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Raffaele Califano

Moderator of

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    MS14 - Molecular Subsets and Novel Targeted Approaches to Small Cell and Neuroendocrine Cancers (ID 77)

    • Event: WCLC 2019
    • Type: Mini Symposium
    • Track: Small Cell Lung Cancer/NET
    • Presentations: 5
    • Now Available
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      MS14.01 - Molecular Subsets of Neuroendocrine Tumors (Now Available) (ID 3519)

      11:30 - 13:00  |  Presenting Author(s): Christine Lee Hann

      • Abstract
      • Presentation
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      Abstract

      Small cell lung cancer (SCLC) is an aggressive tumor with one of the highest case-fatality rates among cancer. Clinically SCLC is hallmarked by early metastatic behavior and rapid development of therapeutic resistance. Over the past decades multiple research teams have used genomic, epigenomic, transcriptomic and proteomic approaches to further characterize SCLC. Long considered a relatively homogeneous tumor, these data have led to a deeper understanding of SCLC biology and support the concept that there are distinct biologic subsets of SCLC. Complementary work using patient-derived xenografts and genetically engineered mouse models have validated some of this data and these models serve as platforms for novel therapeutic development. These studies support translational efforts in SCLC focused on distinct vulnerabilities in subsets of this disease and the development of predictive biomarkers.

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      MS14.02 - Subclonal Architecture and Genomic Evolution of SCLC (Now Available) (ID 3520)

      11:30 - 13:00  |  Presenting Author(s): Jinghui Wang

      • Abstract
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      Abstract

      Small cell lung cancer (SCLC) accounts for 15-20% of all of lung cancer worldwide and it is a highly aggressive and rapidly progressive tumor with rapid growth speed and strongly associated with smoking. SCLC is divided to limited disease and extensive disease. The staging systems for SCLC are Veterans Administration scheme (VA), the AJCC TNM staging systemand NCCN staging, among of these VA is most commonly used. In recent several decades, chemotherapy combined radiotherapy is the main treatment for SCLC. The overall survival (OS) in patients with limited disease-SCLC and extensive disease were 15-18 months and 10-12 months, respectively. Immunotherapy is becoming a promising treatment for SCLC nowadays.

      Targeted therapy based on genotyping in non-small cell lung cancer is a main treatment. However, targeted therapy in SCLC is not successful and studies on the genomic evolution of SCLC are rare. ctDNA (circulating cell-free tumor DNA) is a good tool for monitoring the genomic changing in patients with malignant tumors, especially for monitoring acquired resistance of targeted therapy. ctDNA and CTCs are useful for genomic evolution of cancer. However, isolation and identification of CTCs are not satisfied in lung cancer, though there are more CTCs in small call lung cancer because of tumor cells are more easily to shed to blood stream in SCLC. ctDNA can provide more accurate genomic landscape of SCLC through overcome heterogeneity.

      We conducted a study that aimed to explore the genomic structure and gene evolution pattern of SCLC using next-generation sequencing and who had been followed by dynamic samples after chemotherapy or/and radiotherapy. We found that TP53 and RB1 are the most common mutations in SCLC, and NOTCH1-4, CREBBP, EG300, MYC, MYCL1, and MYCN are also frequently mutated genes and copy number alterations. We also compared the tissue and blood ctNDA genome and we found that a majority of mutations detected in tumor DNA were also detected in paired ctDNA samples suggesting ctDNA sequencing is sensitive and reliable for detecting mutations in SCLC patients. We used the average VAF (Variant allelic frequencies) of mutations from the major clones as a surrogate for overall ctDNA level. We found higher median ctDNA level was associated with shorter progression-free survival (PFS) and overall survival (OS). Dynamic ctDNA levels are correlated with tumor measurements on imaging suggesting that ctDNA sequencing has the potential for monitoring the clinical course of SCLC. The genomic profiles derived from pre-treatment ctDNA to the genomic profiles from ctDNA at different time points during treatment from post-treatment plasma samples available. Some new mutations that were not exist in pre-treatment blood samples.

      Immunotherapy is an important method for lung cancer. PD-L1 expression and tumor mutation burden (TMB) are two common predictors for immunotherapy. In our cohort, tumor mutation burden is not higher based on the large gene panel. PD-L1 expression is about more than 10% in SCLC. The treatment for SCLC is still highly challenging. TMB based on ctDNA is worth further investigation on predicting SCLC immunotherapy. A previous study showed that SCLC with high TMB had a better response to checkpoint inhibitors. Shedding of ctDNA is a complicated process affected by many factors. With the technique development and increasing understanding of tumor biology, the genome of SCLC will be a useful tool for guiding the treatment and predicting the prognosis of SCLC in the future.

