Search

The Tsushima Strait (TS) is the sole passage for volume transport from the East China Sea to the Sea of Japan. To date, the process underlying the interannual variability in volume transport remains unclear. In this study, 27-yr (1993–2019) reanalysis data from the Japan Coastal Ocean Predictability Experiment 2 (JCOPE2M) system and in situ/satellite observations were employed to understand this process. The results suggest that TS transport was generally high in 1999, 2003/04, and 2010 and low in 1995/96, 2005/06, 2008, and 2014/15. The sea level anomaly (SLA) outside the entrance of the TS, that is, the upstream TS forcing, dominates the interannual TS transport variation. A high SLA pumps more water into the Sea of Japan via the TS, and vice versa. By synthesizing JCOPE2M reanalysis data and satellite observations, further analysis revealed that cyclonic mesoscale eddies from the subtropical countercurrent (STCC) could be responsible for this high SLA by reducing Kuroshio transport, enhancing Kuroshio intrusion across the shelf, and increasing the SLA around the upstream TS region. The reverse was true for anticyclonic STCC eddies. Variability in the Kuroshio intrusion southwest of Kyushu induces variations in the TS transport on an interannual time scale. [ABSTRACT FROM AUTHOR]

Background: TP53 mutations are frequent in non‐small cell lung cancer (NSCLC). Different categories of TP53 mutations may be associated with survival in advanced NSCLC, but their effect on prognosis is diverse. To date, a comprehensive comparison of the relationship between different classes of TP53 alterations and survival in advanced NSCLC has rarely been performed. Moreover, the prognostic significance of a novel approach called the evolutionary action of TP53 (EAp53) in advanced NSCLC is unclear. Methods: A total of 210 patients with NSCLC harboring TP53 mutation data were enrolled. Genomic and clinical data for the Memorial Sloan Kettering Cancer Center (MSKCC) cohort with advanced NSCLC were obtained from cBioPortal. Relationship between clinical characteristics and TP53 mutations was performed by Fisher's exact test or χ2 test. Overall survival (OS) analysis was evaluated using Kaplan–Meier method and Cox proportional hazards regression model. Results: TP53 mutations were identified in 51.4% of NSCLC patients and were mainly located in exons 5, 7, and 8. The distribution patterns of missense and truncating mutations of TP53 were remarkably different. Among patients with advanced NSCLC who never received immune checkpoint inhibitor treatments, EAp53 high‐risk mutations were significantly associated with poor OS in both our cohort and the MSKCC cohort. Moreover, marked differences were observed in the mutational landscape between patients with EAp53 high‐risk mutations (HR group) and other patients (OT group). The HR group displayed higher mutation frequencies in the RTK, cell cycle, and DNA damage repair (DDR) pathways than the OT group. In addition, the tumor mutation burden in the HR group was significantly higher than that in the OT group. Conclusions: This study provided important insights into the molecular‐clinical profile of TP53‐mutated NSCLC patients. Moreover, the data revealed that EAp53 high‐risk mutations were an independent prognostic factor for worse OS in advanced NSCLC. [ABSTRACT FROM AUTHOR]