Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Probiotics are viable non-pathogenic micro-organisms which, when ingested, exert a positive influence on host health or physiology. We have critically analysed the evidence for the efficacy of specific probiotic strains in human gastrointestinal diseases. The best evidence can be obtained with randomised controlled trials which avoid bias. Good evidence has been obtained with several strains in the prevention or treatment of antibiotic-associated disorders, in the treatment (and to a lesser extent prevention) of gastroenteritis and acute diarrhoea and in the alleviation of lactose intolerance. We also analysed the recent randomised controlled trials performed in patients with Clostridium difficile or Helicobacter pylori, inflammatory bowel disease, irritable bowel syndrome, non-ulcer dyspepsia and colon cancer.
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PMID:Probiotics and intestinal health effects: a clinical perspective. 1221 85

A variety of malignant complications occur in Crohn's disease, and previous studies have recorded an increased intestinal cancer risk. The present investigation tabulated myeloid and lymphoid malignancies compared with intestinal cancers in 1000 consecutively evaluated patients with Crohn's disease who were followed over an extended period by a single clinician. Myeloid and lymphoid neoplasms were present in 0.5% of patients, while cancer in the intestinal tract was detected in 1%. Most of these patients with a malignancy had Crohn's disease for a prolonged period of more than 20 years and had negative outcomes, including death or presentations with advanced disease. In this cohort, lymphoma was not detected in a single patient after definition of Crohn's disease, possibly reflecting the limited use of immunosuppressives or infused biological agents in this clinical practice. Bypassed rectal 'stumps' were associated with subsequent colorectal cancer in half of all males with colon cancer in this series, suggesting an important risk factor following colectomy in Crohn's disease. Epithelial dysplasia was detected in only a single male patient before colorectal cancer, implying that this histopathological marker may be a poor predictor of subsequent colon cancer development in Crohn's disease, an inflammatory bowel disease process that is typically patchy or focal in distribution in the intestinal tract.
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PMID:Tabulation of myeloid, lymphoid and intestinal malignancies in Crohn's disease. 1246 71

The etiology of almost half of the diarrheal diseases has not been cleared yet, in spite of modern diagnostic methods. Bacteroides fragilis strains which secrete an enterotoxin are termed as enterotoxigenic B.fragilis (ETBF). These strains are associated with diarrheal diseases in children above 1 year of age and in adults. B. fragilis toxin (BFT) stimulates intestinal secretion and in-vitro cytotoxic response in HT29/C1 cells. Recent studies suggest that BFT is related to inflammatory bowel disease and colon cancer by triggering nuclear activation with potential oncogene expression. In this review, the molecular pathogenesis, epidemiology and laboratory diagnosis of ETBF have been reviewed to focus on ETBF as a diarrheal agent.
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PMID:[Enterotoxigenic Bacteroides fragilis as a factor in diarrhea]. 1247 74

Laparoscopic bowel surgery has demonstrated patient care benefits of decreased duration of hospital stay, smaller incisions, lower risk of cardiopulmonary complications, and reduced risk of small-bowel obstruction. Resection of complicated diverticular disease and inflammatory bowel disease can be technically challenging and may be associated with higher conversion rates. The applicability of these techniques to colon cancer is supported by a growing body of evidence that demonstrates similar survival and recurrence rates obtained by open resection and the exaggeration of the risk of port site recurrences. Laparoscopic colorectal surgery has also challenged much of the standard postoperative care plans used for colectomy. Optimal postoperative care of the laparoscopic colectomy patient requires an appreciation of the faster recovery enjoyed by these patients and the fact that ambulation and dietary advancement need to be accelerated. Coordination between the surgical team and the postoperative care team is essential to obtain all the benefits associated with this new approach to the management of colorectal disease.
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PMID:Care of the laparoscopic colectomy patient. 1247 80

