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PubMed1993

Atheroemboli-associated polyps of the sigmoid colon.

Atheroemboli-associated inflammatory type polyps localized to a portion of the sigmoid colon occurred in a 68-year-old diabetic man presenting with a 2-year history of bloody diarrhea and abdominal pain. The patient underwent segmental resection of the sigmoid colon. The specimen contained 15 polyps ranging from 0.3 to 1.9 cm in greatest dimension, localized to an 8-cm length of sigmoid colon. The polyps had an edematous submucosa with a superficially ulcerated mucosa. Microscopically, arterioles within the submucosa of the polyps contained organized atheroemboli. The overlying mucosa was largely replaced by granulation tissue, with foci of coagulation necrosis present in residual mucosa. The remainder of the bowel was unremarkable. The histologic diagnosis of atheroembolization to the gastrointestinal tract is difficult, requiring the inclusion of submucosa with atheroemboli in the biopsy tissue. Ischemic ulcers and erosions as well as inflammatory polyps related to atheroemboli may require deeper biopsy for etiologic diagnosis.

Aged↗
PubMed1997

Effect of aspirin on cell proliferation and differentiation of colon adenocarcinoma Caco-2 cells.

Several lines of evidence suggest that long-term treatment with non-steroidal anti-inflammatory drugs may reduce the risk of colon cancer and the size and number of colonic polyps in patients with familial adenomatous polyposis. Aspirin has also been shown to inhibit cell proliferation in human tumor cell lines and to induce apoptosis in colonic mucosa of familial polyposis patients. To elucidate the molecular mechanisms of the antiproliferative action of aspirin, we studied the effects of aspirin on cell growth and differentiation of the human colon carcinoma Caco-2 cell line. These cells represent a useful tool for studying the mechanisms involved in the regulation of cell growth and differentiation of intestinal epithelial cells since they spontaneously differentiate into polarized cells, expressing brush border enzymes. We show in this study that aspirin (0.1-10 mM) induces a profound inhibition of cell replication as assessed either by cell counts or thymidine incorporation. Moreover, aspirin concentrations of 5 and 10 mM induce apoptosis, whereas concentrations of 1 and 2 mM do not. The inhibition of growth is associated with a dose-dependent reduction in insulin-like growth factor II mRNA expression and with an increase in sucrase activity (a brush border enzyme) and apolipoprotein A-I mRNA expression, 2 specific markers of the differentiative status of this cell line. Our data thus show that aspirin-dependent inhibition of cell growth is associated with the enterocyte-like differentiation of Caco-2 cells.

Adenocarcinoma↗
PubMed2002

Increased membrane type 1 matrix metalloproteinase expression from adenoma to colon cancer: a possible mechanism of neoplastic progression.

PURPOSE: Membrane type 1 matrix metalloproteinase is a membrane-associated matrix metalloproteinase central to the degradation of basement membrane components via the activation of matrix metalloproteinase-2. Although membrane type 1 matrix metalloproteinase is overexpressed in invasive colon cancer, its expression in colonic polyps and carcinoma in situ has not been defined. In addition, the association of membrane type 1 matrix metalloproteinase expression by a primary tumor and recurrence of colon cancers has not been examined. METHODS: Immunoperoxidase staining was performed on randomly selected specimens containing adenoma (n = 17), carcinoma in situ (n = 9), or metastatic colon carcinoma (n = 8) with mouse monoclonal antibody to human membrane type 1 matrix metalloproteinase. Similar staining was also performed on randomly selected node-negative colon cancers that recurred within five years of resection (n = 17), matched for age, gender, stage, grade, and vascular, lymphatic, and perineural invasion, and node-negative colon cancers that did not recur within five years of resection (n = 17). Staining for membrane type 1 matrix metalloproteinase was graded. Mean scores for the groups were compared by Wilcoxon test. RESULTS: We found a progressive and significant increase in the mean score of membrane type 1 matrix metalloproteinase from normal mucosa to adenoma (P < 0.001), carcinoma in situ (P < 0.006), and invasive cancer (P < 0.009). However, there was no difference in membrane type 1 matrix metalloproteinase expression between the recurrent and nonrecurrent groups of node-negative colon cancer (P = not significant). CONCLUSIONS: These data suggest that membrane type 1 matrix metalloproteinase expression increases with progression from normal mucosa to invasive adenocarcinoma; however, it cannot be used as a prognostic indicator on which adjuvant therapy is based in node-negative colon cancer because of its failure to predict recurrence in this patient group.

