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Gregory J Riely



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    MA19 - Genomic Markers of IO Response (ID 922)

    • Event: WCLC 2018
    • Type: Mini Oral Abstract Session
    • Track: Immunooncology
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 15:15 - 16:45, Room 201 BD
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      MA19.09 - Concurrent Mutations in STK11 and KEAP1 is Associated with Resistance to PD-(L)1 Blockade in Patients with NSCLC Despite High TMB (ID 11983)

      16:10 - 16:15  |  Author(s): Gregory J Riely

      • Abstract
      • Presentation
      • Slides

      Background

      Targeted next generation sequencing (NGS) testing for lung cancer patients identifies recurrent patterns of co-mutations. STK11 is known to be associated with poor outcomes with immunotherapy. We have identified that STK11 is commonly co-mutated with KEAP1, but the impact of this pattern of co-mutation on response to immunotherapy is not known.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We identified 308 patients with advanced lung cancer treated at Memorial Sloan Kettering Cancer Center who underwent NGS testing with MSK-IMPACT and received at least one dose of PD-(L)1 inhibitor. Progression free survival (PFS) and overall survival (OS) from treatment initiation of PD-(L)1 blockade were calculated using Kaplan-Meier methodology and compared using logrank method and t-test for continuous variables.

      4c3880bb027f159e801041b1021e88e8 Result

      In a cohort of 308 patients with NSCLC treated with PD-(L)1 blockade, STK11 or KEAP1 mutations occurred frequently (23% and 22% respectively) and concurrent STK11 and KEAP1 mutations (STK11mut/KEAP1mut) were common (56% of all STK11 mutant patients and 13% of all lung cancers, Fisher’s test of association p<0.0001). Other common co-mutations with STK11 included KRAS (50%) and TP53 (48%). STK11mut/KEAP1mut patients had higher TMB than STK11wt/KEAP1wt patients (median 9.4 vs 6.1, Mann-Whitney p= 0.0002).

      STK11mut/KEAP1mut (n=39) patients had diminished PFS and OS compared to patients with STK11wt/KEAP1wt (n=210) (PFS HR 1.5, p=0.02; OS HR 2.3, p=0.001). As context, outcomes in STK11mut/KEAP1mut patients were similarly poor to EGFR mutant patients (n=28) treated with PD-(L)1 blockade (PFS p=0.7) despite substantially different tumor mutation burden (9.4 vs 4.9 mut/Mb, p<0.0001). Among STK11mut/KEAP1mut patients, poor outcomes were unchanged irrespective of KRAS status (PFS p=0.8, OS p=0.5). Patients with mutations in STK11 alone (n=31) or KEAP1 alone (n=28) had outcomes that more closely mirrored STK11wt/KEAP1wt patients (PFS p=0.9 and 0.1 respectively, OS p=0.1 and 0.2 respectively).

      8eea62084ca7e541d918e823422bd82e Conclusion

      KEAP1 plus STK11 co-mutation is a common event in NSCLC that is distinctly associated with poor outcomes with PD-(L)1 blockade despite otherwise favor molecular features.

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    OA02 - Novel Therapies in ROS1, HER2 and EGFR (ID 893)

    • Event: WCLC 2018
    • Type: Oral Abstract Session
    • Track: Targeted Therapy
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 10:30 - 12:00, Room 105
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      OA02.03 - Clinical Activity of Lorlatinib in Patients with ROS1+ Advanced Non-Small Cell Lung Cancer: Phase 2 Study Cohort EXP-6 (ID 12787)

      10:50 - 11:00  |  Author(s): Gregory J Riely

      • Abstract
      • Presentation
      • Slides

      Background

      Among patients with ROS1-positive non-small cell lung cancer (NSCLC), most achieve initial benefit from crizotinib treatment but often develop resistance, and further treatment options are limited. Lorlatinib is a potent, brain-penetrant third-generation ALK/ROS1 TKI with broad mutational coverage. It has shown compelling clinical activity in patients with ALK-positive and ROS1-positive advanced NSCLC, most of whom had CNS metastases and had received prior crizotinib.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      This ongoing Phase 2 study (NCT01970865) enrolled patients with ROS1-positive advanced NSCLC ± asymptomatic CNS metastases without restriction on the type or number of prior lines of therapy (cohort EXP-6). Patients received lorlatinib 100 mg QD. Primary endpoints were overall and intracranial response by independent central review. Secondary endpoints included duration of response and progression-free survival. Safety was assessed in all treated patients (cohorts EXP-1–6); molecular profiling is ongoing.

