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PubMed2004

Prostaglandin E2 synergistically enhances receptor tyrosine kinase-dependent signaling system in colon cancer cells.

Cyclooxygenase (COX)-generated prostaglandin E(2) (PGE(2)) plays critical roles in colorectal carcinogenesis. Recently, we have shown that PGE(2) and transforming growth factor-alpha synergistically induces the expression of amphiregulin (AR) in colon cancer cells (Shao, J., Evers, B. M., and Sheng, H. (2003) Cancer Res. 63, 5218-5223). In this study, we demonstrated synergistic actions of PGE(2) and the receptor tyrosine kinase signaling system in AR expression and in tumorigenic potential of colon cancer cells. Activation of the Ras/Raf/MAPK pathway induced AR transcription in colon cancer LS-174 cells that was enhanced by PGE(2) in a synergistic fashion. The cAMP-responsive element within the AR promoter was required for the synergistic activation of AR transcription. An Sp1 element was responsible for the basal transcription of AR and significantly enhanced the synergy between PGE(2) and the epidermal growth factor receptor (EGFR) signaling system. Furthermore, activation of both PGE(2) and EGFR signaling pathways synergistically promoted the growth and migration of colon cancer cells. Our results suggest that COX-2/PGE(2) may exert pro-oncogenic effects through synergistic induction of receptor tyrosine kinase-dependent signaling pathway, thus, provide a novel mechanism for the combinatorial treatment of colonic neoplasms targeting both COX-2/PGE(2) and the EGFR system that has demonstrated remarkable advantages.

Antineoplastic Agents↗
PubMed1978

Progress in radiology: colorectal tumors: pathology and detection.

The prognosis in colorectal neoplasia has not improved in the past 20 years despite improved diagnostic techniques. The greatest promise lies in wider screening and earlier radiographic and endoscopic detection. To clarify the radiologist's role in finding large bowel tumors, the clinical, pathologic, and radiologic literature is reviewed. Since individuals over 40 years of age harbor the bulk of colon neoplasms, the most diligent efforts to detect these lesions should be made in this group. Controlled studies comparing single and double contrast barium enema techniques are lacking, but available data suggest that the double contrast examination is more sensitive for detection of the numerous small, but potentially malignant colon tumors. Careful radiographic technique, including a thoroughly clean colon, is critical for accurate detection regardless of which technique is used.

Adenoma↗
PubMed1991

Loss of heterozygosity of p53 gene and p53 protein expression in human colorectal carcinomas.

The p53 gene is a tumor suppressor gene located on chromosome 17p. Deletions of this chromosome and point mutations of p53 have been implicated in the development of colonic neoplasms. We have analyzed the loss of heterozygosity of the human p53 tumor suppressor gene in 40 cases of colorectal carcinoma using two restriction fragment length polymorphisms detected by BglII and AccII restriction enzymes. p53 gene product expression was studied immunohistochemically in 64 colorectal carcinomas, 18 adenomas, and 40 normal colonic mucosae using an anti-human p53 monoclonal antibody (Pab 1801) and the avidin-biotin-peroxidase complex technique. Twelve of the 40 patients (30%) were polymorphic for the p53 gene. In ten of these informative patients (83%), the tumor samples showed the loss of one allele when compared with normal colorectal samples of the same patient. One of the homozygous patients showed a loss of both p53 alleles. p53 immunostaining was observed in 43 of 64 carcinomas (67%) but only in two adenomas (11%). These two positive adenomas showed areas of carcinoma in situ. The normal mucosa was always negative. No relation could be found between p53 immunostaining and the degree of differentiation, the extension of the tumor, or the Ki-67 proliferative index. Mucinous carcinomas and right-side carcinomas were less p53 immunoreactive (25% and 52%, respectively) than the usual adenocarcinomas (73%) and distal tumors (72%). These findings suggest that p53 may be a target of chromosome 17 deletions and that this gene may play a role in the malignant transformation of adenomas. BglII and AccII restriction fragment length polymorphism analysis of the p53 gene may be a useful and direct technique to detect allelic loss of this gene in tumors.

Adenocarcinoma↗
PubMed1998

Use of self-expanding metallic stents in the management of obstruction of the sigmoid colon.

OBJECTIVE: The purpose of our study was to evaluate the clinical efficacy of a new self-expanding metallic endoprosthesis in the management of distal colonic obstruction in seven patients. CONCLUSION. The Wallstent enteral endoprosthesis is safe and effective in relieving obstruction in patients with resectable colonic tumors. Once in place, the Wallstent permits planned elective surgery and avoids a temporary stoma. In addition, the Wallstent can palliate patients with obstruction due to advanced colonic neoplasms. The results of our preliminary study are promising and show a low incidence of complications.

Acute Disease↗
PubMedDate not supplied

Colorectal cancer detection in a Community Hospital Screening Program.

In its first 4 1/2 years of operation in the Long Beach Community Hospital Cancer Detection Center, among the 5,595 persons examined, 16 cases of colorectal cancer were discovered. Fourteen of the 16 had symptoms referable to neoplasms. Eight had lesions found on proctosigmoidoscopic examination. Nine had positive findings for occult blood in stool samples, a 7.5% cancer detection rate among the 120 with positive stool sample findings. Six patients with cancer submitted one to four stool specimens that showed negative findings on occult blood testing, and one patient submitted no specimen. Although valuable in screening, stool testing for occult blood will not detect all colonic neoplasms. The complaints of pain, altered bowel habits, or tenesmus warrant sigmoidoscopic examination, barium enema studies, or both, whether findings in stool samples are positive or negative.

