Introduction: The G protein-coupled oestrogen receptor 1 (GPER-1) is a potential prognostic marker in breast cancer. However, its role in male breast cancer (MBC) is still unknown. This study evaluates the expression of GPER-1 in MBC samples and correlates these data with clinical and pathological parameters including patients' survival.
View Article and Find Full Text PDFWe recently reported that dysregulated c-Jun N-terminal kinases (JNK) activity causes defective cell cycle checkpoint control, inducing neoplastic transformation in a cellular ulcerative colitis (UC) model. In the quiescent chronic phase of UC, p-p54 JNK was down-regulated and p-p46 JNK was up-regulated. Both were up-regulated in the acute phase.
View Article and Find Full Text PDFUnusual locations of the appendix vermiformis can result in delay in appropriate diagnosis and treatment of appendicitis. So an inflamed appendix in a sub-hepatic caecum caused by caecal maldescent for example can mimic cholecystitis, the pain being localized in the right upper quadrant. Here, we present a case of perforated sub-hepatic appendicitis with peritonitis, requiring open ileocaecal resection.
View Article and Find Full Text PDFThe production of hydrogen peroxide (H2 O2 ) drives tumourigenesis in ulcerative colitis (UC). Recently, we showed that H2 O2 activates DNA damage checkpoints in human colonic epithelial cells (HCEC) through c-Jun N-terminal Kinases (JNK) that induces p21(WAF1) . Moreover, caspases circumvented the G1/S and intra-S checkpoints, and cells accumulated in G2/M.
View Article and Find Full Text PDFBackground: Previous studies have suggested that affective disorders are characterized by glial pathology. In this context, it has been hypothesized that elevated S100B serum and cerebrospinal fluid levels may represent a suitable surrogate marker. However, brain studies on the cellular distribution pattern of S100B in depressed patients are lacking so far.
View Article and Find Full Text PDFOxidative stress, caused by reactive oxygen species (ROS), is a major contributor to inflammatory bowel disease (IBD)-associated neoplasia. We mimicked ROS exposure of the epithelium in IBD using non-tumour human colonic epithelial cells (HCEC) and hydrogen peroxide (H2 O2 ). A population of HCEC survived H2 O2 -induced oxidative stress via JNK-dependent cell cycle arrests.
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