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R. Herbst



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    ED 07 - How to Treat Advanced Squamous Carcinoma of the Lung (ID 7)

    • Event: WCLC 2015
    • Type: Education Session
    • Track: Treatment of Advanced Diseases - NSCLC
    • Presentations: 1
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      ED07.03 - Lung Master Protocol in Squamous Cell Lung Cancer (Lung-MAP, S1400) (ID 1800)

      03:00 - 03:20 PM  |  Author(s): R. Herbst

      • Abstract
      • Presentation

      Abstract:
      In recent years, our understanding of non-small cell lung cancer (NSCLC) has evolved from thinking of this malignancy as a single disease, or a small number of histologic subtypes, to now a multitude of genomically-defined subsets, both in adenocarcinoma and squamous lung cancer. In development of new targeted therapies against these abnormalities, so-called Master Protocols offer a number of advantages over traditional single study designs for drug-biomarker approval, including a common infrastructure, homogeneous patient populations with consistent eligibility across multiple independent sub-studies, and the ability to screen large numbers of patients in rapid fashion. Thus, the Lung-MAP project was designed to facilitate approval of targeted therapy-predictive biomarker combinations in squamous lung cancer, a recognized area of unmet need. Lung-MAP is constructed as a unique public-private partnership engaging the National Cancer Institute (NCI) and its Thoracic Malignancies Steering Committee (TMSC), the Foundation of the NIH (FNIH), the pharmaceutical industry and advocacy groups such as Friends of Cancer Research (FOCR), along with an advisory role by the Federal Drug Administration (FDA). The design is multiple simultaneously running Phase II/III trials, each capable of independently opening and/or closing without affecting the other sub-studies, in which patients eligible for 2[nd] line therapy for lung SCC have their cancers genomically screened through a next generation sequencing (NGS) platform (Foundation Medicine). Patients are then randomized into one of several sub-studies, each comparing an experimental targeted therapy with standard of care therapy, based on identification of candidate predictive biomarkers associated with each sub-study. At launch, drug targets under study consisted of “match sub-studies” for PI3K, FGFR, CDK 4/6 and HGF, and a non-match sub-study testing PD-L1-directed therapy, as described below. Rapid turn-around time of NGS screening results, within 2 weeks, allows real time assignment into the appropriate sub-study. For those patients with cancers that do not “match” into a biomarker-driven sub-study, there is a ‘non-match” sub-study, in which a predictive biomarker is not yet of sufficient validation to utilize it in a drug-biomarker registration strategy. Due to changes in the therapeutic landscape since the launch of Lung-MAP, a number of amendments and modifications have been implemented, which will be discussed during this presentation.

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    MINI 27 - Biology and Other Issues in SCLC (ID 152)

    • Event: WCLC 2015
    • Type: Mini Oral
    • Track: Small Cell Lung Cancer
    • Presentations: 1
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      MINI27.08 - NOTCH3 Protein Expression and Outcome in Small Cell Lung Cancer (SCLC) and Therapeutic Targeting with Tarextumab (Anti-Notch 2/3) (ID 2999)

      05:25 - 05:30 PM  |  Author(s): R. Herbst

      • Abstract
      • Presentation
      • Slides

      Background:
      NOTCH expression is associated with cancer cell survival via effects on cancer stem/progenitor cells. Targeting NOTCH2 and 3 decreases growth and survival of SCLC patient-derived human tumor xenografts (PDX). Phase1b/2 trials testing Tarextumab (TRXT) anti-NOTCH2/3 therapy are underway (NCT01647828 and NCT01859741) and show promising anti-tumor activity. Here, we studied NOTCH3 protein expression using immunohistochemistry (IHC) in SCLC human tissues and correlated with survival. Also, we studied NOTCH3 gene expression in phase 1b patients (pts) treated with TRXT.

