (p = 0.003), and high number of alterations (≥ 5) (p = 0.003) significantly shortened mPFS. tTMB was correlated with bTMB (rPearson = 0.9, p < 0.0001), with a concordance rate of 90% for TMB-H and TMB-L classification. Interestingly, 9.8% of the EGFR positive pts were bTMB-H, and mPFS was shorter in bTMB-H pts (6 mo, 95% CI: 5 - NR) than in bTMB-L pts (NR, 95%: 13 - NR) (p = 0.2).

      Conclusion

      Deep sequencing with the pan-cancer panel effectively detected mutations and evaluated TMB in both tissue and plasma with a high consistence. Moreover, the presence of structure variation, high tumor heterogeneity and concomitant mutations in genes such as CDKN2A were associated with worse prognosis. Further studies of predictive factors are ongoing (NCT03059641).

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      P1.14-38 - Identification of FGFR1-3 Fusions in Lung Cancers Using Comprehensive Next-Generation Sequencing (Now Available) (ID 2071)

      09:45 - 18:00  |  Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      Fusions have been described in the fibroblast growth factor receptors (FGFR) 1-3 genes with multiple partners in a variety of tumors. Here we focused on the prevalence of FGFR fusions in lung cancers for whom might benefit from FGFR inhibitors in clinical development.

      Method

      We reviewed FGFR alterations in 10833 lung cancer patients (pts) who underwent genetic testing at our institute from 2016 to 2019. Mutation profiles were analyzed using hybridization capture based next-generation sequencing (NGS), which covers all exons of FGFR1-3 and specific intron regions containing the break points of fusions. All patients were also analyzed for mutations in EGFR, KRAS, HER2, BRAF, ALK, RET, MET, ROS1, as well as other oncogenes.

      Result

      FGFR fusions were identified in 25 lung cancer pts, including 9 adenocarcinoma pts, 4 squamous-cell carcinoma pts, 1 patient with large cell neuroendocrine carcinoma and 11 pts with non-specific pathology. FGFR3-TACC3 fusion was detected in 72% (18/25) of pts and the remaining were previously unreported fusions (table). Concurrent EGFR mutations were identified in 44% (11/25) of pts with FGFR fusions (32%, treated with EGFR tyrosine kinase inhibitors (EGFR-TKIs); 12%, not treated with EGFR-TKIs). PI3K-AKT-MTOR signaling pathway was also activated in 28% (7/25) of pts, and cell-cycle gene alterations were also detected in 16% (4/25) of pts.

      Table. Frequency of FGFR fusions

      Fusions

      Fusion region

      N (%)

      FGFR3-TACC3

      EX17:EX11

      6 (24%)

      EX18E:EX11

      4 (16%)

      EX18E:EX13

      2 (8%)

      EX17:EX10

      2 (8%)

      others

      4 (16%)

      FGFR1-chr8:21672159

      EX1:chr8:21672159

      1 (4%)

      FGFR1-MTUS1

      EX19E:EX8

      1 (4%)

      EFHA2-FGFR1

      EX2:EX3

      1 (4%)

      TNRC18-FGFR1

      PMT:EX10

      1 (4%)

      ZMAT4-FGFR1

      EX2:EX2

      1 (4%)

      ZNF696-FGFR1

      EX2:EX18E

      1 (4%)

      OPALIN-FGFR2

      EX6E:EX2

      1 (4%)

      Total

      25 (100%)

      Conclusion

      FGFR1-3 fusions define a unique molecular subtype of lung cancer. Depending on the concurrent genetic alterations, combined targeted therapy might be an optimal strategy to control tumor growth for these pts.

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      P1.14-47 - ctDNA NGS for Guiding Crizotinib Treatment in ALK-Rearranged Advanced NSCLC Patients (Pts) (Now Available) (ID 1522)

      09:45 - 18:00  |  Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      FISH and IHC are commonly used and the golden standard for testing ALK rearrangement. However, they provide no information on fusion types or mutation status of other genes, which could be important prognostic factors. In addition, a tissue biopsy is not always applicable/preferred by pts.

      Method

      43 ALK-rearranged treatment naïve advanced NSCLC pts were included. ALK-rearrangement was confirmed by ctDNA NGS with a panel of 59 tumor-related genes in 25 pts (ctDNA arm) and by IHC/FISH/tissue NGS in 18 pts (control arm). All pts received crizotinib as first-line therapy. PFS was estimated using Kaplan-Meier method and compared using log-rank test.