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      MS14.03 - Targeting Transcription (Including Lurbinectedin) (Now Available) (ID 3521)

      11:30 - 13:00  |  Presenting Author(s): Manuel Cobo

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      MS14.04 - Targeting DNA Damage and Repair (Now Available) (ID 3522)

      11:30 - 13:00  |  Presenting Author(s): Charles M Rudin

      • Abstract
      • Presentation
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      Abstract

      Genomic profiling of small cell lung cancer has revealed nearly universal inactivation of the key tumor suppressor genes TP53 and RB1. Loss of these critical regulators of cell cycle entry and DNA damage response together results in selective sensitivity to DNA damaging agents, inhibitors of DNA damage repair, and inhibitors of the remaining late phase cell cycle checkpoints. Multiple preclinical studies and recent clinical data nominate these pathways as potential synthetic lethal vulnerabilities in small cell lung cancer. Recent study has also demonstrated that targeting DNA damage response can activate the anti-tumor immunity and potentiate the response of immune checkpoint blockade antibodies. This talk will review these recent studies, focusing on opportunities and future directions in investigational therapy for patients with small cell lung cancer.

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      MS14.05 - DLL3 Targeting Agents (Now Available) (ID 3523)

      11:30 - 13:00  |  Presenting Author(s): John T Poirier

      • Abstract
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      Abstract

      Delta-like ligand 3 (DLL3) is a single-pass transmembrane Notch ligand that interacts with full-length, unprocessed NOTCH1 in the Golgi apparatus, inhibiting the pathway in cis. DLL3 is selectively overexpressed in the subtype of small cell lung cancer (SCLC) driven by the transcription factor ASCL1 (SCLC-A) that accounts for ~70% percent of SCLC diagnoses (95% CI [60 – 79])1. In one study immunoreactivity was observed in 1,040/1,363 (70.4%) of SCLC specimens, consistent with this incidence2. Overexpression of DLL3 leads to low-level cell surface expression of the protein on the order of 10,000 proteins per cell while expression in normal tissues is restricted to intracellular compartments: the same study demonstrated only low to moderate cytoplasmic or nuclear immunoreactivity in normal adult tissues3. High expression of DLL3 has also been reported in low-grade glioma4,5, neuroendocrine prostate6, and occasionally in other cancer types when neuroendocrine features are present7,8. The exquisitely selective expression of surface DLL3 on cancer cells presents an attractive target for a variety of therapeutic strategies.

      Rovalpituzumab teserine (Rova-T; SC16LD6.5) is an antibody drug conjugate consisting of a monoclonal antibody targeting DLL3, a cathepsin-cleavable linker, and a pyrrolobenzodiazepine (PBD) warhead4. The first-in-human clinical trial of Rova-T in recurrent SCLC demonstrated
      encouraging activity despite often severe side-effects attributable to the PBD warhead9; however, the phase 2 TRINITY study showed a disappointing 16% objective response rate while reporting a similar toxicity profile (NCT02674568). Subsequently, the phase 3 TAHOE study was halted due to shorter overall survival in the treatment arm. An active phase 3 trial of Rova-T in the maintenance setting (MERU) is ongoing (NCT03033511).

      Other DLL3-targeting therapies under active investigation include the bispecific T cell engager (BiTE) AMG 757 (NCT03319940), and a chimeric antigen receptor CAR-T AMG119 (NCT03392064). These agents have shown significant anti-tumor activity in preclinical models of SCLC; however, AMG 119 required direct delivery of the engineered T cells for activity. AMG 757 was therefore the more potent of the two strategies in preclinical models and may therefore be better suited to overcome known barriers to CAR-T activity in solid tumors.

      Alternative strategies remain under exploration including the use of 89Zr-SC16, a PET radiotracer, for in vivo imaging and as a companion diagnostic to optimize the selection of patients for treatment with DLL3-directed therapeutic agents. 89Zr-labeled-SC16 antibody successfully delineated normal tissue from subcutaneous and orthotopic SCLC tumor xenografts. Radiotracer accumulation in tumors was directly correlated with the degree of DLL3 expression and, also correlated with response to SC16LD6.5 therapy in SCLC patient–derived xenograft models.