      Methods:
      For NOTCH IHC staining, murine monoclonal antibodies were generated by immunizing mice with a NOTCH3 extracellular domain (ECD) protein, then creating hybridomas. Clones were screened by FACS and western blots for specificity to NOTCH3.ECD. A lead clone was selected for NOTCH3 protein measurement in 47 SCLC samples represented in a tissue microarray from Yale Pathology Tissue Services (YPTS). NOTCH3 signal was determined in tumors using H-scores generated by Leica Aperio Scanscope IHC membrane image analysis. For survival analysis, NOTCH3 signal was binarized with cutoffs defined by X-tile software. For the phase 1b clinical trial, a standard 3+3 dose escalation design was employed with cohorts of 3 to 6 pts treated at each dose level. TRXT was given IV on Day 1 of each 21 day cycle with etoposide 100 mg/m[2] (Days 1-3) and cisplatin 80 mg/m[2 ]or carboplatin at AUC 5 (Day 1) for 6 cycles, followed by TRXT alone every 21 days until progression of disease or unacceptable toxicities. Then, the MTD TRXT plus etoposide and carboplatin was confirmed in a cohort of 6 subjects. All pts are required to submit tissues for Notch 3 gene expression and IHC staining.

      Results:
      A single hybridoma clone demonstrating specific reproducible membranous staining with a dynamic range for NOTCH3.ECD in control and PDX tissues was chosen for IHC analysis in SCLC human FFPE tissues (n=47). Forty cases (85.1%) demonstrated NOTCH3 signal, with eighteen (38.3%) having none to very low signal. Of the 31 cases with adequate follow-up, there was a strong trend with worse outcome and high NOTCH3 expression in the extensive stage (p=0.063), but not in limited stage (p=0.857). The level of significance was a function of the experimental cut-point and can only be considered exploratory. Finally, 27 pts were treated with TRXT in the phase 1b trial, with an overall response rate of 84%. The median duration of treatment was 128 days (6 cycles) with mPFS and mOS of 124 and 228 days, respectively. The median follow-up for PFS and OS was 86 and 107 days, respectively. Twenty-five pts have tissues evaluable for NOTCH3 gene expression and the analysis is underway.

      Conclusion:
      NOTCH3 IHC staining showed expression in most SCLC cases, with high NOTCH3 trending towards worse survival in extensive stage. This supports the rationale of targeting NOTCH3 by TXRT in SCLC pts. Further evaluation of the prognostic and predictive value of TRXT for anti-Notch therapies in SCLC is underway in an ongoing Phase 2 clinical trial.

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    MS 04 - Harnessing the Full Potential of the Immune System (ID 22)

    • Event: WCLC 2015
    • Type: Mini Symposium
    • Track: Treatment of Advanced Diseases - NSCLC
    • Presentations: 1
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      MS04.01 - PD1/PDL1 Studies (ID 1860)

      02:20 - 02:40 PM  |  Author(s): R. Herbst

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    MTE 02 - Patients, Investigators and Pharmaceuticals Working Together to Accelerate Research and Access: The Lung Cancer Master Protocol (Lung-MAP) Clinical Trial (Ticketed Session) (ID 54)

    • Event: WCLC 2015
    • Type: Meet the Expert (Ticketed Session)
    • Track: Advocacy
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/07/2015, 07:00 AM - 08:00 AM, 105
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      MTE02.01 - Patients, Investigators and Pharmaceuticals Working Together to Accelerate Research and Access: The Lung Cancer Master Protocol (Lung-MAP) Clinical Trial (ID 1979)