      4c3880bb027f159e801041b1021e88e8 Result

      As of the data cut-off (02 Feb 2018), 47 patients with ROS1+ NSCLC were treated; 25 had baseline CNS metastases; 34 had received prior crizotinib and 13 were crizotinib-naïve. Treatment with lorlatinib led to rapid and durable responses in both crizotinib-naïve and crizotinib-pre-exposed patients (Table).

      ICR-assessed endpoint Crizotinib-naïve Crizotinib-pre-exposed Total EXP-6
      Overall, N 13 34 47
      ORR, % (95% CI) 61.5 (31.6, 86.1) 26.5 (12.9, 44.4) 36.2 (22.7, 51.5)
      Confirmed response, n 8 9 17

      Response lasting at least 12 months, n

      5 5 10
      Median time to tumor response, months (range) 1.4 (1.3–8.3) 2.5 (1.4–4.2) 1.4 (1.3–8.3)
      Intracranial (IC), N 6 19 25
      IC ORR, % (95% CI) 66.7 (22.3, 95.7) 52.6 (28.9, 75.6) 56.0 (34.9, 75.6)
      Confirmed IC response, n 4 10 14

      IC response lasting at least 12 months, n

      1 4 5
      Median PFS, months (95% CI)a 21.0 (4.2, 26.7) 8.5 (4.4, 18.0) 9.9 (5.5, 21.0)

      ICR, independent central review; PFS, progression-free survival.

      aPer Kaplan-Meier method.

      The most common treatment-related adverse events (TRAEs) in EXP-6, were hypercholesterolemia (83%) and hypertriglyceridemia (60%). In EXP-6, 36% and 23% of patients had TRAEs leading to dose interruptions and dose reductions, respectively. No permanent treatment discontinuations due to TRAEs or treatment-related deaths occurred.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Lorlatinib showed clinically meaningful benefit in patients with ROS1-positive NSCLC, including those who had received prior crizotinib or were crizotinib-naive, as demonstrated by rapid and durable responses. These findings further suggest that the activity of lorlatinib differs depending on prior exposure to crizotinib. The safety profile of lorlatinib in ROS1 patients was comparable to that previously reported in the overall ALK/ROS1 population.

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    OA12 - Novel Therapies in MET, RET and BRAF (ID 921)

    • Event: WCLC 2018
    • Type: Oral Abstract Session
    • Track: Targeted Therapy
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 15:15 - 16:45, Room 106
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      OA12.02 - Updated Antitumor Activity of Crizotinib in Patients with MET Exon 14-Altered Advanced Non-Small Cell Lung Cancer (ID 13453)

      15:25 - 15:35  |  Author(s): Gregory J Riely

      • Abstract
      • Presentation
      • Slides

      Background

      MET exon 14 alterations occur in ~3% of non-squamous non-small cell lung cancer (NSCLCs) and 20–30% of sarcomatoid lung carcinomas. Here we present updated antitumor activity for crizotinib in patients with advanced NSCLC whose tumors are positive for MET exon 14 alterations (hereafter MET exon 14-positive NSCLC), including updated biomarker analyses in circulating tumor DNA (ctDNA).

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Patients with MET exon 14-positive NSCLC by local molecular profiling were treated with 250 mg crizotinib BID in an expansion cohort of the ongoing PROFILE 1001 study (NCT00585195). Responses were based on derived investigator assessment per RECIST v1.0. Prospective plasma profiling for MET exon 14 alterations in plasma ctDNA was performed (PlasmaSELECT-R64; Personal Genome Diagnostics, Boston, MA).

      4c3880bb027f159e801041b1021e88e8 Result

      As of Jan 31, 2018, 69 patients (65 response-evaluable) with MET exon 14-positive NSCLC had been treated. Median age was 72 y (range: 34, 91). Tumor histology was: 84% adenocarcinoma, 9% sarcomatoid adenocarcinoma, 4% squamous cell carcinoma and 3% adenosquamous carcinoma. 61% were former-smokers, 38% never-smokers and 1% a current smoker. Median duration of treatment was 7.4 mo (95% CI: 5.5, 9.1), with 29% of patients ongoing. Confirmed responses were 3 CRs and 18 PRs (ORR, 32% [95% CI: 21, 45]); 29 patients had SD as their best overall response (Figure).

      crizo cmet ex14 waterfall_4may2018-v3.jpg

      Median time to response was 7.6 weeks (range: 3.7, 16.3). Median DOR was 9.1 mo (95% CI: 6.4, 12.7). Median PFS was 7.3 mo (95% CI: 5.4, 9.1). MET exon 14 alterations were detected in ctDNA from 18/37 (49%) patients with analyzable samples.