      Result

      On average, Pts in ctDNA arm were significantly older at diagnosis than pts in the control arm (56 vs. 45, p = 0.02), indicating the preferability of ctDNA NGS in elderly pts. Though older, pts in ctDNA arm had a similar mPFS with pts in the control arm (8 vs. 10 mo, p = 0.9). ALK fusion types in ctDNA arm and their associated statistics were listed in Table 1. Concomitant mutations were identified in 15 genes in 9 pathways. Frequently mutated pathways include p53 (in 8 pts) and DNA repair pathways (in 3 pts). Mutations in DNA repair pathway (5 vs. 10 mo, p = 0.06), high frequency of EML4-ALK (>= 1.5%) (6 mo vs. NR, p = 0.06), and bone metastasis (6 vs. NR, p = 0.05) were associated with shorter mPFS.

      Table 1. ALK fusion types and associated statisticss
      ALK fusion types # of pts (Median) age at diagnosis (year) (m)PFS (mo) Average # of mutations per pt
      V1 11 52 10 1.5
      V3 10 61 6 2.8
      V2 1 60 - 1
      V5' 1 65 - 1
      V7 1 49 3 2
      DCTN1-ALK 1 47 - 2

      Conclusion

      Information on ALK fusion types, concomitant mutations, and mutation frequencies provided by NGS could be valuable prognostic factors and deserves further investigation. ctDNA NGS could be used as an effective alternative to identify ALK+ pts, especially for elderly pts, when tissue biopsy is inapplicable or not preferred.

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    P2.04 - Immuno-oncology (ID 167)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Immuno-oncology
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.04-54 - Characteristic of MSI-H Lung Cancer Patients Identified with Targeted Next-Generation Sequencing (Now Available) (ID 2435)

      10:15 - 18:15  |  Presenting Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      MSI-H/dMMR predicts response to immune oncology (IO) agents and is an approved biomarker for pembrolizumab therapy irrespective of histologic diagnosis. In this study, we retrospectively analyzed a large cohort of lung cancer patients using targeted next generation sequencing to examine the prevalence and clinicopathologic associations of MSI-H in lung cancers.

      Method

      MSI and TMB status was derived from a 1021 gene targeted next generation sequencing panel. MSI was analyzed using MSIsensor 0.5, that relies on an empirically defined cutoff of MSI score>10%, as MSI-H. TMB analysis interrogated single nucleotide variants, small insertion and deletion, with VAF ≥3 %. TMB-H pts were identified with ≥9 mut/MB (upper quartile of data from geneplus).

      Result

      5592 lung cancer patients were interrogated in the study, with 4753 lung adenocarcinoma, 559 lung squamous cell carcinoma, 112 small cell lung carcinomas (SCLC), and 168 rare lung cancer types including pulmonary sarcomatoid carcinoma, carcinoid and so on. A total of 12 lung tumors were identified as MSI-H (0.21%), and 5 were lung adenocarcinoma (0.1%), 3 were small cell lung cancer (2.7%), 1 was lung squamous cell carcinoma (0.18%), 2 were pulmonary sarcomatoid carcinomas, and 1 was pulmonary carcinoid (1.8%). The incidence was higher in small cell lung cancer and rare lung cancer subtypes. The average diagnosis age of the 12 patients were 53 years (range: 16-74). All the patients were TMB-H, with the TMB averaged 51.23 mut/Mb (range: 10-70 mut/Mb). Two of the 5 lung adenocarcinoma patients carried EGFR L858R or 19del mutation. One patient who had both NRAS G12V and EGFR Ex20 mutation had tried nivolumab (120mg) for one cycle with deteriorating of cough and progression of disease.

      Conclusion

      MSI-H is very rare in lung tumors, where it appears to enrich in small cell lung cancer and rare lung cancer subtypes. MSI-H lung cancer patients tend to have a younger diagnosis age. MSI-H may coexist with other driver alterations, including those negatively associated with IO response. Additional investigation is needed to determine efficacy of IO in these patients.