Adenoma↗
PubMed2005

Polypoid pleomorphic sarcoma of the colon.

In contrast to common colonic epithelial neoplasms, polypoid mesenchymal tumors of the colon are extremely rare. The majority of uncommon gastrointestinal mesenchymal tumors are associated with the so-called gastrointestinal stromal tumors (GIST). We present a case of a rare colonic pleomorphic sarcoma, macroscopically mimicking a common epithelial colonic polyp, which did not match the criteria of GIST. In this case report we discuss the clinical and pathological characteristics of a rare polypoid-shaped, pleomorphic colonic sarcoma and refer a mark-off to other rare mesenchymal neoplasms of the gut.

Aged↗
PubMed1996

Microscopic colitis is a cause of large bowel diarrhea in Northern India.

Chronic diarrhea is a common clinical problem. To determine the possible causes in North India, we studied prospectively 71 patients with chronic diarrhea of the large bowel type. A definite diagnosis could be established in 70 patients. Ulcerative colitis was found in 18 patients, colorectal malignancies in three, colonic polyps in three, and irritable bowel syndrome in 32. In addition, seven patients with seronegative polyarthritis and chronic diarrhea were found to have chronic inflammation of the colon on histology. Two patients had pseudodiarrhea, and no diagnosis could be established in one patient. The remaining five patients with chronic diarrhea showed histologic evidence of chronic colonic inflammation with predominantly mononuclear cell infiltration of the lamina propria and increased intraepithelial lymphocytes, but results of their radiologic and endoscopic studies were normal. These five patients were classified as having microscopic (lymphocytic) colitis. We conclude that the causes of chronic diarrhea in North India patients are similar to a large extent to those seen in Western populations. Microscopic (lymphocytic) colitis is a definite clinicopathologic entity that should be considered in the differential diagnosis of chronic diarrhea.

Adolescent↗
PubMedDate not supplied

Arginine metabolism in benign and malignant disease of breast and colon: evidence for possible inhibition of tumor-infiltrating macrophages.

L-Arginine concentrations have been measured in benign and malignant breast and colonic neoplasms and compared with the macrophage content and arginase activity within these tumors. Our study confirmed previous findings of elevated plasma arginine concentrations in malignancy and demonstrated that tissue free-arginine concentrations are substantially higher in malignant (mean 9.8 mumol/g protein) than benign (2.8 mumol/g protein) breast disease. Similarly, malignant colonic neoplasms had a higher free-arginine concentration than benign colonic polyps (14.0 vs. 7.0 mumol/g protein). The macrophage content of the malignant tumors was also significantly higher than in the benign conditions (278 vs 29/high power field in breast disease), but despite this, there was no detectable difference in the arginase activity. These findings suggest that tumor-infiltrating macrophages are not able to produce this enzyme, and/or its activity is inhibited within the tumor cell milieu. The differences observed in the arginine concentrations within these lesions has potentially important implications for the pathway of arginine metabolism and local host antitumor responses.

Arginase↗
PubMed1992

Cigarette smoking, alcohol use and adenomatous polyps of the sigmoid colon.