      8eea62084ca7e541d918e823422bd82e Conclusion

      In patients with MET exon 14-positive advanced NSCLC, crizotinib treatment led to objective responses that were rapid and durable, with CRs in some cases. Plasma ctDNA profiling detected MET exon 14 alterations in a subset of patients who harbor MET exon 14 alterations by tumor testing.

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

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 3
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.01-74 - MET Exon 14-Altered Lung Cancers: Central Nervous System (CNS) Metastases and Patterns of CNS Progression on MET Inhibition. (ID 14263)

      16:45 - 18:00  |  Author(s): Gregory J Riely

      • Abstract
      • Slides

      Background

      MET exon 14 (METex14) alterations are targetable drivers found in 3-4% of lung cancers. The frequency of intracranial disease and patterns of central nervous system (CNS) progression on MET tyrosine kinase inhibitors (TKI) are not well characterized.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Patients with advanced METex14-altered lung cancers identified by next-generation sequencing (MSK-IMPACT) between January 2014 and March 2018 were eligible for analysis. A retrospective review of clinical features, patterns of metastases, and CNS progression on MET-TKI was performed. The frequency of intracranial disease was compared to cohorts single-center of EGFR-mutant (n=200), ERBB2-mutant (n=98) and KRAS-mutant (n=200) lung cancers.

      4c3880bb027f159e801041b1021e88e8 Result

      82 patients with metastatic METex14-altered lung cancers were identified. The median age was 73; 56% (n=46) were female and 54% (n=44) were former smokers. The frequency of brain metastases at baseline was 11% (n=9/82). The lifetime frequency of intracranial metastases from diagnosis of metastatic disease was 34% (n=28/82). By comparison, the frequency of brain metastases was 47% (94/200, p=0.05) with EGFR-, 47% (46/98), p=0.09) with ERBB2-, and 32% (64/200, p=0.78) with KRAS-driven tumors. 6% (n=5/82) of patients developed leptomeningeal disease. The overall survival (OS) of patients who developed intracranial disease on therapy compared to those who did not develop intracranial disease was not significantly different (HR 0.66, 95% CI 0.30-1.43, p=0.29). 51 patients received crizotinib, 26 of whom developed progressive disease. The frequency of intracranial (alone), intracranial and extracranial, and extracranial (alone) progression was 8% (2/26), 19% (5/26), and 73% (19/26), respectively.

      8eea62084ca7e541d918e823422bd82e Conclusion

      A third of patients with METex14-altered lung cancers develop intracranial disease. This proportion is lower than that seen in EGFR- and ERBB2-mutant lung cancers and comparable to KRAS-mutant lung cancers. The frequency of CNS failure on crizotinib was lower than expected compared to historical rates in ALK-rearranged lung cancers.

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      P1.01-75 - Utility of cfDNA Testing for Acquired Resistance: The Memorial Sloan Kettering Experience with Plasma EGFR T790M Clinical Testing. (ID 12514)

      16:45 - 18:00  |  Author(s): Gregory J Riely

      • Abstract
      • Slides

      Background

      Liquid biopsy for circulating tumor DNA (ctDNA) has been increasingly adopted for the detection of oncogenic drivers and drug resistance mechanisms. Practice guidelines for liquid biopsy are lacking and biologic factors influencing ctDNA detection and shedding are poorly understood. We evaluated factors influencing ctDNA detection, using EGFR-T790M as a case-study, in patients with acquired resistance to first/second-generation EGFR tyrosine kinase inhibitors (EGFR-TKI).

      a9ded1e5ce5d75814730bb4caaf49419 Method

      This single-center study included metastatic sensitizing EGFR-mutant lung cancer patients (exon 19 deletions, L858R, G719) who underwent plasma EGFR-T790M testing after acquired resistance to erlotinib, gefitinib, or afatinib between January 2016 and August 2017. Plasma T790M was performed by digital PCR. Variant allele fraction (VAF) was calculated as mutant/(wildtype+mutant) allele. Concordance between plasma and tissue testing was examined if tissue analysis (MSK-IMPACT and/or targeted PCR) occurred within 90 days of blood draw. Turnaround time (TAT) was measured from date of blood draw and/or biopsy to result. ctDNA results were correlated with metastatic site and the number of organs involved.