      1 Rudin, C. M. et al. Molecular subtypes of small cell lung cancer: a synthesis of human and mouse model data. Nat Rev Cancer 19, 289-297, doi:10.1038/s41568-019-0133-9 (2019).
      2 Huang, R. S. P. et al. Delta-like Protein 3 Prevalence in Small Cell Lung Cancer and DLL3 (SP347) Assay Characteristics. Arch Pathol Lab Med, doi:10.5858/arpa.2018-0497-OA (2019).
      3 Sharma, S. K. et al. Non-invasive Interrogation of DLL3 Expression in Metastatic Small Cell Lung Cancer. Cancer Res, doi:10.1158/0008-5472.CAN-17-0299 (2017).
      4 Saunders, L. R. et al. A DLL3-targeted antibody-drug conjugate eradicates high-grade pulmonary neuroendocrine tumor-initiating cells in vivo. Sci Transl Med 7, 302ra136, doi:10.1126/scitranslmed.aac9459 (2015).
      5 Spino, M. et al. Cell Surface Notch Ligand DLL3 is a Therapeutic Target in Isocitrate Dehydrogenase-mutant Glioma. Clin Cancer Res 25, 1261-1271, doi:10.1158/1078-0432.CCR-18-2312 (2019).
      6 Puca, L. et al. Delta-like protein 3 expression and therapeutic targeting in neuroendocrine prostate cancer. Sci Transl Med 11, doi:10.1126/scitranslmed.aav0891 (2019).
      7 Koshkin, V. S. et al. Transcriptomic and Protein Analysis of Small-cell Bladder Cancer (SCBC) Identifies Prognostic Biomarkers and DLL3 as a Relevant Therapeutic Target. Clin Cancer Res 25, 210-221, doi:10.1158/1078-0432.CCR-18-1278 (2019).
      8 Ding, X., Li, F. & Zhang, L. Knockdown of Delta-like 3 restricts lipopolysaccharide-induced inflammation, migration and invasion of A2058 melanoma cells via blocking Twist1-mediated epithelial-mesenchymal transition. Life Sci 226, 149-155, doi:10.1016/j.lfs.2019.04.024 (2019).
      9 Rudin, C. M. et al. Rovalpituzumab tesirine, a DLL3-targeted antibody-drug conjugate, in recurrent small-cell lung cancer: a first-in-human, first-in-class, open-label, phase 1 study. Lancet Oncol 18, 42-51, doi:10.1016/S1470-2045(16)30565-4 (2017).

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    OA15 - Targeted Agents and Immunotherapy for Small Cell Lung Cancer (ID 152)

    • Event: WCLC 2019
    • Type: Oral Session
    • Track: Small Cell Lung Cancer/NET
    • Presentations: 7
    • Now Available
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      OA15.01 - Combination Olaparib and Temozolomide in Relapsed Small Cell Lung Cancer: Updated Results from Phase 1/2 Clinical Trial (Now Available) (ID 1394)

      14:30 - 16:00  |  Presenting Author(s): Anna F Farago  |  Author(s): Beow Yeap, Rebecca S Heist, J Paul Marcoux, Deepa Rangachari, David Barbie, Elizabeth Kennedy, Mari Mino-Kenudson, Alice T. Shaw

      • Abstract
      • Presentation
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      Background

      DNA damage repair inhibition is an emerging strategy for treating small cell lung cancer (SCLC). Combining poly(ADP-ribose) polymerase (PARP) inhibition with the DNA alkylating agent temozolomide has shown activity in both preclinical models and early phase clinical trials.

      Method

      This is a single-arm phase 1/2 study combining the PARP inhibitior olaparib (tablet formulation) with temozolomide in patients with SCLC. Key eligibility criteria include histologically or cytologically confirmed incurable SCLC which progressed following ≥ 1 platinum-based chemotherapy. In cohort 1, olaparib and temozolomide are administered orally on days 1-7 of 21-day cycles. After cohort 1 completed enrollment, cohort 2 was added in a protocol amendment, in which olaparib is administered continuously days 1-21 and temozolomide is administered days 1-7 of 21-day cycles. For each cohort, the phase 1 portion is a conventional 3+3 design, with the primary objective to determine the maximum tolerated dose (MTD) or recommended phase 2 dose (RP2D). The primary objective of the phase 2 dose expansion portion is to determine the objective response rate (ORR). Response assessments are performed every 6 weeks, with treatment continued until progression, unacceptable toxicity, or investigator’s discretion. Treatment post-progression is allowed for patients with ongoing clinical benefit.

