No Abstract Available.
Protein-Serine-Threonine Kinases* ; Receptors, Cell Surface* ; Transforming Growth Factor beta*

Current evidences have expended the concept that chronic inflammation might play a crucial role in the development and progression of colorectal cancer. For instance, chronic ulcerative colitis (UC) is associated with a 10- to 40-fold increased risk of developing colorectal cancer (CRC) compared to the general population. However, the specific mechanistic link between chronic inflammation and carcinogenesis in colon has not been integrated into molecular understanding. In this current review, we will provide an update on the molecular pathogenesis of colitis-associated colorectal cancer, focused on 1) the differences of molecular mechanism between the colitis-associated colorectal cancer (CAC) and the sporadic colorectal cancer (SCC), 2) the plausible and contributive role of chronic inflammation in colon carcinogenesis, and 3) lessons learned from colitis-associated animal model. Understanding of molecular pathogenic mechanism underlying the colitis-associated colorectal cancer will facilitate the development of novel treatment strategies for prevention of colitis-associated colorectal cancer.
Carcinogenesis* ; Colitis, Ulcerative ; Colon* ; Colorectal Neoplasms ; Inflammation* ; Inflammatory Bowel Diseases ; Models, Animal

No abstract availble.
Animals ; *Cell Line ; *Helicobacter Infections ; *Helicobacter pylori ; Humans

Gastrointestinal hemangioma is a relatively uncommon benign vascular tumor that can occur anywhere in the gastrointestinal tract. It is the second most common vascular lesion of the colon and a clinically important entity because of the possibility of massive hemorrhage when complicated. In gross appearance, hemangioma presents variously as a pedunculated, subpedunculated, or flat elevated lesion similar to a submucosal tumor. A typical case of hemangioma is relatively easy to diagnose because the lesion presents as translucent blue-purple vessels under the mucosa. However, it can be difficult to diagnose in some cases, especially if it does not have its usual characteristic color or is covered with normal mucosa. We incidentally found a colonic hemangioma that had the unusual appearance of a pedunculated polypoid lesion with normal mucosa. It was misdiagnosed as a pedunculated polyp with a long, thick neck and treated by using an endoscopic mucosal resection.
Caves ; Colon ; Gastrointestinal Tract ; Hemangioma ; Hemangioma, Cavernous ; Hemorrhage ; Mucous Membrane ; Neck ; Polyps

No abstract available.
Helicobacter pylori* ; Helicobacter*

No abstract available.
Helicobacter pylori* ; Helicobacter*

No abstract available.
Capsule Endoscopy*

BACKGROUND/AIMS: Transforming growth factor-beta (TGF-β) is a cytokine implicated in the susceptibility, development, and progression of gastrointestinal cancer and certain other neoplasms. In the later stages of cancer, TGF-β not only acts as a bystander of host-immune response, but also contributes to cell growth, invasion, and metastasis. In the current study, we generated gastric mucosal cells that stably express Smad7, and explored the Helicobacter pylori-associated biological changes between mock-transfected and Smad7-transfected RGM1 cells. METHODS: RGM1 cells stably transfected with Smad7 were infected with H. pylori, and molecular changes in apoptotic markers and inflammatory mediators were examined. Several candidate genes were explored in Smad7-overexpressing cells after H. pylori infection. RESULTS: Overexpression of Smad7 in RGM1 cells significantly increased the H. pylori-induced cytotoxicity compared to mock-transfected cells. Exaggerated increases in inflammatory mediators, cyclooxygenase 2, inducible NO synthase, and augmented apoptosis were noted in Smad7-overexpressing cells, whereas mitigated heme oxygenase 1 was noted in Smad7- overexpressing cells. These phenomena were reversed in cells transfected with Smad7 siRNA. CONCLUSIONS: These data suggest that inhibition of Smad7 is a possible target for mitigating H. pylori-associated inflammation.
Apoptosis ; Cyclooxygenase 2 ; Gastritis ; Gastrointestinal Neoplasms ; Helicobacter pylori ; Helicobacter* ; Heme Oxygenase-1 ; Inflammation ; Neoplasm Metastasis ; Nitric Oxide Synthase ; RNA, Small Interfering ; Transforming Growth Factor beta

No abstract available.

BACKGROUND/AIMS: The p53 mutations have been described as the most common genetic alteration during development and progression of malignancy in a wide range of human cancers. Mutant p53 proteins have a prolonged half-life accounting for increased levels of p53 protein frequently detected in tumors. This can induce the production of anti-p53 in the senzn of patients with HCC. We determined the relationship of serum anti-p53 with p53 expression in the liver tissue of chronic liver disease and the correlation of serum anti-p53 with serum alpha- fetoprotein(AFP) in patients with HCC. METHODS: In sera of same patients, we analysed the anti- p53 using ELISA system As controls we tested 50 healthy individuals and 20 patients with chronic hepatitis. Immaiohistochemical study for the presence of mutant p53 was performed on liver tissue from 50 patients with cirrhosis and 30 patients with HCC using monoclonal antibody clone DO-7 and LSAB kit by ABC method. RESULTS: Anti-p53 was positive in 9(30%) of 30 patients with HCC. Among nine patients with positive anti-p53, only two patients had detectable p53 expression in their tumor tissues. Anti-p53 was positive in 5(10%) of 50 patients with liver cirrhosis. The AFP was elevated in 21(70%) of 30 patients with HCC. Among the 9 AFP- negative HCC patients, 4(44.4%) were found to be positive for anti-p53. P53 expression was detectable in 9(30%) of 30 HCCs and 1(3.3%) of RO surrounding non-tumorous cirrhotic tissues. CONCLUSION: Mese findings suggest that anti-p53 was not correlated with the status of p53 expression in liver tissue and serological testing for anti-p53 antibody may be complementary to serum AFP for diagnosing of HCC with normal serum AFP.
Carcinoma, Hepatocellular ; Chronic Disease* ; Clone Cells ; Enzyme-Linked Immunosorbent Assay ; Fibrosis ; Half-Life ; Hepatitis, Chronic ; Humans ; Liver Cirrhosis ; Liver Diseases ; Liver* ; Serologic Tests