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Breast cancer metastasis to the gastrointestinal tract is relatively rare. Patients with such disease often develop gastrointestinal symptoms, but it is sometimes asymptomatic. Endoscopic findings of gastric metastasis from breast cancer markedly vary from benign to malignant, and even in suspected malignant cases, it is often difficult to differentiate between primary and metastatic disease. We experienced a case in which an endoscopic examination performed during the treatment for metastatic breast cancer resembled an early-stage gastric cancer. A 71-year-old woman underwent curative surgery for right breast cancer 16 years previously. She underwent endoscopic submucosal dissection for early-stage gastric cancer 5 years ago. Two years ago, she developed metastatic disease in the lungs and mediastinal lymph nodes, and endocrine therapy was administered. At the same time, a follow-up endoscopy revealed a new elevated lesion, suspected to be an early-stage gastric cancer. However, histological diagnosis of the biopsy was metastasis of breast cancer. One and a half years later, a follow-up endoscopy revealed a gastric lesion that had reduced in size. She is still alive, having received a variety of systemic treatments. Patients with metastatic breast cancer are experiencing prolonged survival. Thus, follow-up endoscopy should be considered after the diagnosis of gastrointestinal metastasis considering the risk of lethal conditions, such as gastrointestinal bleeding and perforation. Our case serves as a reminder to clinicians how difficult it is to determine whether a gastric lesion is primary or metastatic based on endoscopic findings and the importance of communication with endoscopists and pathologists.

Background The occurrence of sarcoid reactions has been recognized in various cancers. The common location for observing these granulomas is mainly the lymph nodes, but a rare occurrence in the spleen has been reported. Almost all splenic sarcoid reactions associated with gastric cancer have been resected synchronously and diagnosed accidentally, and a rare metachronous occurrence of a sarcoid reaction in the spleen after distal gastrectomy can mimic cancer metastasis. We describe a rare case of a splenic sarcoid reaction recognized in a patient with gastric cancer 6 months after distal gastrectomy. Case presentation An 82-year-old man underwent laparoscopic distal gastrectomy for gastric cancer (T3N0M0, stage IIA). Six months after gastrectomy, CT and 18F-fluorodeoxyglucose (FDG)-PET/CT showed the appearance of a splenic mass. We diagnosed solitary splenic metastasis from gastric cancer and performed laparoscopic-assisted splenectomy. His splenic tumor was diagnosed as a sarcoid reaction by histopathological examination. Conclusion To our knowledge, this is the first report of a splenic sarcoid reaction recognized 6 months after distal gastrectomy for gastric cancer without any chemotherapy. The splenic sarcoid reaction and cancer metastasis to the spleen were undistinguishable from the CT and FDG-PET/CT findings. The present case and literature review showed that cases of splenic sarcoid reactions associated with gastric cancer can also be accompanied by the occurrence of these granulomas in lymph nodes. When the appearance of a solitary mass is observed in the spleen after resection of primary cancer, it is necessary to consider not only cancer metastasis but also sarcoid reactions. Retrospective histopathological confirmation of the existence of sarcoid reactions in lymph nodes from resected specimens might possibly avoid incorrect diagnosis and intervention.

Synovial sarcoma (SS) is genetically characterized by chromosomal translocation, which generates SYT-SSX fusion transcripts. Although SS can occur in any body part, primary gastric SS is substantially rare. Here we describe a detection of the fusion gene sequence of gastric SS in plasma cell-free DNA (cfDNA). A gastric submucosal tumor was detected in the stomach of a 27-year-old woman and diagnosed as SS. Candidate intronic primers were designed to detect the intronic fusion breakpoint and this fusion sequence was confirmed in intron 10 of SYT and intron 5 of SSX2 by genomic polymerase chain reaction (PCR) and direct sequencing. A locked nucleic acid (LNA) probe specific to the fusion sequence was designed for detecting the fusion sequence in plasma and the fusion sequence was detected in preoperative plasma cfDNA, while not detected in postoperative plasma cfDNA. This technique will be useful for monitoring translocation-derived diseases such as SS.