Inflammatory bowel diseases, including ulcerative colitis and Crohn's disease, increase the risk of colorectal cancer in humans. It has been recently shown in humans and animal models that intestinal microbiota and host immunity are integral in the progression of large bowel diseases. Lymphocytes are widely believed to prevent bacterially induced inflammation in the bowel, and lymphocytes are also critical in protecting against primary tumors of intestinal epithelia in mice. Taken together, this raises the possibility that lymphocytes may inhibit colon carcinogenesis by reducing bacterially driven inflammation. To examine the role of bacteria, lymphocytes, and inflammatory bowel disease in the development of colon cancer, 129/SvEv Rag-2-deficient and congenic wild-type mice were orally inoculated with a widespread enteric mouse bacterial pathogen, Helicobacter hepaticus, or sham-dosed with media only. H. hepaticus-infected Rag2-/-, but not sham-dosed Rag2-/- mice, rapidly developed colitis and large bowel carcinoma. This demonstrated a link between microbially driven inflammation and cancer in the lower bowel and suggested that innate immune dysregulation may have an important role in inflammatory bowel disease and progression to cancer. H. hepaticus-infected wild-type mice did not develop inflammation or carcinoma showing that lymphocytes were required to prevent bacterially induced cancer at this site. Adoptive transfer with CD4+ CD45RBlo CD25+ regulatory T cells into Rag-deficient hosts significantly inhibited H. hepaticus-induced inflammation and development of cancer. These results suggested that the ability of CD4+ T cells to protect against intestinal cancer was correlated with their ability to reduce bacterially induced inflammatory bowel disease. Further, regulatory T cells may act directly on the innate immune system to reduce or prevent disease. These roles for T cells in protection against colon carcinoma may have implications for new modes of prevention and treatment of cancer in humans.
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PMID:CD4+ CD25+ regulatory T lymphocytes inhibit microbially induced colon cancer in Rag2-deficient mice. 1254 27

Luminal nutrition is important for maintenance of gastrointestinal mucosal structure and function. In particular, short chain fatty acids (SCFAs), metabolic products of anaerobic bacterial fermentation of dietary fiber and resistant starch, are particularly important as the preferred respiratory fuel of the colonocytes. A variety of biological effects of SCFAs have been reported, and there is now increasing number of experimental works showing new aspects of these molecules. For example, as the mechanisms mediating anti-inflammatory effects of SCFAs, several investigators identified the inhibitory effect of butyrate on proinflammatory cytokine-induced NF-kappaB activation. Various inflammatory responses are now discussed with the central role of NF-kappaB activation, and thus the inhibition of NF-kappaB activation represents the efficacy of dietary fiber and SCFAs in the treatment with inflammatory bowel disease. Furthermore, recent advance in molecular technology has identified mechanisms mediating anti-tumor effects of SCFAs. SCFAs modulate expression of cell cycle-regulating proteins and induce apoptosis in colon cancer cells. SCFAs increase the susceptibility of colon cancer cells to complement-mediated cell injury. In this review, new aspects of functions of SCFAs are focused and summarized.
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PMID:Role of dietary fiber and short-chain fatty acids in the colon. 1257 Aug 25

The association of Streptococcus bovis endocarditis with colonic neoplasia is classically described and exceeds 50 percent. The prevalence of Streptococcus bovis in fecal cultures from patients with carcinoma of the colon is significantly increased (56%) as compared to that in controls (10%) and also in patients with inflammatory bowel disease (28%). Streptococcus bovis endocarditis is relatively benign, but it stresses the frequency of the associated colonic carcinoma, requiring colonoscopy and making the treatment of the high-risk lesion mandatory. The article covers a literature review and a case report.
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PMID:[Streptococcus bovis endocarditis - predictor of colonic carcinoma? ]. 1262 71

Non-steroidal anti-inflammatory drugs (NSAID) may inhibit colon cancer development through affecting proliferation and apoptosis. However, their use in cancer chemoprevention is still limited due to toxicities. There is longstanding clinical experience with the aminosalicylate mesalazine in the treatment of patients with inflammatory bowel disease with very few side effects. So far, most studies on the cellular effects of mesalazine were focused on its anti-inflammatory properties. Recent data, however, indicate that mesalazine may also reduce cell growth in vivo. We therefore investigated the growth inhibitory effect of mesalazine on human colon cancer cells in vitro compared with established chemopreventive agents. We also wished to determine the underlying cellular mechanisms of the effect. Here we show that mesalazine dose- and time-dependently inhibited the proliferation of colon cancer cells. Mesalazine was less potent in reducing cell growth than sulindac sulfide or indomethacin but growth effective mesalazine concentrations were comparable with concentrations achievable in vivo under standard mesalazine treatment. While other NSAID induced a robust G(1) arrest, mesalazine specifically blocked cells in mitosis although microtubule polymerization or spindle orientation was not affected. In addition, mesalazine induced apoptosis in colon cancer cells possibly through activation of caspase-3 whereas the levels of bcl-2 family proteins were not altered. We conclude that mesalazine inhibits growth of colon cancer cells largely through a mitotic arrest, which has not been reported for NSAID so far. Mesalazine also induces apoptosis through partial activation of caspases similar to, although weaker than, established chemopreventive agents. These findings may suggest a potential of mesalazine as a chemopreventive agent for colorectal cancer.
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PMID:Mesalazine causes a mitotic arrest and induces caspase-dependent apoptosis in colon carcinoma cells. 1266 3