      07:00 - 07:30 AM  |  Author(s): R. Herbst

      • Abstract
      • Presentation
      • Slides

      Abstract:
      The traditional obstacles to approval of oncologic therapeutic agents, especially targeted therapies that address a rare-biomarker defined group of patients are the long processes from initial drug discovery to clinical implementation, the difficulties in recruitment for these clinical trials and high number of screen failures and the overall low rate of enrollment in clinical trials. The Lung Master Protocol (Lung-MAP, S1400) is a precedent-setting clinical trial designed to advance the efficient development of targeted therapies for squamous cell cancer of the lung (SCCA). There are few new effective therapeutic options for patients with advanced lung SCCA. Immunotherapies, including nivolumab, have already shown clear benefit for patients with SCCA in 2015 leading to approval by the FDA which has been an unprecedented step forward for the treatment of patients, however we are still lacking predictive markers for these therapies that are reliably selecting patients more likely to benefit. Lung-MAP (S1400) is aiming to identify biomarker-drug pairs that will lead to successful therapeutic outcomes and registration of new agents. It is a registration-intent master protocol that includes a screening component and clinical trial component; the clinical trial component includes multiple sub-studies which independently evaluate investigational therapies. The clinical trial component is designed to be modular such that new sub-studies can be added either as other sub-studies close or as new biomarker-drug pairs are identified for testing in this patient population. Lung-MAP is utlilizing a broad NGS screening platform capitalizing on the expanding application of genomic sequencing in oncology that has through the Cancer Genome Atlas and other sequencing initiatives revealed targetable genetic aberrations including gene mutations, rearrangements, amplifications, and deletions, and creating an immense opportunity to implement personalized therapy with a high potential to improve patients outcomes. Immunotherapy has been integrated in the design of Lung-MAP from its launch in June of 2014. The original study design and structure is shown in the figure. Figure 1 The modular design of the study has allowed for the flexibility to adapt to the approval of nivolumab and the hault in further development of AMG102 (rilotumumab) with discontinuation of the corresponding sub-study by implementing timely modifications which include the following:1)Eligibility has changed from exclusively second line therapy to second-or more line therapy 2)Pre-screening, while patient receive first line therapy has been added to boost accrual 3)the unmatched arm has been changed to a single (not randomized) arm study with the anti-PD-L1 agent MEDI-4736. Theses changes are reflected in the figure. Each independently conducted and analyzed sub-study specifies investigator-assessed progression-free survival (IA-PFS) and overall survival (OS) as the co-primary endpoints for the phase 3 primary objectives. The primary objectives for the phase 3 are to determine if there is a statistically significant difference in OS and to determine if there is both a clinically meaningful and statistically significant difference in IA-PFS. The conduct of Lung-MAP relies on close collaboration (a public-private partnership) among the NCI and NCTN (spearheaded by SWOG), the pharmaceutical industry, the Foundation for the NIH (FNIH), Friends of Cancer Research, advocates, and FDA. This Master Protocol will improve genomic screening of SCC patients for clinical trial entry, and improve time lines for drug-biomarker testing, allowing for inclusion of the maximum numbers of otherwise eligible patients. The clinical trial continues to be updated following science and alterations in the therapeutic landscape, with adaptations in design and incorporation of new agents against matched targets and the implementation of novel immunotherapy approaches for the unmatched arm. Figure 2





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    ORAL 31 - PD1 Axis Inhibition (ID 143)

    • Event: WCLC 2015
    • Type: Oral Session
    • Track: Treatment of Advanced Diseases - NSCLC
    • Presentations: 1
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      ORAL31.07 - A Phase II Trial of Pembrolizumab for Untreated Brain Metastases from Non-Small Cell Lung Cancer (ID 824)

      05:50 - 06:01 PM  |  Author(s): R. Herbst

      • Abstract
      • Presentation
      • Slides

      Background:
      Patients with advanced non-small cell lung cancer (NSCLC) often develop brain metastases (BrMs), and standard therapy such as surgery or radiation can cause toxicity and delay systemic treatment. Pembrolizumab is a PD-1 inhibitor with promising clinical activity and a favorable toxicity profile in patients with advanced NSCLC, however the efficacy of pembrolizumab in the central nervous system (CNS) is unknown. This trial aims to determine the safety and activity of pembrolizumab in patients with advanced NSCLC and untreated brain metastases.