      Result

      Between October 2015 and April 2018, 50 patients were enrolled to cohort 1. The median age was 63 (range 39-85), median number of prior therapies was 2 (range 1-7), and 72% were platinum sensitive. The RP2D was olaparib 200 mg PO BID d1-7 and T 75 mg/m2 QD d1-7. The confirmed ORR was 41.7%. After a median follow-up of 7.1 months among 22 surviving patients, the median progression-free survival (mPFS) was 4.2 months, median overall survival (mOS) was 8.5 months, and median duration of response (mDoR) was 4.3 months. The ORR among platinum-sensitive and platinum-resistant patients was 47.1% and 28.6%, respectively, with no significant differences in mPFS, mOS or mDOR. The most common grade 3/4 treatment related adverse events were neutropenia (38%), anemia (28%) and thrombocytopenia (26%). Among 41 pts treated at the RP2D, dose reductions occurred in 44% overall and 64% of those who received at least 3 cycles. Enrollment to the phase 1 portion of cohort 2 began in November 2018 and is ongoing. Updated results from cohorts 1 and 2 will be presented at the meeting.

      Conclusion

      Combination olaparib and temozolomide has an acceptable tolerability profile and shows promising clinical activity in relapsed SCLC. Clinical trials identifier NCT02446704.

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      OA15.02 - Carboplatin-Etoposide Versus Topotecan as Second-Line Treatment for Sensitive Relapsed Small-Cell Lung Cancer: Phase 3 Trial (Now Available) (ID 546)

      14:30 - 16:00  |  Presenting Author(s): Isabelle Monnet  |  Author(s): Nathalie Baize, Laurent Greillier, Margaux Geier, Hervé Lena, Henri Janicot, Alain Vergnenegre, Jacqhy Crequit, Regien Lamy, Jean Bernard Auliac, Jacques Le Treut, Hervé Le Caer, Radj Gervais, Eric Dansin, Anne Madroszyk, Patrick Renault, Gwenaëlle Legarff, Roland Schott, Patrick Saulnier, Christos Chouaid

      • Abstract
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      Background

      Topotecan is currently the only drug approved in Europe in second line setting for small-cell lung cancer (SCLC). This study investigates whether the doublet carboplatin-Etoposide was superior to topotecan monotherapy as second-line treatment in patients with sensitive relapsed SCLC.

      Method

      this open-label, multicenter, phase 3 trial randomized patients with SCLC that responded to first-line platin etoposide doublet treatment but showed evidence of disease relapse or progression at least 90 days after completion of the first-line treatment. Enrolled patients were randomly assigned (1:1) to receive combination chemotherapy (Six cycles of 3-weeks Carboplatin, AUC 5, day 1 and Etoposide 100 mg/Sqm/d 1-3, intra-venous) or oral Topotecan (2.3 mg/Sqm/d 1-5, every 3 weeks). Primary endpoint was progression free survival (PFS). Secondary endpoints were overall survival (OS), objective response rate (ORR), quality of life and tolerance in the intention-to-treat population, (clinical trialgouv: NCT02738346)

      Result

      178 patients were screened and 164 randomized in 36 centers, with 82 assigned to each treatment group (age: 64.5 ± 7.2 years, men: 72.8%, PS 0/1/>1: 34.7%/56.3%/ 9%. Median PFS was significantly longer in combination chemotherapy group (4.7 months, 95% CI: 3.9-5.5) compare to topotecan group (2.7 months, 95% CI: 2.3-3.2), HR: 0.6, 95% CI 0.4-0.8, p < 0.002. The ORR were significantly more important in the combination chemotherapy than in topotecan arm (ORR 49 % vs 25 %, p < 0,002), but without difference in term of median OS, 7.5 months (95% CI: 5.4-8.7) in combination chemotherapy group versus 7.4 months (95% CI.6.0-9.3) in topotecan arm. Grade 3/4 neutropenia were significantly more common in the topotecan group than in the combination chemotherapy group (35.8% vs 19.7 %, p < 0.001. There is a non-significant trend for more febrile neutropenia in topotecan arm compare to combination arm (13.6 % 6.2 %, p = 0.19, and no difference for grade 3/4 thrombopenia, 35.8 % vs 30.9 %, and anemia, 24.6 % vs 21 %, for topotecan and combination arms, respectively. Two treatment-related deaths occurred in the topotecan arm (febrile neutropenia with sepsis), none in the combination arm. Results of quality of life outcomes will be presented at the meeting.

      Conclusion

      platin - etoposide re-challenge can be considered as a standard second-line chemotherapy for sensitive relapsed SCLC.

