Abstract. The COordinated Regional Downscaling EXperiment (CORDEX) is a diagnostic model intercomparison project (MIP) in CMIP6. CORDEX builds on a foundation of previous downscaling intercomparison projects to provide a common framework for downscaling activities around the world. The CORDEX Regional Challenges provide a focus for downscaling research and a basis for making use of CMIP6 global climate model (GCM) output to produce downscaled projected changes in regional climates and assess sources of uncertainties in the projections, all of which can potentially be distilled into climate change information for vulnerability, impacts and adaptation studies. CORDEX Flagship Pilot Studies advance regional downscaling by targeting one or more of the CORDEX Regional Challenges. A CORDEX-CORE framework is planned that will produce a baseline set of homogeneous high-resolution, downscaled projections for regions worldwide. In CMIP6, CORDEX coordinates with ScenarioMIP and is structured to allow cross comparisons with HighResMIP and interaction with the CMIP6 VIACS Advisory Board.

Introduction: EGFR-mutant NSCLC displays diverse outcomes to tyrosine kinase inhibitor (TKI) treatment. Because cooccurring genomic alterations might describe different biological subsets of patients with this cancer, exploring co-occurring genomic alterations that impact patients' outcomes using a comprehensive gene panel is potentially important.

The success of crizotinib in ALK-positive patients has elicited efforts to find new oncogenic fusions in lung cancer. These efforts have led to the discovery of novel oncogenic fusion genes such as ROS1 and RET. However, the molecular and clinicopathologic characteristics associated with RET or ROS1 fusion, compared with ALK fusion-positive lung cancer, remain unclear. We accordingly analyzed the clinicopathologic characteristics of RET-and ROS1-fusion-positive lung adenocarcinomas. We further performed immunohistochemistry and fluorescence in situ hybridization analysis (FISH) in 15 cases of RET and 9 cases of ROS1 fusion tumors by identified NanoString's nCounter screening. RET fusion-positive patients were younger in age, never-smokers, and in early T stage; ROS1 fusion-positive patients had a higher number of never-smokers compared with patients with quintuple-negative (EGFR À /KRAS À /ALK À /ROS1 À /RET À ) lung adenocarcinoma. Histologically, RET and ROS1 fusion tumors share the solid signet-ring cell and mucinous cribriform pattern, as previously mentioned in the histology of ALK fusion tumors. Therefore, it can be presumed that fusion gene-associated lung adenocarcinomas share similar histologic features. In immunohistochemistry, the majority of 15 RET and 9 ROS1 fusion-positive cases showed positivity of more than moderate intensity and cytoplasmic staining for RET and ROS1 proteins, respectively. In FISH, the majority of RET and ROS1 rearrangement showed two signal patterns such as one fusion signal and two separated green and orange signals (1F1G1O) and an isolated 3 0 green signal pattern (1F1G). Our study has provided not only characteristics of fusion gene-associated histologic features but also a proposal for a future screening strategy that will enable clinicians to select cases needed to be checked for ROS1 and RET rearrangements based on clinicohistologic features.