The relationship of adenomatous polyps of the sigmoid colon with cigarette smoking and alcohol use was investigated in male self-defense officials in Japan. In the comparison between 116 cases and 930 controls, total ethanol intake was not at all associated with the risk of adenomatous polyps, but cigarette smoking was strongly related to adenomatous polyps. After adjustment for total ethanol intake, body mass index and rank, odds ratios (and 95% confidence interval) for the categories of 0, 1-399, 400-799, and 800 or more cigarette-years were 1.0 (referent), 2.3 (1.1-4.6), 2.9 (1.5-5.4) and 3.2 (1.6-6.5), respectively. Among five alcoholic beverages (sake, shochu, beer, whiskey including brandy, and wine), only whiskey consumption was weakly related to the risk of adenomatous polyps. Because the present findings disagree with an earlier observation on self-defense officials, we examined the association with smoking and alcohol use separately for small (less than 5 mm) and large (greater than or equal to 5 mm) adenomas, combining data from these two studies. Cigarette smoking was more strongly associated with small adenomas while the positive association with certain alcoholic beverages were largely confined to large adenomas. These findings suggest that cigarette smoking and alcohol use may be linked with the development of adenoma at different stages of colon tumorigenesis.

Adenoma↗
PubMed1991

Oncogene-mediated transformation. An in vitro model for colon carcinogenesis.

Evaluation of molecular events in human colon polyps and tumors has revealed constitutive elevated expression of c-myc, activation of both ras and src proto-oncogenes, and allelic deletion events involving inactivation of putative regulatory genes, including p53. To evaluate the contribution of each of these events to colon carcinogenesis, it is desirable to establish epithelial cell lines representing different stages of neoplastic progression. Such in vitro models can be used to establish a primary role for different genes implicated in neoplastic transformation, identifying events involved in multistep carcinogenesis and delineating the factors modulating cellular transformation. We present herein a summary of such an in vitro model for colon carcinogenesis using the introduction of relevant genetic elements into normal mucosa to identify the molecular steps and accompanying cellular events underlying neoplastic progression in the colon.

Animals↗
PubMed2002

Challenge in the differentiation between attenuated familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer: case report with review of the literature.

The clinical differentiation between hereditary nonpolyposis colorectal cancer (HNPCC) and attenuated familial adenomatous polyposis (AFAP) is very difficult. The 62-yr-old proband presented with duodenal adenocarcinoma. His history of subtotal colectomy for colon cancer, the rarity of duodenal adenocarcinoma in the general population, and his family history of colon cancer made us suspect that he might have FAP. We investigated this family by obtaining medical records and performing gene analysis. The proband had only 10 adenomatous colon polyps when he underwent subtotal colectomy for the cancer, so classic FAP was excluded. His family history included rectal cancer in his brother at 69 yr of age, colon cancer in his mother at 75 yr, and colon cancer in one maternal cousin at 42 yr. Three months after we started to study this family, the proband's 32-yr-old son presented with rectal cancer. His family fulfilled the Amsterdam criteria for HNPCC, but AFAP could not be excluded. Upon gene testing, the proband was negative for APC gene germline mutation, which made AFAP highly unlikely. Moreover, high microsatellite instability (MSI) was detected in his adenomas and cancer tissues. The fulfillment of Amsterdam criteria, the exclusion of FAP and AFAP, and the high MSI established the diagnosis of HNPCC in this family. We also summarize the differences between FAP, AFAP, and HNPCC; extend the graphic description of the MSI mechanism; and propose a diagnostic strategy for HNPCC.

Adenomatous Polyposis Coli↗
PubMed2000

Influence of K-ras activation on the survival responses of Caco-2 cells to the chemopreventive agents sulindac and difluoromethylornithine.