      Methods:
      Eligibility for patients with NSCLC in this Phase II trial includes the presence of at least 1 BrM between 5 and 20 mm that is asymptomatic, untreated or progressing after prior local therapy, and not requiring urgent local therapy. PD-L1 expression in tumor obtained since the most recent systemic therapy is required. Patients are treated with pembrolizumab 10mg/kg every 2 weeks. Systemic response is determined by RECIST 1.1, and BrM response is determined by modified RECIST (mRECIST) in which brain lesions ≥ 5mm are considered measurable and up to 5 target lesions are allowed. The primary endpoint of this trial is BrM response rate.

      Results:
      Fifteen patients with NSCLC and untreated BrMs were treated with pembrolizumab, none of whom had a drug-related Grade ≥ 3 adverse event (AE) or any grade AE attributed to BrMs. Of the 10 patients evaluable for response, 5 (50% with 95% CI: 0.24-0.76) had a BrM response (4 partial and 1 complete) and 5 had a systemic response. Only one patient who responded in the body had progressive disease in the brain; all other patients who had a systemic response also had a CNS response. The duration of response in the brain was at least 12 weeks for 4 of the 5 responders, and all responses are ongoing at the time of data analysis.

      Conclusion:
      To our knowledge this is the first study to demonstrate that the PD-1 inhibitor pembrolizumab has activity in the CNS in patients with NSCLC and untreated brain metastases. To date there have been no drug-related neurologic or significant toxicity identified. Patient enrollment and biomarker analysis are ongoing.

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    ORAL 41 - Immune Biology, Microenvironment and Novel Targets (ID 159)

    • Event: WCLC 2015
    • Type: Oral Session
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      ORAL41.08 - Discussant for ORAL41.05, ORAL41.06, ORAL41.07 (ID 3440)

      07:46 - 07:56 PM  |  Author(s): R. Herbst

      • Abstract
      • Presentation

      Abstract not provided

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    ORAL 42 - Drug Resistance (ID 160)

    • Event: WCLC 2015
    • Type: Oral Session
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      ORAL42.04 - Rictor Alterations Elicit Mechanisms of Survival Advantage and Resistance to Targeted Therapy in Non-Small Cell Lung Cancer (NCSLC) (ID 2991)

      07:02 - 07:13 PM  |  Author(s): R. Herbst

      • Abstract
      • Presentation

      Background:
      Rictor (RPTOR independent companion of MTOR, complex 2) is a highly conserved protein and is a critical component for assembly and functionality of the mTORC2 complex. Alterations of the PI3K/mTOR/AKT pathway are hallmark of many cancer types, underscoring the potential important role of Rictor. The goal of our current study was to characterize the functional consequences of genomic alterations of Rictor in advanced refractory NSCLC. Our preliminary data suggest that Rictor alterations have the potential to, not only signal canonically (via activation of AKT), but also provide cancer cells with alternate, more advantageous oncogenic signaling via non-canonical mechanisms.

      Methods:
      We correlated genomic data (DNA next generation sequencing (NGS), Foundation Medicine, Inc) gene expression profiling, and clinical outcome in the context of the ongoing BATTLE-2 clinical trial of targeted therapies in chemo-refractory NSCLC(198 cases). We further (1) surveyed early stage NSCLC cases(230 cases) in The Cancer Genome Atlas (TCGA) database to perform two-way hierarchical clustering comparing gene expression profiling in amplified vs diploid cases; (2) utilized a single-nucleotide polymorphism array to select Rictor amplified and diploid NSCLC cell lines; (3) assessed Rictor protein and RNA expression by Western blot and qRT-PCR, respectively; (4) performed Rictor knockdown (siRNA), and (5) performed drug sensitivity to targeted therapies by MTS assay.

