Endoscopic resection is a safe and effective modality for treating well-differentiated rectal carcinoids smaller than 10 mm in diameter. Discrepancies were observed between CR-E and CR-P. The risk factors for metastasis were tumor size, increased mitotic rate, and lymphovascular invasion.

No abstract

Toxic epidermal necrolysis (TEN) is a severe adverse drug reaction involving extensive keratinocyte death in the epidermis. Histologically, the skin from TEN patients exhibits separation at the dermo-epidermal junction and accompanying necrosis of epidermal keratinocytes. Receptor-interacting protein kinase-3 (RIP3 or RIPK3) is an essential part of the cellular machinery that executes "programmed", or "regulated", necrosis and has a key role in spontaneous cell death and inflammation in keratinocytes under certain conditions. Here we show that RIP3 expression is highly upregulated in skin sections from TEN patients and may therefore contribute to the pathological damage in TEN through activation of programmed necrotic cell death. The expression level of mixed lineage kinase domain-like protein (MLKL), a key downstream component of RIP3, was not significantly different in skin lesions of TEN. However, elevated MLKL phosphorylation was observed in the skin from TEN patients, indicating the presence of RIP3-dependent programmed necrosis. Importantly, in an in vitro model of TEN, dabrafenib, an inhibitor of RIP3, prevented RIP3-mediated MLKL phosphorylation and decreased cell death. Results from this study suggest that the high expression of RIP3 in keratinocytes from TEN patients potentiates MLKL phosphorylation/activation and necrotic cell death. Thus, RIP3 represents a potential target for treatment of TEN.

Background/AimsTechniques for endoscopic evaluation of gastrointestinal subepithelial lesions include conventional endoscopy, jumbo biopsy, endoscopic ultrasonogrphy (EUS), EUS-guided fine needle aspiration, and endoscopic submucosal resection. However, these procedures have many limitations, such as low diagnostic yields and high complication rates. We therefore evaluated the diagnostic yield for tissue sampling of incidental subepithelial lesions using the bite-on-bite technique.MethodsOne hundred and forty subepithelial lesions were found in 129 patients during conventional diagnostic esophagogastroduodenoscopy by one examiner from October 2003 to November 2004. Bite-on-bite biopsies with conventional-sized forceps were taken from 36 patients having 37 lesions that did not appear to be hypervascular or to have a thick overlying epithelium. Two to eight bites were performed to obtain submucosal tissue for one lesion.ResultsThe bite-on-bite technique was diagnostic in 14 of the 37 lesions (38%). Blood oozing for more than 30 seconds occurred in five cases, but was easily controlled by epinephrine injection (2 cases) or hemoclip (3 cases). The diagnostic yield tended to be higher in the esophagus than in the stomach and duodenum (54% vs. 28%, p=0.109).ConclusionsThe bite-on-bite technique for subepithelial lesions is an effective and safe method in selected cases. This technique may be useful for incidental subepithelial lesions, especially those of the esophagus, except for ones with a high risk of bleeding or thick overlying epithelium.

Background/AimsThe aim of this study was to determine whether the routine closure of mucosal defects after endoscopic submucosal dissection (ESD) can enhance mucosal healing and reduce ESD-associated bleeding.MethodsPatients with gastric epithelial neoplasias and no obvious submucosal invasion were prospectively enrolled. Mucosal defects were left untreated in the control group. In the study group, mucosal closure was attempted with a 2-channel endoscope, a detachable snare, and clips. All participants received a second-look endoscopy the day after ESD, and coagulation therapy was administered to patients with visible vessels and active bleeding points.ResultsFifty-two patients were enrolled in the study, and 26 patients were assigned to each group. Complete mucosal defect closure occurred in 16 patients (61%) in the study group; incomplete closure occurred in 8 patients (31%) in the study group, and failed closure occurred in 2 patients (8%). Coagulation therapy at the second-look endoscopy was performed more often in the control group than in the study group (31% vs 4%, p=0.024). There were no significant differences in the incidence of immediate or delayed bleeding or in the two-week decrease in hemoglobin between the groups. The prevalence of open ulcers after 8 weeks was significantly lower in the study group than in the control group (18% vs 43%, p=0.012).ConclusionsRoutine mucosal closure after ESD supports earlier healing of artificial ulcers. A larger-scale trial is necessary to determine whether mucosal closure can reduce ESD-associated bleeding.

Endoscopic repair using clips can be effective for the treatment of colon perforations that occur during diagnostic colonoscopy.

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RAP80 localizes to sites of DNA insults to enhance the DNA-damage responses. Here we identify TRAIP/RNF206 as a novel RAP80-interacting protein and find that TRAIP is necessary for translocation of RAP80 to DNA lesions. Depletion of TRAIP results in impaired accumulation of RAP80 and functional downstream partners, including BRCA1, at DNA lesions. Conversely, accumulation of TRAIP is normal in RAP80-depleted cells, implying that TRAIP acts upstream of RAP80 recruitment to DNA lesions. TRAIP localizes to sites of DNA damage and cells lacking TRAIP exhibit classical DNA-damage response-defect phenotypes. Biochemical analysis reveals that the N terminus of TRAIP is crucial for RAP80 interaction, while the C terminus of TRAIP is required for TRAIP localization to sites of DNA damage through a direct interaction with RNF20–RNF40. Taken together, our findings demonstrate that the novel RAP80-binding partner TRAIP regulates recruitment of the damage signalling machinery and promotes homologous recombination.