The nonsteroidal anti-inflammatory drug sulindac and the ornithine decarboxylase inhibitor difluoromethylornithine (DFMO) are both potent inhibitors of colon carcinogenesis in experimental models of this disease. The combination of these two agents is undergoing evaluation as a strategy for colon cancer chemoprevention in humans with resected colon polyps. We evaluated the effects of the major sulfide and sulfone metabolites of sulindac and DFMO alone, or in combinations, on the growth and survival of Caco-2 colon cancer-derived cells and in clones of these cells transfected with an activated K-ras oncogene. Both the sulfide and sulfone metabolites of sulindac reduced cell viability, measured by colony-forming assays, primarily by inducing apoptosis. Expression of an activated K-ras oncogene caused cells treated with either sulindac sulfide or sulfone to undergo apoptosis earlier than nontransfected controls. However, clonogenic survival, measured 2 weeks after drug treatment, was the same in both Caco-2 and ras-transfected Caco-2 cells treated with sulindac metabolites. A 24-h treatment with DFMO caused a dose-dependent decrease in the colony-forming ability of cells expressing an activated K-ras but had no effect on the viability of the parental Caco-2 cells. The DFMO-dependent decrease in colony formation in K-ras-activated cells occurred in the absence of apoptosis. Assessment of cell survival by colony-forming assays indicated that these two agents acted in an additive manner when combined. These data indicate that K-ras can influence the kinetics of apoptosis induction by sulindac metabolites and cell survival in response to DFMO. However, cytotoxicity induced by these agents occurs via unique mechanisms. These studies suggest that the combination of DFMO and sulindac may be useful in human cancer prevention strategies.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

The clinical correlates of a 3' truncating mutation (codons 1982-1983) in the adenomatous polyposis coli gene.

Familial adenomatous polyposis (FAP) is caused by mutations in the adenomatous polyposis coli (APC) gene, and different mutations may produce different clinical pictures. Most mutations occur in the 5' half of the gene, and mutations toward the 3' end are rare. The aim of this study was to document the phenotypes in a family with a truncating mutation at codons 1982-1983, one of the most 3' mutations on record. Colonic polyps in this family were much less numerous, and their growth was delayed compared with the classical FAP picture, and malignant degeneration occurred considerably later. Two individuals had sparse colonic but profuse gastric fundic gland polyposis. Gardner's syndrome stigmata were variable, and a desmoid tumor was recorded in 1 person.

Adenomatous Polyposis Coli↗
PubMed1992

Cellular distribution of a colonic adenoma-associated antigen as defined by monoclonal antibody Adnab-9.

Adenomatous colonic polyps constitute a precursor for colorectal cancer. Antibodies to these precancerous lesions might identify specific early tumor antigens. Adnab-9 is a murine monoclonal antibody raised against membranes of colonic adenomas. Adnab-9 binding in colonic washings (effluent) correlates with the presence of colorectal cancer. Immunohistochemical staining with Adnab-9 shows cytoplasmic reactivity in scattered cells in 4 of 31 adenomatous tissue sections, 0 of 14 sections of colorectal cancer cells, and 1 of 8 normal-appearing colonic mucosa specimens examined. Adnab-9 recognized a dominant M(r) 87,000 protein species in tissue extracts in the membrane-bound fraction of effluent by Western blotting. Adnab-9 binding by enzyme-linked immunosorbent assay in adenomatous extracts is higher than cancer or normal tissue, is membrane-bound, and is absent from established colorectal cancer cell lines. This distribution and nature of immunostaining suggest that Adnab-9 recognizes a determinant associated with the membrane component of a subpopulation of adenoma cells which may have a role in early colorectal neoplasia.

Adenoma↗
PubMed1993

Exclusion of the APC gene as the cause of a variant form of familial adenomatous polyposis (FAP)

Familial adenomatous polyposis (FAP) is a premalignant disease inherited as an autosomal dominant trait, characterized by hundreds to thousands of polyps in the colorectal tract. Recently, the syndrome has been shown to be caused by mutations in the APC (adenomatous polyposis coli) gene located on chromosome 5q21. We studied two families that both presented a phenotype different than that of the classical form of FAP. The most important findings observed in these two kindreds are (a) low and variable number of colonic polyps (from 5 to 100) and (b) a slower evolution of the disease, with colon cancer occurring at a more advanced age than in FAP in spite of the early onset of intestinal manifestations. To determine whether mutations of the APC gene are also responsible for this variant syndrome, linkage studies were performed by using a series of markers both intragenic and tightly linked to the APC gene. The results provide evidence for exclusion of the APC gene as the cause of the variant form of polyposis present in the two families described.

