Mass balance and latest fluxes of radiocesium derived from the fukushima accident in the western North Pacific Ocean and coastal regions of Japan

This article summarizes and discusses mass balance calculations of the activities of Fukushima-derived 137Cs released to the atmosphere and ocean prior to 2018 as well as the 137Cs inventories on land and in the ocean, biota, and sediment. We propose that the consensus value of the total amount of 137Cs released to the atmosphere was 15–21 PBq; atmospheric deposition of 137Cs on land was 3–6 PBq; atmospheric deposition of 137Cs on the North Pacific was 12–15 PBq; and direct discharge of 137Cs to the ocean was 3–6 PBq. We also evaluated the movement of 137Cs from one domain to another for several years after the accident. We calculated that the amount of 137Cs transported by rivers might be 40 TBq. The annual deposition of 137Cs due to resuspension at Okuma during the period 2014–2018 was 4–10 TBq year−1. The 137Cs discharged to the ocean was 0.73–1.0 TBq year−1 in 2016–2018. The integrated amount of FNPP1-derived 137Cs that entered the Sea of Japan from the Pacific Ocean from 2011 until 2017 was 270 ± 20 TBq, 6.4% of the estimated amount of FNPP1-derived 137Cs in Subtropical Mode Water in the North Pacific. The integrated amount of FNPP1-derived 137Cs that returned to the North Pacific Ocean through the Tsugaru Strait from the Sea of Japan was 110 ± 10 TBq. Decontamination efforts removed 134 TBq of 137Cs from surface soil prior to February 2019, an amount that corresponded to 4% of the137Cs deposited on land in Japan

Adrenal Corticomedullary Mixed Tumor Associated With the FGFR4-G388R Variant

Adrenal corticomedullary mixed tumors (CMMTs) are extremely rare; with only 20 cases being reported to date, the pathogenesis has remained elusive. A 31-year-old woman developed gestational hypertension with psychiatric disturbances persistent to postpartum and was diagnosed with pheochromocytoma, for which adrenalectomy was performed. Histological findings showed mixed adrenocortical adenoma and pheochromocytoma. Double immunostaining of inhibin and INSM1 (insulinoma-associated protein 1) showed that the 2 tumor components had distinct functional properties. Exome analysis of peripheral leukocytes and tumor (singular, as anatomically it is only 1 mass) revealed a homozygous germline FGFR4-0388R variant. As a readout of the variant, serine phosphorylation of signal transducer and activator of transcription 3 (STAT3) was detected only in the nucleus of adrenocortical adenoma component but not in the pheochromocytoma component. No tyrosine phosphorylation of STAT3 was detected. We report a case of CMMT with the germline FGFR4-G388R variant. Although additional studies are required, our immunohistochemical analysis suggests that the variant may play a role in the development of the adrenocortical component within the pheochromocytoma, leading to CMMT

Identification of a Biomarker Combination for Survival Stratification in pStage II/III Gastric Cancer after Curative Resection

Background: We sought to identify an optimal combination of survival risk stratification markers in patients with pathological (p) stage II/III gastric cancer (GC) after curative resection. Methods: We measured the expression levels of 127 genes in pStage II/III GC tissues of two patient cohorts by quantitative polymerase chain reaction (qPCR) and the expression of 1756 proteins between two prognosis (good and poor) groups by proteomic analysis to identify candidate survival stratification markers. Further, immunohistochemistry (IHC) using tumor microarrays (TMAs) in another cohort of patients was performed to identify an optimal biomarker combination for survival stratification in GC patients. Results: secreted protein acidic and rich in cysteine (SPARC), erb-b2 receptor tyrosine kinase 2 (ERBB2), inhibin subunit beta A (INHBA), matrix metallopeptidase-11 (MMP11), tumor protein p53 (TP53), and platelet-derived growth factor receptor-beta (PDGFRB) were identified as candidate biomarkers from qPCR analysis, and SPARC and galectin-10 were obtained from the proteomic analysis. The combination of PDGFRB, INHBA, MMP11, and galectin-10 was identified as the optimal combination of survival risk stratification markers. Conclusions: A combination of four proteins in GC tissues may serve as useful survival risk stratification markers in patients with pStage II/III GC following curative resection. Our results may facilitate future multicenter prospective clinical trials

Comprehensive genomic profiling of a unique liposarcoma arising in a patient with Li–Fraumeni syndrome and the novel detection of c-myc amplification: a case report

Abstract Background Germline TP53 mutations have been frequently reported in patients with Li–Fraumeni syndrome (LFS), resulting in a predisposition to various malignancies. Mutations other than germline TP53 mutations can also cause LFS-associated malignancies, but their details remain unclear. We describe a novel c-myc amplification in a unique liposarcoma in a patient with LFS. Case presentation A female patient with LFS developed breast cancer twice at the age of thirty; both were invasive ductal carcinomas harboring HER2 amplifications. Computed tomography revealed an anterior mediastinal mass, which was surgically resected. Histological analysis revealed three different lesions corresponding to myxoid liposarcoma-, pleomorphic liposarcoma-, and well-differentiated liposarcoma-like lesions. Fluorescence in-situ hybridization (FISH) analysis did not detect MDM2 amplification, Rb1 deletion, break apart signals of EWS, FUS, DDIT3, or c-myc, or c-myc-IGH fusion signals, but it did detect more c-myc signals. Further FISH analysis and comprehensive genomic profiling revealed c-myc amplification. We considered two differential diagnoses, dedifferentiated liposarcoma lacking MDM2 amplification and myxoid pleomorphic liposarcoma (MPLPS), and determined that this case is most likely MPLPS. However, definite diagnosis could not be made because a clear-cut differentiation of the case from liposarcomas was not possible. Conclusions A previous study demonstrated that c-myc amplification could not be detected in various liposarcomas, but the present unique liposarcoma showed c-myc amplification, so the c-myc amplification may indicate that the present liposarcoma is an LFS-related tumor. The present case further clarifies the pathological features of MPLPS and LFS-related liposarcomas by broadening their histopathological and genetic diversities