A 75-year-old asymptomatic man presented with an anterior mediastinal cyst without a solid component on computed tomography. Pathologic examination of the specimens obtained by thoracoscopic resection showed a thymic cyst with a 1.6-mm type A microthymoma in the surrounding thymic tissue. In addition, there were multiple hyperplastic nodules smaller than 1 mm histologically corresponded to microscopic thymomas. The patient underwent completion thymectomy through median sternotomy; thereafter, there was no residual thymic neoplasm detected. This was the first case report of a type A microthymoma. Microthymoma or microscopic thymoma could be present concomitantly with a thymic cyst without a solid component.

Apparent hydrodynamic radii ( R happ ) of nonionic surfactant micelles in aqueous solutions of hepta- and hexa-ethyleneoxide monoalkylether (C 14 E 7 , C 16 E 7 , and C 16 E 6 ) were measured at 20–40 °C. Fluorescence spectra of pyrene in aqueous solutions of the nonionic surfactants were measured as a function of surfactant concentration and temperature. The cloud point of C 16 E 6 was about 35 °C at concentration range of 10 −3 to 10 −2 M. However, even at a higher temperature than the cloud point, the fluorescence intensity ratio of pyrene monomer, I m1 / I m3 , in C 16 E 6 solution behaves similarly to other surfactants (C 16 E 7 and C 14 E 7 ), indicating that the pyrene molecules reside in a similar location of surfactants. The slope for the temperature dependence of the I m1 / I m3 ratio also changed with the surfactant concentration, and the micelle size differed among the surfactants (C 16 E 6 , C 16 E 7 , and C 14 E 7 ). The activation enthalpy of pyrene diffusion was evaluated using Stevens–Ban plot, and the value of 20–30 kJ mol −1 was obtained for surfactant concentrations of 5 × 10 −4 to 10 −2 M. The results were compared with those reported for ionic and nonionic surfactant micelles.

The aims of this study were to elucidate sonographic and histologic features of pure mucinous carcinoma (P-MC) of the breast using quantitative analysis and to evaluate the relationship between quantitative analysis and visual qualitative assessment. Eleven P-MCs (nine patients) were evaluated qualitatively and quantitatively. Three experts assessed these sonographic images using the Breast Imaging Reporting and Data System (BI-RADS) lexicon. For assessment of internal echoes and posterior echoes, quantitative measures were determined using ImageJ software. Histologic thin sections were stained for classification into separate parts of the tumor (stroma, mucin and cancer cells) and were digitized. Internal echoes were isoechoic in 7 of 11 (63.6%) tumors and hypoechoic in 4 of 11 (36.4%); all P-MCs were "enhanced" in qualitative evaluation. As internal echoes increased, the proportion of stroma increased and that of mucin decreased. The high level of internal echoes is correlated with reflection and back-scattering, which are caused mainly by the interface between mucin and stroma.

Viral protein R (Vpr), an accessory protein of human immunodeficiency virus type 1 (HIV-1), induces the G2 cell cycle arrest in fission yeast for which host factors, such as Wee1 and Rad24, are required. Catalyzing the inhibitory phosphorylation of Cdc2, Wee1 is known to serve as a major regulator of G2/M transition in the eukaryotic cell cycle. It has been reported that the G2 checkpoint induced by DNA damage or incomplete DNA replication is associated with phosphorylation and upregulation of Wee1 for which Chk1 and Cds1 kinase is required. In this study, we demonstrate that the G2 arrest induced by HIV-1 Vpr in fission yeast is also associated with increase in the phosphorylation and amount of Wee1, but in a Chk1/Cds1-independent manner. Rad24 and human 14-3-3 appear to contribute to Vpr-induced G2 arrest by elevating the level of Wee1 expression. It appears that Vpr could cause the G2 arrest through a mechanism similar to, but distinct from, the physiological G2 checkpoint controls. The results may provide useful insights into the mechanism by which HIV-1 Vpr causes the G2 arrest in eukaryotic cells. Vpr may also serve as a useful molecular tool for exploring novel cell cycle control mechanisms.