Purpose: Although multiple primary colorectal cancer has been recognized as a significant clinical entity, its clinical and pathological features and its prognosis are still controversial. The purpose of this study was to clarify clinical and pathological features of multiple primary colorectal cancer.Materials and Methods: Among 1669 patients who underwent surgery for primary colorectal cancer from January 1997 to June 2005, 26 patients (1.6%) with multiple primary colorectal cancer were identified. We reviewed clinical characteristics including diagnostic interval, lesions, operating methods, and TNM stage, and we defined the index lesion as the most advanced lesion among the synchronous lesions. For the purposes of the study, the colon and rectum were classified into three segments. The right-side colon included the appendix, cecum, ascending colon, hepatic flexure, and transverse colon, and the left-side colon included the splenic flexure, descending colon, and sigmoid colon.Results: Of the 26 patients with multiple primary colorectal cancers, nineteen patients were male and seven patients were female, with a mean age of 61.5 years. Nineteen patients had synchronous colorectal cancers and seven patients had metachronous colorectal cancers. In the metachronous cases, the mean diagnostic interval was 36.8 months. The site of the first lesion in metachronous colorectal cancers was the right colon in five cases (71.4%) and the left colon in two cases (28.6%), and the site of the second lesion was the rectum in six cases (55.5%), the right colon in three cases (33.3%), and the left colon in one case. The TNM stage of the second lesions in the metachronous colorectal cancers was stage II in four cases (57.1%), stage III in one case (14.3%), and stage IV in one case (14.3%). For the synchronous colorectal cancers, the operation methods were single-segment resection combined with endoscopic mucosal resection in five cases (26.3%), single-segment resection alone in six cases, two-segment resection in six cases, and total colectomy in two cases.
Peroxiredoxin is a well-studied antioxidant enzyme. Enzymes in this category eliminate ROS in order to protect cells from oxidative stresses. PRX-1 exerts a protective antioxidant role in cells through its peroxidase activity, reCorrespondence Kwang Woo Hwang, Laboratory of Host Defense Modulation, College of Pharmacy, Chung-Ang University, 221 Heukseok-dong, Dongjakgu, Seoul, Korea. Tel: +82 2 820 5597; Fax: +82 2 823 5597; e-mail: khwang@cau.ac.kr List of Abbreviations: DMEM, Dulbecco's modified Eagle's medium; dNTP, deoxyribonucleotide triphosphate; FACS, fluorescence-activated cell sorting; GFP, green fluorescent protein; IL, interleukin; IκBα, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; iNOS, inducible nitric acid synthase; LPS, lipopolysaccharide; NF-κB , nuclear factor kappa-light-chain-enhancer of activated B cells; NK, natural killer; PMA, phorbol 12-myristate 13-acetate; PRX, peroxiredoxin; ROS, reactive oxygen species; shPRX-1, shRNA lentiviral vector targeting peroxiredoxin-1; STAT, signal transducers and activators of transcription; TNF, tumor necrosis factor. ducing H 2 O 2 , peroxynitrite, and a wide range of organic hydroperoxides for detoxification (1).The mammalian PRX family can be classified into six distinct groups (types I through VI). Other,
Activated T cells express inhibitory receptors such as CTLA-4 that can downregulate immune responses. Blockade of or genetic deficiency in CTLA-4 can result in autoimmunity. Therefore, strategies to increase the inhibitory function of CTLA-4 may be attractive in settings of undesirable T cell responses such as autoimmunity or transplant rejection. We have tested the hypothesis that transgenic constitutive expression of CTLA-4 can further attenuate immune responses when compared with normal inducible expression. Our results indicate that transgenic expression of CTLA-4 in mouse T cells (CTLA-4-Tg T cells) results in reduced cell cycle progression and increased apoptosis of TCR-stimulated T cells. CTLA-4-Tg T cells display reduced T cell proliferation in an in vivo model of graft versus host disease (GVHD). These results further our understanding of how CTLA-4 can be manipulated to inhibit immune responses and may help development of new therapeutic strategies for clinical settings of autoimmunity and transplantation.
Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic β-cell death and destabilization of glucose homeostasis. One of the major characteristics of T1D pathogenesis is the production of inflammatory mediators by macrophages that result in destruction or damage of pancreatic β-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic β-cells respectably. In this setting, peroxiredoxin-1, an anti-oxidant enzyme was knocked down to observe its functions in the pathogenesis of T1D. RAW264.7 cells were primed with lipopolysaccharide and co-cultured with MIN6 cells while PRX-1 was knocked down in one or both cell types. Our results suggest that hindrance of PRX-1 activity or the deficiency of this enzyme in inflammatory conditions negatively affects pancreatic β-cell survival. The observed decrease in viability of MIN6 cells seems to be caused by nitric oxide production. Additionally, it seems that PRX-1 affects previously reported protective activity of IL-6 in pancreatic β cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity.
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