The gastrointestinal epithelium is known to undergo constant and rapid renewal resulting in millions of cells being shed into the fecal stream every day. The conventional wisdom was that these cells disintegrate upon exfoliation and will not survive the transit through the intestinal tract. In 1990, we (P.N.) made the discovery that a significant number of these cells remain intact and viable and that they can be isolated. The implications of this important discovery became apparent when we demonstrated that these cells are exclusively of colonic origin, are anatomically representative of the entire colon, and can be used for clinical investigations of disease processes. The term coprocytobiology (CCB) was coined to encompass the broad range of applications of this new technology. The somatic cell sampling and recovery (SCSR) process involves the isolation of exfoliated colonocytes from a small sample of stool ( approximately 1 g) collected and transported in a unique medium at ambient temperature, providing cells for the detection of a number of biomarkers of disease propensity. These exfoliated colonocytes express cytokeratins indicating epithelial lineage as well as colon-specific antigen. Over the years, the study of exfoliated colonocytes has provided striking new insights into the biology of colon cancer and inflammatory bowel disease, including detection of p53 gene mutations, reverse transcriptase polymerase chain reaction amplification, and identification of CD44 splice variants, neoplasia-associated specific binding of plant lectins, and expression of COX-2, the inducible form of cyclooxygenase. The functional diversity of cells isolated by SCSR is revealed by the demonstration of cell surface markers such as secretory component, IgA, and IgG on the one hand and the amplification and cloning of the human insulin receptor and the expression of the multidrug resistance gene mdr-1 on the other hand. This review portrays the immense potential of CCB as a powerful tool for investigating the pathophysiology of disease, identifying genetic variants in pharmacogenetics, assessment of mucosal immunity, and several other applications that use somatic cells.
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PMID:Coprocytobiology: on the nature of cellular elements from stools in the pathophysiology of colonic disease. 1270 72

Ulcerative colitis and Crohn's disease (together known as Inflammatory Bowel Disease or IBD) are both associated with increased risk for colorectal cancer. Although it is conventional to emphasise differences between IBD-associated and sporadic colon cancer, such as a lower rate of Adenomatosis Polyposis Coli mutations and earlier p53 mutations, IBD-associated cancer has a similar dysplasia-cancer sequence to sporadic colon cancer, similar frequencies of major chromosomal abnormalities and of microsatellite instability and similar glycosylation changes. This suggests that IBD-associated colon cancer and sporadic colon cancer might have similar pathogenic mechanisms. Because the normal colon is arguably in a continual state of low-grade inflammation in response to its microbial flora, it is reasonable to suggest that both IBD-associated and sporadic colon cancer may be the consequence of bacteria-induced inflammation. We have speculated that the glycosylation changes might result in recruitment to the mucosa of bacterial and dietary lectins that might otherwise pass harmlessly though the gut lumen. These could then lead to increased inflammation and/or proliferation and thence to ulceration or cancer. The glycosylation changes include increased expression of onco-fetal carbohydrates, such as the galactose-terminated Thomsen-Friedenreich antigen (Gal beta1,3GalNAc alpha-), increased sialylation of terminal structures and reduced sulphation. These changes cannot readily be explained by alterations in glycosyltransferase activity but similar changes can be induced in vitro by alkalinisation of the Golgi lumen. Consequences of these changes may be relevant not only for cell-surface glycoconjugates but also for intracellular glycoconjugates.
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PMID:Altered glycosylation in inflammatory bowel disease: a possible role in cancer development. 1282 Jul 18


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