A case of duodenal duplication cyst mimicking a pancreatic pseudocyst with intracystic hemorrhage.

BACKGROUND: Duodenal duplication cysts in adults are rare, and a preoperative diagnosis remains difficult because clinical manifestations are nonspecific and variable. We describe a case of a duodenal duplication cyst mimicking a pancreatic pseudocyst with repeated intracystic hemorrhage. CASE PRESENTATION: A 47-year-old male who complained of upper abdominal pain and vomiting was referred to our hospital. He was a heavy drinker and had a past history of hospitalization for alcoholic chronic pancreatitis. Plain abdominal computed tomography (CT) showed a cystic lesion of 7 cm in size in the lumen near the second part of the duodenum. The cystic lesion showed high density inside. Gastrointestinal endoscopy revealed that the lumen of the duodenum was deformed by a submucosal tumor-like mass and the endoscope could not pass through it, but active bleeding was not seen in the lumen of the duodenum. On the fourth day of hospitalization, anemia progressed and contrast-enhanced CT demonstrated a high-density spot on the wall of the cystic lesion. A pancreatic pseudocyst complicated with intracystic hemorrhage was preliminarily considered. Angiography was immediately performed, and a pseudoaneurysm was identified in the branch of the anterior superior pancreaticoduodenal artery (ASPDA). Transcatheter arterial embolization (TAE) was performed. Anemia did not progress after that, and follow-up CT showed reduction in the size of the cystic lesion. Afterward, the same symptoms recurred twice and surgical treatment was performed for the pancreatic pseudocyst with repeated intracystic hemorrhage. Macroscopically, a cystic mass of 5 cm in size was adjacent to the second part of the duodenum on the pancreas side. A pinhole-sized communication was identified between the cyst and the duodenum lumen. Microscopically, the cyst wall was composed of gastric mucosa and shared a common proper muscle layer with the duodenum. Chronic ulcers and erosions were seen in the cyst. Based on these findings, a diagnosis of duodenal duplication cyst was made. CONCLUSIONS: Duodenal duplication cysts in adults have seldom been reported and should be considered as a differential diagnosis for a patient with a cystic lesion adjoining the duodenum.

[A Case of Effective Chemoradiotherapy Using mFOLFOX6 for Locally Advanced Rectal Cancer].

We report a case of locally advanced rectal cancer, treated effectively with chemotherapy consisting of mFOLFOX6 combined with radiotherapy. A 63-year-old man was admitted to our hospital in March 2012 for diarrhea and anal and perineal pain. Advanced rectal cancer with invasion ofthe right perineum was diagnosed based on computer tomography(CT) findings. Surgery was performed; however, the rectal cancer was unresectable. A sigmoid colostomy was performed, and a central venous port was implanted. In April 2012, the patient was treated with chemotherapy using 3 courses ofmFOLFOX6 and concurrent radiotherapy. Radiotherapy at 2 Gy/day was administered 25 times(total dose, 50 Gy). After chemoradiotherapy, the patient underwent 3 courses ofmFOLFOX6 as an additional therapy. By June 2012, CT showed resolution ofthe tumor in the right perineum and a marked decrease in the size ofthe primary rectal cancer. Because the patient refused surgery, we started treatment with combination chemotherapy using oral S-1 and intravenous CPT-11 in August 2012. After 18 courses, the treatment was changed to oral administration ofS -1 alone, which was continued for 1 year. The patient remained well without recurrence for 54 months since the original diagnosis. Therefore, chemoradiotherapy with mFOLFOX6 is a possible option for the management of advanced rectal cancer.

Immunohistochemical and sequencing analyses of the Wnt signaling components in Japanese anaplastic thyroid cancers.

We investigated the status of the components and target genes of the Wnt signaling pathway in Japanese anaplastic thyroid cancers (ATCs) in the present study. Nuclear and cytoplasmic positive staining of beta-catenin, which might indicate the existence of alterations in the Wnt signaling pathway, were found in 40.9% and 63.6% of the 22 ATC samples, respectively. The beta-catenin, adenomatous polyposis coli (APC) and Axin 1 gene mutations were observed in 4.5%, 9.0%, and 81.8% of the 22 ATC samples, respectively. Overexpression of cyclin D1 and c-myc, which are the target genes of the Wnt signaling pathway, was observed in 27.3% and 59.1% of the ATC samples, respectively. There was no significant correlation between nuclear or cytoplasmic positive staining of beta-catenin and nuclear positive staining of cyclin D1 or c-myc. Taken together, the results of beta-catenin immunohistochemistry suggest that alterations in the Wnt signaling pathway are associated with carcinogenesis of ATC, but the frequency of beta-catenin gene mutation in our series is lower than that previously reported. Furthermore, cyclin D1 and c-myc frequently accumulated in ATC, independently of dysfunction in the Wnt signaling pathway.

Yeast glycogen synthase kinase-3 activates Msn2p-dependent transcription of stress responsive genes.

The yeast Saccharomyces cerevisiae has four genes, MCK1, MDS1 (RIM11), MRK1, and YOL128c, that encode homologues of mammalian glycogen synthase kinase 3 (GSK-3). A gsk-3 null mutant in which these four genes are disrupted showed growth defects on galactose medium. We isolated several multicopy suppressors of this growth defect. Two of them encoded Msn2p and phosphoglucomutase (PGM). Msn2p is a transcription factor that binds to the stress-response element (STRE). PGM is an enzyme that interconverts glucose-1 phosphate and glucose-6 phosphate and is regulated by Msn2p at the transcriptional level. Expression of the mRNAs of PGM2 and DDR2, whose promoter regions possess STRE sequences, on induction by heat shock or salt stress was reduced not only in an msn2 msn4 (msn2 homologue) double mutant but also in the gsk-3 null mutant. STRE-dependent transcription was greatly inhibited in the gsk-3 null mutant or mck1 mds1 double mutant, and this phenotype was suppressed by the expression of Mck1p but not of a kinase-inactive form of Mck1p. Although Msn2p accumulated in the nucleus of the gsk-3 null mutant as well as in the wild-type strain under various stress conditions, its STRE-binding activity was reduced in extracts prepared from the gsk-3 null mutant or mck1 mds1 double mutant. These results suggest that yeast GSK-3 promotes formation of a complex between Msn2p and DNA, which is required for the proper response to different forms of stress. Because neither Msn2p-GSK-3 complex formation nor GSK-3-dependent phosphorylation of Msn2p could be detected, the regulation of Msn2p by GSK-3 may be indirect.

PY motifs of Rod1 are required for binding to Rsp5 and for drug resistance.

In Saccharomyces cerevisiae, the overexpression of ROD1 confers resistance to o-dinitrobenzene (o-DNB), a representative of target drugs of glutathione S-transferase. The roles of Rod1 in drug resistance have remained to be determined. We isolated the rog3 mutation as a suppressor mutation of the temperature sensitivity of the strain, in that two of the total four glycogen synthase kinase 3 homologs were deleted. Rog3 is homologous to Rod1, and its overexpression also conferred resistance to o-DNB. Furthermore, these two proteins have PY-motifs, and bound to Rsp5, a hect-type ubiquitin ligase. The rsp5-101 mutant showed sensitivity to o-DNB as did the rod1 mutant, a mutant Rod1 containing altered PY motifs was defective in ability to bind to Rsp5 and in conferring o-DNB resistance. These results suggest that interaction of Rod1 and Rsp5 is important for drug resistance.