Adenomatous Polyposis Coli↗
PubMed1999

The onset and extent of genomic instability in sporadic colorectal tumor progression.

Cancer cell genomes contain alterations beyond known etiologic events, but their total number has been unknown at even the order of magnitude level. By sampling colorectal premalignant polyp and carcinoma cell genomes through use of the technique inter-(simple sequence repeat) PCR, we have found genomic alterations to be considerably more abundant than expected, with the mean number of genomic events per carcinoma cell totaling approximately 11,000. Colonic polyps early in the tumor progression pathway showed similar numbers of events. These results indicate that, as with certain hereditary cancer syndromes, genomic destabilization is an early step in sporadic tumor development. Together these results support the model of genomic instability being a cause rather than an effect of malignancy, facilitating vastly accelerated somatic cell evolution, with the observed orderly steps of the colon cancer progression pathway reflecting the consequences of natural selection.

Adenomatous Polyps↗
PubMed1997

[Ulcerative colitis: activity of antioxidant enzymes of the colonic mucosa].

OBJECTIVES: Reactive oxygen species are regarded as mediators of inflammation in ulcerative colitis. Antioxidant enzymes are the primary defense against reactive oxygen species. We investigated the activities of antioxidant enzymes-superoxide dismutase, catalase and glutathion peroxidase-in colonic mucosa biopsy specimens obtained at different phases of the disease in patients given vitamin E therapy or not and in controls. PATIENTS AND METHODS: Biopsy specimens were obtained from 29 patients with ulcerative colitis and from 18 healthy controls. Ten patients on maintenance drug therapy were also given a 300 mg daily oral dose of vitamin E. RESULTS: Enzyme activities were significantly increased in inflamed non-polypous colonic mucosa in patients with active ulcerative colitis, while they were similar to activities observed in controls during quiescent phases of the disease. Antioxidant enzyme activities in specimens from inflammatory polyps remained high even in patients in clinical remission. Administration of vitamin E resulted in a significant reduction of glutathion peroxidase activity in the colonic mucosa. CONCLUSION: These findings indirectly confirm that important quantities of reactive oxygen species are formed in ulcerative colitis. Further studies are needed to elucidate the relationship of these changes with the pathogenesis of ulcerative colitis.

Adult↗
PubMed1981

[Leukocyte-adherence-inhibition reactivity in patients with colorectal and pancreatic cancer (author's transl)].

The immunoreactivity of patients with colorectal or pancreatic cancer was investigated by a modified leukocyte adherence inhibition test (LAI). The microcapillary-LAI-test was easy to practise and measurements had a low intra-assay coefficient of variation. The number of false positive results was low, only 1 of 39 patients with benign disease and not one of 13 healthy volunteers reacted in the presence of colorectal carcinoma extracts. In 43 patients with colorectal cancer 17 of 25 (68%) with Dukes' B & C and 15 of 18 (83%) with Dukes' D cancer were LAI positive. Of the 19 patients with colon polyps 6 positive results were observed, exclusively in case of large villous adenomas, polyposis coli and one polyp with a focal carcinoma. 10 of 11 patients with pancreatic cancer reacted in the test. Leukocytes from patients with limited cancer of other source, when tested with colorectal or pancreatic carcinoma extracts, showed a negative LAI response. However, in case of metastatic diseases some crossreactions were observed, which resulted in false positive tests. Following our results, the LAI test could be of value in the diagnosis of gastrointestinal carcinoma.

Aged↗