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      OA15.03 - Discussant - OA15.01, OA15.02 (Now Available) (ID 3804)

      14:30 - 16:00  |  Presenting Author(s): Mary O'Brien

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      OA15.04 - Genomic and TCR Intratumor Heterogeneity of Small-Cell Lung Cancer by Multiregion Sequencing: An Association with Survival (Now Available) (ID 1458)

      14:30 - 16:00  |  Presenting Author(s): Jianjun Zhang  |  Author(s): Runzhe Chen, Ying Jin, Jun Li, Jiexin Zhang, Junya Fujimoto, Won-Chul Lee, Xiao Hu, Yamei Chen, Carmen Behrens, Chi-Wan Chow, Edwin Parra, Latasha Little, Curtis Gumbs, Xingzhi Song, Emily Roarty, Jianhua Zhang, Don Lynn Gibbons, John Victor Heymach, J. Jack Lee, William N. William Jr, Bonnie Glisson, Ignacio Wistuba, P. Andrew Futreal, Lauren Averett Byers, Alexandre Reuben, Ming Chen

      • Abstract
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      Background

      Small cell lung cancer (SCLC) is an aggressive cancer. Although sensitive to initial therapy, recurrence is almost inevitable. The molecular mechanisms underlying recurrence are unknown. We have previously demonstrated that complex genomic and T cell receptor (TCR) intratumor heterogeneity (ITH) was associated with increased risks of relapse in non-small cell lung cancers (NSCLC). Genomic ITH and TCR architecture of SCLC and its clinical impact have not been well studied, largely due to lack of tumor specimens as surgery is rarely used to treat SCLC.

      Method

      We performed multiregion whole-exome sequencing and TCR sequencing of 49 tumor samples from 18 resected limited-stage SCLCs to delineate the immunogenomic ITH of SCLC. We compared the results to those in NSCLC and assessed the association of genomic and TCR attributes with patient’s survival.

      Result

      On average, 544 mutations/sample were detected. The median proportion of trunk mutations (mutations identified in all regions within the same tumors) was 80.4% versus 70% in NSCLC (TRACERx, Jamal-Hanjani, NEJM, 2017, p=0.08) and all TP53 and RB1 mutations were trunk mutations, suggesting these mutations were early events during carcinogenesis of this cohort of SCLCs. A higher non-synonymous tumor mutational burden (TMB) was associated with a higher T cell density (infiltration) in the tumor (r=0.46, p=0.005). Compared to the TCR repertoire of NSCLC (Reuben, WCLC, 2017), these SCLC tumors demonstrated significantly lower T-cell density (0.05 versus 0.24, p<0.0001), richness (diversity, 1,043 versus 3,666, p<0.0001) and clonality (reactivity, average 0.02 versus 0.15, p<0.0001) despite similar non-synonymous TMB (average 187 in SCLC versus 176 mutations/sample in NSCLC). Only 0.2% to 14.6% of T cells were detectable across all regions from the same tumors, suggesting substantial TCR ITH. Jaccard index (JI), a parameter quantifying TCR ITH was significantly lower in SCLC than in NSCLC (0.06 versus 0.1, p<0.0001) implying higher level of TCR ITH in SCLC than NSCLC. Interestingly, higher T-cell density, richness or clonality appeared to be associated with lower risk of recurrence numerically. Furthermore, higher TCR JI (less degree of ITH) was associated with significantly longer overall survival (HR=0.15, p=0.04).

      Conclusion

      Limited-stage SCLC tumors have distinct TCR repertoire and genomic ITH architecture. Overall, SCLC may have a more pronounced immunosuppressive microenvironment and higher level of TCR repertoire ITH than NSCLC. Nevertheless, higher degree of T cell infiltration and clonal expansion as well as more homogeneous T cell response may be associated with more favorable clinical outcome in patients with limited-stage SCLC.

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      • Abstract
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      As requested by the author, the abstract for this presentation will not be published

      Information from this presentation has been removed upon request of the author.

      Information from this presentation has been removed upon request of the author.

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      OA15.06 - Discussant - OA15.04, OA15.05 (Now Available) (ID 3805)

      14:30 - 16:00  |  Presenting Author(s): Hidehito Horinouchi

      • Abstract
      • Presentation
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      Abstract not provided

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      OA15.07 - Heine H. Hansen Lectureship Award for Small Cell Lung Cancer (Now Available) (ID 3861)

      14:30 - 16:00  |  Presenting Author(s): Caroline Dive

      • Abstract
      • Presentation
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      Abstract not provided

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