      4c3880bb027f159e801041b1021e88e8 Result

      177 patients underwent plasma T790M testing; 65% female, 47% current/former smokers. Plasma T790M was positive in 32% (56/177) of patients, tissue testing was T790M-positive in 46% (45/97), and overall T790M-positivity by either platform was 49% (86/177). The median TAT was shorter for plasma T790M compared to tissue PCR (9 vs 15 days, p<0.0001), and led to osimertinib use in 84% (47/56) of positive patients. Concordance between plasma and tissue T790M was 80% (32/40). 15 patients with positive plasma had matched tissue, 87% (13/15) were concordant on tissue. 76% (19/25) of the patients that were T790M-negative on plasma also tested negative on tissue. Median plasma T790M-VAF was 0.98% (range 0.1–49.5%), lower than tissue T790M-VAF (12.8%, range 2.58–27.8, p<0.0001). Plasma T790M-VAF did not correlate with time on osimertinib (p=0.72). Plasma T790M status correlated with a higher number of metastatic sites (4 vs 3, p<0.0001). Plasma T790M detection by organ sites were: pleura (58% with metastases vs 34% without metastases, p=0.14), bone (80% vs 21%, p=0.0002), hepatic (61% vs 41%, p=0.28), nodal (61% vs 33%, p=0.07), adrenal (64% vs 44%, p=0.60), brain (71% vs 38%, p=0.08), and bone/hepatic concurrently (94% vs 98%, p=0.04).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Using plasma T790M as an archetypal example, cfDNA testing showed concordance and a shorter turnaround compared to tissue testing. cfDNA was more likely to result positive in patients with more metastatic sites, or osseous and hepatic metastases possibly driven by increased ctDNA shedding.

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      P1.01-81 - Phase 3 Study of Pemetrexed-Platinum with or without Pembrolizumab for TKI-Resistant/EGFR-Mutated Advanced NSCLC: KEYNOTE-789 (ID 14192)

      16:45 - 18:00  |  Presenting Author(s): Gregory J Riely

      • Abstract
      • Slides

      Background

      In the phase 3 KEYNOTE-189 study, pembrolizumab plus pemetrexed-platinum improved OS and PFS over chemotherapy plus placebo in first-line, metastatic NSCLC without targetable EGFR mutations (Gandhi et al. NEJM 2018). The phase 3 KEYNOTE-789 (ClinicalTrials.gov, NCT03515837) study evaluates pemetrexed-platinum combined with pembrolizumab vs placebo in EGFR-TKI–resistant, EGFR-mutated, metastatic nonsquamous NSCLC.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Eligibility for this multicenter, randomized, double-blind, placebo-controlled study requires age ≥18 years; EGFR-TKI–resistant EGFR-mutated (exon 19 deletion or L858R mutation), histologically/cytologically confirmed stage IV, nonsquamous NSCLC; measurable disease per RECIST version 1.1; ECOG PS 0/1; and archival/newly obtained pretreatment tumor sample to evaluate PD-L1 expression. If progression on prior EGFR-TKI occurred with first- or second-generation TKIs (eg, erlotinib, afatinib, gefitinib) and T790M mutation is present, patients must have had subsequent progression on osimertinib; patients with progression on first-line osimertinib are eligible regardless of EGFR T790M mutation status. Patients are randomized 1:1 to pembrolizumab 200 mg or placebo, each in combination with pemetrexed 500 mg/m2 plus platinum chemotherapy (carboplatin AUC 5 or cisplatin 75 mg/m2; investigator’s choice) Q3W for 4 cycles. Patients continue allocated treatment (pembrolizumab or placebo) plus pemetrexed for up to 35 cycles, followed by pemetrexed maintenance therapy until documented disease progression or intolerable toxicity. Randomization is stratified by PD-L1 tumor proportion score ≥50% vs <50%, prior osimertinib vs no prior osimertinib, and geographic region of East Asia vs non-East Asia. Tumor response is assessed radiographically at baseline, week-6, then every 9 weeks through week-54 and every 12 weeks thereafter, per RECIST version 1.1 by blinded, independent central review. Treatment decisions are based on iRECIST criteria by investigator review. PFS and OS are dual primary endpoints, which will be tested with one-sided alphas of 0.001 and 0.02, respectively. Secondary endpoints are ORR; duration of response; change from baseline global health status and quality-of-life scores on the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-Core 30; time to true deterioration in composite endpoint of cough, chest pain, or dyspnea on EORTC QLQ-Lung Cancer Module 13; and safety and tolerability. Severity of AEs will be graded per NCI CTCAE version 4.0. Approximately 480 patients will be enrolled beginning June 1, 2018.

