ATS 2019 Virtual Final Program

BEHAVIORAL • CLINICAL • TRANSLATIONAL SCIENTIFIC SYMPOSIUM CME Credits Available: 2 D85 UNFOLDING CIRCADIAN CLOCKS AND ER STRESS IN LUNG DISEASES Assemblies on Respiratory Structure and Function; Allergy, Immunology and Inflammation; Clinical Problems; Environmental, Occupational and Population Health; Respiratory Cell and Molecular Biology; Sleep and Respiratory Neurobiology 1:30 p.m. - 3:30 p.m. KBHCCD Ballroom D One (Level 3) Target Audience Basic and clinical researchers who are interested in learning role of circadian rhythm and ER stress in several pathologies of the lung and to establish projects in this area of lung biology Objectives At the conclusion of this session, the participant will be able to: • learn how circadian rhythm and ER stress play are culprits in pathogenesis of chronic lung disease. Circadian clocks have been conserved throughout evolution to allow anticipation of physiology and behaviour of the organisms to the environmental changes. As a consequence, most aspects of animal metabolism are under the control of this molecular clock. The endoplasmic reticulum (ER) is a sophisticated luminal network in which protein synthesis, maturation, folding, and transport take place. The unfolded protein response (UPR) is a stress-activated signalling pathway that regulates cell proliferation, metabolism and survival. The circadian clock coordinates metabolism and signal transduction with light/dark cycles. Accumulation of non-functional and potentially cytotoxic, misfolded proteins disease is believed to contribute to lung cell apoptosis, inflammation, and autophagy. Because of its fundamental role as a quality control system in protein metabolism, the UPR is of potential importance in the pathogenesis of many lung diseases such as asthma, COPD and IPF. Both sleep disruption and ER stress are emerging as a common culprit in the pathogenesis of chronic lung diseases which is a result of common environmental stressors or infections leading to the perturbation of the metabolic pathway in the body. Chairing: P. Sharma, PhD, MPH, Ultimo, Australia S.S. Sohal, PhD, Launceston, Australia R.C. Chambers, PhD, London, United Kingdom 1:30 Introduction P. Sharma, PhD, MPH, Ultimo, Australia 1:35 Regulation of Lung Inflammation by Circadian Clocks D. Ray, MBChB, PhD, Oxford, United Kingdom 2:05 The Autophagy-Inflammation-Cell Death Axis in Lung Disease A.M.K. Choi, MD, New York, NY 2:35 Exosomes and ER Stress as Mediators of Sleep Apnea Morbidity D. Gozal, MD, MBA, ATSF, Columbia, MO 3:03 Oxidative Stress and Aging in Lung Disease: Revealing New Pathways for Treatment Y.S. Prakash, MD, PhD, Rochester, MN BASIC • TRANSLATIONAL SCIENTIFIC SYMPOSIUM CME Credits Available: 2 D86 METABOLISM AS A LINK BETWEEN LUNG CANCER AND ITS MICROENVIRONMENT Assemblies on Thoracic Oncology; Respiratory Cell and Molecular Biology 1:30 p.m. - 3:30 p.m. KBHCCD Ballroom A One (Level 2) Target Audience Basic scientists and clinicians interested in new research on how metabolism is altered in lung cancer Objectives At the conclusion of this session, the participant will be able to: • gain new findings about alterations in metabolism in lung cancer and the tumor microenvironment; • obtain a better understanding about new therapies that target metabolic alterations in lung cancer; • obtain a better understanding of molecular interactions between lung cancers and their microenvironment that may promote or hinder tumor growth. The development and growth of lung cancers are dependent on complex interactions between cancer cells and the surrounding microenvironment, which includes stromal, inflammatory, and vascular cells. Much work has focused on cytokine and chemokine signaling between these cells. It is becoming clear that metabolic alterations that occur during malignant transformation serve as potent signals as well. These alterations have the potential to serve as diagnostic and therapeutic targets. This session will explore metabolic signaling in the tumor microenvironment. Chairing: E. Ostrin, MD, PhD, Houston, TX R. Savai, PhD, Bad Nauheim, Germany S.J. Moghaddam, MD, Houston, TX 1:30 Metabolic Heterogeneity and Liabilities in Lung Cancer R.J. Deberardinis, MD, PhD, Dallas, TX 1:50 Cystine and Glutamate Transport and Metabolic Reprogramming in Lung Tumor Development P.P. Massion, MD, Nashville, TN 2:10 Metabolic Changes in Tumor Cells and Tumor-Associated Macrophages: A Mutual Relationship R. Savai, PhD, Bad Nauheim, Germany 2:30 Implications of Cigarette Smoke Induced Metabolic Alterations in Lung Cancer Progression F. Kheradmand, MD, Houston, TX 2:50 Aberrant Tryptophan Catabolism Marked by High Kynureninase Expression Contributes to Immunomodulation and Poor Outcome in Lung Adenocarcinoma E. Ostrin, MD, PhD, Houston, TX 3:10 Targeting Cytokine Networks as an Immunotherapeutic Modality for Lung Cancer S.J. Moghaddam, MD, Houston, TX ATS 2019 • Dallas, TX 374 WEDNESDAY • MAY 22