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    P2.14 - Targeted Therapy (ID 183)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Targeted Therapy
    • Presentations: 2
    • Now Available
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.14-09 - Concurrent TP53 Mutation Adversely Impact the Efficacy of Crizotinib in ROS1-Rearranged Lung Cancer Patients (ID 2158)

      10:15 - 18:15  |  Author(s): Rongrong Chen

      • Abstract

      Background

      ROS1 tyrosine kinase inhibitors (TKIs) are now standard of care for patients with advanced ROS1-rearranged NSCLC. But factors that may affect the efficacy of ROS1 TKIs remain to be explored.

      Method

      We conducted a retrospective multicenter study of lung cancer patients with ROS1 rearrangements. Treatment and survival follow-up was done and clinical records were reviewed. PFS distribution was analyzed by Kaplan-Meier method with log-rank test.

      Result

      In total, we included 94 lung cancer patients with ROS1 fusion genes profiled by next-generation sequencing from May 2016 to September 2018. Fifty of them were female. The median diagnosis age was 54 (25-83). The most common histologic type was adenocarcinoma, which was confirmed in 75 of 78 patients with available pathological results. The most common fusion partners were CD74, EZR, SDC4 and SLC34A2 identified in 42, 19, 12 and 8 patients respectively. Concurrent actionable mutations were uncommon for ROS1 fusion-positive patients. The most frequent concomitant mutated gene was TP53, which was detected in 33% of all the patients. After excluding 29 patients who were lost to follow-up at the very start, the median follow-up time was 8.5 (0-28) months from the moment when mutation profiling was performed. Thirty-nine patients received treatment with crizotinib, among whom 27 were treatment-naïve patients. The median PFS of the 39 patients with crizotinib was not reached yet. Patients with baseline CNS metastasis tend to have shorter PFS compared to patients without (median, 12 vs NR, p = 0.0073). Besides, concurrent TP53 mutations were correlated with worse PFS (median, both NR, p = 0.0417). Mutation profiles of 10 patients were derived from ctDNA testing. No difference was found in PFS between these 10 patients with others whose genomic profiles were based on fresh tissue or FFPE specimens, suggesting that plasma ctDNA serves as good specimen source for mutation profiling to monitor clinical treatment.

      Conclusion

      Concurrent TP53 mutation and presence of CNS metastasis are associated with decreased PFS of ROS1-positive patients treated with crizotinib.

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      P2.14-38 - ATAD2B-ALK, a Novel Fusion in Lung Adenocarcinoma Identified Using Next-Generation Sequencing (NGS) (Now Available) (ID 1844)

      10:15 - 18:15  |  Author(s): Rongrong Chen

      • Abstract
      • Slides

      Background

      Anaplastic lymphoma kinase (ALK) rearrangements is an important molecular subtype of non-small cell lung cancer (NSCLC), and patients with this variant are sensitive to ALK inhibitors. Since the discovery of the EML4-ALK fusion ten years ago, several fusion partners of ALK in NSCLC have been reported, including KIF5B, KLC1, HIP1, TPR and so on. According to previous reports, different fusion partner lead to various function and activity of the fusion product. Here, we identified a novel fusion partner for ALK in a lung adenocarcinoma patient.

      Method

      A 46-year-old smoking Chinese male was diagnosed with lung adenocarcinoma of left lower lobe. In Oct 2017, the patient accepted lobectomy and lymph node dissection, then received 4 cycles of adjuvant chemotherapy. Lymph node metastasis occurred one and a half years after his surgery. The lymph node biopsy sent for genomic testing with a NGS-based pan-cancer 1021-gene panel. Immunohistochemistry (IHC) of ALK was performed to confirm the ALK fusion.

      Result

      A novel ATPase family AAA domain containing 2B(ATAD2B)-ALK fusion was identified in the lymph node biopsy tissue. The fusion occurred in intron 1 of ATAD2B gene and intron 19 of ALK gene located on short arm of chromosome 2 (ATAD2B(PMT..IVS1)_ALK(IVS19..END)). ATAD2B is a phylogenetically conserved nuclear protein expressed during neuronal differentiation and it was also reported to play a role in tumorigenesis. As IHC confirmed the expression of ALK, we proposed the fused promoter of ATAD2B had driven the expression of ALK kinase domain. The patient is currently treated with crizotinib.

      Conclusion

      The novel ALK fusion gene probably served as oncogenic driver of the patient’s tumor. This case is the first report of ATAD2B-ALK fusion in clinical tumor samples and could provide a new diagnostic and therapeutic candidate target for patients with lung cancer.

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