      4c3880bb027f159e801041b1021e88e8 Result

      Section not applicable

      8eea62084ca7e541d918e823422bd82e Conclusion

      Section not applicable

      6f8b794f3246b0c1e1780bb4d4d5dc53

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

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.13-44 - Safety, PK, and Preliminary Antitumor Activity of the Oral EGFR/HER2 Exon 20 Inhibitor TAK-788 in NSCLC (ID 12373)

      16:45 - 18:00  |  Author(s): Gregory J Riely

      • Abstract
      • Slides

      Background

      TAK-788 (AP32788) is an investigational tyrosine kinase inhibitor (TKI) with potent, selective preclinical activity against activating EGFR and HER2 mutations, including exon 20 insertions. We report early results of a phase 1/2 first-in-human, open-label, multicenter study of TAK-788 (NCT02716116).

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Patients with advanced non-small cell lung cancer (NSCLC) refractory to standard therapy received daily oral doses (5–120 mg) of TAK-788 in the ongoing dose-escalation phase (3+3 design). Preliminary antitumor activity (by RECIST v1.1), safety, and PK are reported for patients who received ≥1 dose.

      4c3880bb027f159e801041b1021e88e8 Result

      As of 8-Sep-2017, 34 patients (median age, 60 y; female, 65%; ≥2 prior anticancer therapies, 88%; Table) were treated with TAK-788; 10 remain on treatment at data cutoff. AUC0‑24,ss increased in a dose-proportional manner over the dose range evaluated; the effective t1/2 was ~16 (range 6–28) h. The most common treatment-emergent AEs (TEAEs; ≥20%) were diarrhea (47%), nausea (26%), and fatigue (21%). Grade ≥3 TEAEs in ≥2 patients (excluding disease progression) were dyspnea (n=3, 9%) and anemia, asthenia, dehydration, lung infection, pleural effusion, pneumonia, and pneumonitis (n=2 each, 6%). Two DLTs, both pneumonitis, were reported (80 mg, grade 3; 120 mg, grade 5). Of 14 evaluable patients, 3 had PR (80 mg, n=2, both confirmed; 120 mg, single PR awaiting confirmation), 6 had SD (40 mg, n=3; 80 mg, n=2; 120 mg, n=1), and 5 had PD as best response (40 mg, n=3; 80 mg, n=1; 120 mg, n=1). All patients with PR had EGFR exon 20 insertions.

      8eea62084ca7e541d918e823422bd82e Conclusion

      TAK-788 exhibits antitumor activity in patients with EGFR exon 20 insertions with an AE profile consistent with other EGFR TKIs. Phase 2 will begin after determination of the RP2D, with 4 molecularly defined cohorts in NSCLC. Updated data will be presented, including the recommended phase 2 dose (RP2D).

      Baseline Characteristics

      5 mg

      (n=4)

      10 mg

      (n=5)

      20 mg

      (n=5)

      40 mg

      (n=6)

      80 mg

      (n=7)

      120 mg

      (n=7)

      Total

      (n=34)

      Mutation type,a %

      Common EGFR mutations (exon 19 deletion / L8585R) 25 20 0 0 0 0 6
      EGFR-T790M+ 0 0 0 0 14 0 3
      EGFR exon 20 insertion 50 40 60 83 71 57 62
      HER2 0 20 40 17 14 29 21
      a One patient (20 mg) had both EGFR and HER2 mutations; 1 patient (80 mg) had EGFR exon 20 insertion + T790M.

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    SH02 - Highlight of the Previous Day Sessions (ID 994)

    • Event: WCLC 2018
    • Type: Highlight of the Day Session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 07:00 - 08:00, Room 202 BD
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      SH02.03 - IO (ID 14783)

      07:24 - 07:36  |  Presenting Author(s): Gregory J Riely

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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