岸本 充

A 50-year-old male with a pancreatic tail tumor underwent distal pancreatectomy. At 14 and 27 months after the primary surgery, metachronous liver metastases were identified and partial hepatectomies were performed for each. Pathologic findings of the primary pancreatic tumor were heterogeneous, but they essentially categorized into two components based on their cytologic features: (i) clear cell component and (ii) epithelioid cell component. The metastatic hepatic tumor was entirely composed of the epithelioid cell component. SMARCB1 expression was lost by immunohistochemistry and heterozygous deletion of SMARCB1 was identified by fluorescence in situ hybridization for both the primary and metastatic tumors. Targeted DNA sequencing of a metastatic hepatic tumor sample was performed and SMARCB1 loss was identified. Based on the morphologic, immunohistochemical, and molecular analyzes, the present case was difficult to classify into any of the existing entities. SMARCB1 deficiency might play a key role in the tumorigenesis.

Retained placenta can lead to septic shock; however, sepsis-induced cardiomyopathy (SICM) due to retained placenta has not been reported previously. This report presents a rare case of SICM following septic shock due to retained placenta after miscarriage in a 40-year-old woman, accompanied by the "shark fin sign" on an electrocardiogram, a pattern typically linked to myocardial ischemia. She experienced ventricular tachycardia and required venoarterial extracorporeal membrane oxygenation; however, she was successfully treated. We also reviewed previous cases of shark fin sign in patients without myocardial infarction. A review showed that half of the cases experienced lethal arrhythmias, even without myocardial infarction.

Keratins are intermediate filament proteins in epithelial cells, and they are important for cytoskeletal organization. Keratin 6A (KRT6A), classified as a type II keratin, is normally expressed in stratified squamous epithelium and squamous cell carcinomas. Little is known about the expression and role of KRT6A in adenocarcinomas. We investigated the clinicopathological and molecular biological significance of KRT6A in colorectal adenocarcinoma. Immunostaining of our institution's colorectal adenocarcinoma cases demonstrated that KRT6A showed significantly stronger expression at the invasive front than the tumor center (p < 0.0001). The high-KRT6A-expression cases (n = 47) tended to have a high budding grade associated with significantly worse prognoses. A multivariate analysis revealed that the KRT6A expression status was an independent prognostic factor for overall survival (p = 0.0004), disease-specific survival (p = 0.0097) and progression-free survival (p = 0.0033). The correlation between KRT6A and patient prognoses was also validated in an external cohort from a published dataset. To determine the function of KRT6A in vitro, KRT6A was over-expressed in three colon cancer cell lines, DLD-1, SW620, and HCT 116. KRT6A overexpression increased migration and invasion in DLD-1, but did not in SW620 and HCT116. In three-dimensional sphere-forming culture, KRT6A expression enhanced the irregular protrusion around the spheroid in DLD-1. Our findings in the present study indicated that KRT6A expression is a valuable prognostic marker of colorectal cancer and KRT6A may be involved the molecular mechanism in the progression of invasive areas of colorectal cancer.