      Results:
      In the Battle-2 cases, we identified 15% of Rictor alterations (9% gene amplifications, 6.6% mutations, non-concomitant). Among the mutations, 1 was mapped to an N-terminal phosphorylation site, while all others are of unknown significance to date. Rictor alterations were significantly associated with lack of 8-week disease control in the AKTi+MEKi therapeutic arm. In the TCGA we found: (1) 10% Rictor amplifications and 3% mutations; (2) significant correlation between amplification and elevated Rictor gene expression; (3) a putative functional gene expression signature associated with Rictor amplification. In diploid cell lines we found concordance between AKT phosphorylation and activation of other downstream mTORC2 targets (i.e. SGK1 and PKCα), but in Rictor amplified cell lines we witnessed a discordant activation of these pathways. Furthermore, following Rictor knockdown in our amplified cell lines, a significant reduction of colony formation, migratory, and invasive potential was seen in a pathway-differential manner. Thus, suggesting that Rictor amplifications may provide survival advantage in select cancer cells by tipping the signaling balance toward a non-canonical oncogenic pathway (AKT-independent[I1] ).Also in a differential pathway manner, Rictor gene amplification and overexpression contributed to resistance to a number of targeted therapies

      Conclusion:
      Rictor alterations may constitute a potential novel mechanism of targeted therapy resistance via the activation of non-canonical signaling pathways. These alterations could define new molecular NSCLC subtypes with distinct biology that expose unique avenues for therapeutic implication. Ongoing studies are exploring therapeutic vulnerabilities, non-canonical signaling and Rictor mutations.

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    PLEN 04 - Presidential Symposium Including Top 4 Abstracts (ID 86)

    • Event: WCLC 2015
    • Type: Plenary
    • Track: Plenary
    • Presentations: 1
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      PLEN04.01 - A Randomized, Phase III Study Comparing Carboplatin/Paclitaxel or Carboplatin/Paclitaxel/Bevacizumab with or without Concurrent Cetuximab in Patients with Advanced Non-Small Cell Lung Cancer (NSCLC): SWOG S0819 (ID 3612)

      10:45 - 10:57 AM  |  Author(s): R. Herbst

      • Abstract
      • Presentation
      • Slides

      Background:
      This abstract is under embargo until September 9, 2015 and will be distributed onsite on September 9 in a Late Breaking Abstract Supplement.

      Methods:


      Results:


      Conclusion:


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    PRC 04 - Press Conference 4 (ID 199)

    • Event: WCLC 2015
    • Type: Press Conference
    • Track: Other
    • Presentations: 1
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      Abstract – A Randomized, Phase III Study Comparing Carboplatin/Paclitaxel or Carboplatin/Paclitaxel/Bevacizumab with or without Concurrent Cetuximab in Patients with Advanced Non-Small Cell Lung Cancer (NSCLC): SWOG S0819 - Dr. Roy Herbst, Ensign Professor of Medicine, Professor of Pharmacology, Chief of Medical Oncology, Director, Thoracic Oncology Research Program, Associate Director for Translational Research, Yale Comprehensive Cancer Center, Yale School of Medicine, New Haven, Connecticut (ID 3638)

      10:17 - 10:25 AM  |  Author(s): R. Herbst

      • Abstract
      • Presentation
      • Slides

      Abstract:
      Background: Cetuximab, a chimeric monoclonal antibody targeting the epidermal growth factor receptor (EGFR), moderately increases survival in patients with advanced NSCLC. Our prior work suggested that EGFR gene copy number measured by fluorescent in-suit hybridization (FISH) could identify those patients most likely to benefit.Methods: Patients eligible for this NCTN multicenter open-label, phase III trial had histologically or cytological confirmed Stage IV NSCLC that was newly diagnosed or recurrent after previous surgery or radiation. Patients with controlled brain metastases were allowed entry. All patients were required to have tumor tissue available for EGFR FISH testing. Randomization was stratified by appropriateness for bevacizumab treatment, smoking status and M-substage. The co-primary objectives were progression-free survival (PFS) in EGFR-FISH positive (FISH+) patients and overall survival (OS) in the overall study population (OSP). Secondary objectives were OS in FISH-positive patients and clinical outcomes (PFS and OS) comparison among bevacizumab-appropriate (BA) and inappropriate (BI) patients.Results: The final accrual was 1,333 total and 1,313 eligible patients (control arm: 657 total, 275/382 BA/BI; cetuximab-containing arm: 656 total, 279/377 BA/BI). EGFR FISH status was determined on 976 patients, with 400 (41%) FISH+. Squamous carcinoma (SCCA) represented 24-25% of patients. PFS and OS were not significantly different in the OSP (HR (95%CI) =0.98 (0.87-1.09) and 0.94(0.84-1.06), respectively). There is some indication of benefit in PFS and OS (HR 0.91 (0.74-1.12) and 0.83 (0.67-1.04), respectively) in FISH+ patients, albeit not statistically significant. However, among FISH+ BI and SCCA patients, effect estimates for OS were 0.75 (0.57-1.00) and 0.56 (0.37-0.84), respectively. Cetuximab was generally well tolerated with a spectrum of adverse events consistent with prior reportsConclusion: The addition of cetuximab had minimal effect in unselected advanced NSCLC patients. In FISH+ patients there is a suggestion of benefit, predominantly in SCCA and BI. These data support using a new marker for determining who should receive an EGFR antibody inhibitor with chemotherapy.Support: NIH/NCI/NCTN grants SWOG: CA180888, CA180819; ECOG/ACRIN: CA180820; Alliance: CA180821; and in part by Bristol-Myers Squibb Co.

      N PFS OS
      Analysis Group OSP FISH+ OSP FISH+ OSP FISH+
      All Patients
      Cetuximab-Containing Arm, Median, 95% CI 656 199 4.6(4.2-5.2) 5.4(4.5-5.7) 10.9(9.6-12.0) 13.4(11.7-14.8)
      Control Arm, Median, 95% CI 657 201 4.5(4.2-4.9) 4.8(3.9-5.5) 9.4(8.7-10.3) 9.8(8.7-12.1)
      Hazard Ratio, 95% CI 0.98(0.87-1.09) 0.91(0.74-1.12) 0.94(0.84-1.06) 0.83(0.67-1.04)
      2-sided p-value 0.68 0.37 0.34 0.10
      BA
      Cetuximab-Containing Arm, Median, 95% CI 279 86 5.6(5.3-6.1) 6.2(5.7-7.4) 12.7(10.9-13.4) 15.5(13.4-18.4)
      Control Arm, Median, 95% CI 275 80 5.9(5.5-6.6) 6.7(5.7-8.0) 11.6(10.5-13.8) 13.2(11.2-19.1)
      Hazard Ratio, 95% CI 1.05(0.88-1.25) 1.07(0.77-1.47) 1.04(0.86-1.25) 0.97(0.69-1.38)
      2-sided p-value 0.57 0.70 0.70 0.88
      BI
      Cetuximab-Containing Arm, Median, 95% CI 377 113 4.1(3.6-4.4) 4.5(3.8-5.2) 9.2(8.2-10.9) 11.2(8.6-12.9)
      Control Arm, Median, 95% CI 382 121 3.8(3.1-4.2) 3.7(2.8-4.6) 8.2(7.3-8.7) 8.7(5.9-9.7)
      Hazard Ratio, 95% CI 0.93(0.80-1.07) 0.82(0.63-1.07) 0.88(0.76-1.03) 0.75(0.57-1.00)
      2-sided p-value 0.31 0.14 0.12 0.05
      SCCA
      Cetuximab-Containing Arm, Median, 95% CI 160 55 4.2(3.7-4.6) 4.5(3.8-5.2) 9.6(8.2-11.5) 11.8(8.6-13.5)
      Control Arm, Median, 95% CI 161 56 3.7(2.8-4.3) 2.8(2.6-4.1) 8.0(7.1-8.9) 6.4(4.2-8.7)
      Hazard Ratio, 95% CI 0.88(0.70-1.11) 0.68(0.46-1.01) 0.85(0.67-1.08) 0.56(0.37-0.84)
      2-sided p-value 0.29 0.06 0.18 0.006


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