Adult↗
PubMed1987

Repeat colonoscopy after endoscopic polypectomy.

The records of all patients undergoing endoscopic polypectomy between December 1979 and December 1982 were reviewed. One hundred seventy-two patients underwent colonoscopic polypectomy in the absence of carcinoma or inflammatory bowel disease. Of these, the polyp could not be retrieved in 4, and 19 were lost to follow-up. One hundred forty-nine patients underwent subsequent endoscopy from one to four years after the initial polypectomy. Seventy-five (50.3 percent) of the patients developed new polyps. Although 61 of the 75 patients with new polyps were identified in the first two years, new polyps were noted throughout all four years. The presence of multiple polyps on the initial examination was statistically significant in predicting new polyps. The age and sex of the patients, size of the polyps, and the presence of atypia did not identify patients at higher risk for new polyps. The data indicate that new polyps are more likely to develop in patients who had a previous polyp. It would appear that annual examinations should be performed until two successive examinations are negative. Following a second negative examination, reexamination at two- or three-year intervals, unless symptomatic, would appear to be adequate.

Adenoma↗
PubMed1995

Sialosyl-Tn antigen: initial report of a new marker of malignant progression in long-standing ulcerative colitis.

BACKGROUND & AIMS: Expression of the mucin-associated carbohydrate antigen sialosyl-Tn (STn) correlates with malignant transformation in sporadic colonic neoplasms. The aim of this study was to analyze STn antigen expression in patients with long-standing ulcerative colitis (UC). METHODS: STn antigen was assessed by immunohistochemistry in archival tissues. Study A was a retrospective chronological case-control study. Serial surveillance colonoscopic biopsy specimens without inflammation or dysplasia were analyzed in 7 patients who developed colon cancer and in 8 controls who did not develop colon cancer. Study B analyzed the anatomic distribution of STn expression in 17 cancer-bearing (case) and 6 cancer-free (control) colectomy specimens from patients with UC. In some colectomy specimens, STn was compared with aneuploidy, which was determined by flow cytometry. RESULTS: In study A, among the 7 patients with UC who developed cancer, 6 patients (86%) expressed STn in at least one prior nondysplastic surveillance biopsy specimen from the same site. Only 3 of 8 control patients (38%) expressed STn. In study B, STn was expressed in 40 of 82 specimens (49%) from cancer-bearing colons but only 8 of 62 specimens (13%) from cancer-free colons. STn was expressed in most aneuploid areas but was also found in diploid, nondysplastic mucosa. CONCLUSIONS: STn antigen seems to be a promising marker of cancer risk in patients with UC.

Aneuploidy↗
PubMed1998

p53 and bcl-2 protein expression in rectosigmoid adenomas.

OBJECTIVE: The aim of this study was to evaluate whether p53 or bcl-2 protein expression in rectosigmoid adenomas is associated with histological characteristics of the adenomas and with presence of synchronous advanced proximal neoplasms. METHODS: Seventy-six average-risk patients who underwent total colonoscopy and had rectosigmoid adenoma(s) were studied. An adenoma was considered advanced if villous histology and/or severe dysplasia and/or diameter > 1 cm were present. p53 and bcl-2 protein expression was immunohistochemically examined using specific monoclonal antibodies. RESULTS: p53 protein was detected in 43% and bcl-2 in 93% of the 76 rectosigmoid adenomas. Advanced compared with nonadvanced adenomas were significantly more frequently p53-positive (28 of 44 or 63.6% vs five of 32 or 15.6%, p < 10(-4)) or had a bcl-2 score of 12 (20 of 44 or 45.5% vs five of 32 or 15.6%, p = 0.007). Proximal advanced neoplasms were mainly found in patients with rectosigmoid adenomas positive for p53 and with a bcl-2 score of 12 (six of 17 or 35.3% vs 2/59 or 3.4%, OR: 15.6, p = 0.001) and in particular in those with advanced rectosigmoid adenomas positive for p53 and with a bcl-2 score of 12 (six of 13 or 46.2% vs two of 31 or 6.5%, OR: 12.4, p = 0.007). CONCLUSION: p53 expression and bcl-2 protein overexpression in rectosigmoid adenomas are associated with advanced histology and a high risk of synchronous advanced proximal colon neoplasm.

Adenoma↗
PubMed1989

Heterogeneity in the response of familial polyposis epithelial cells and adenomas to increasing levels of calcium in vitro.

A biomarker of increased risk for colon cancer is abnormally high proliferation of colonic epithelial cells. The authors developed an in vitro assay that measures the ability of human colonic epithelial cells that are in progressive stages of abnormal development to respond to direct application of calcium as the chloride in tissue culture medium. Incorporation of 3H-thymidine and autoradiography in situ was employed to measure the number of proliferating cells cultured at 0.1 mM CaCl2, the optimum level for growth, and 2.2 to 5 mM, both levels achievable in the colonic lumen. Abnormal cell proliferation was reduced in biopsies from 13 of 14 patients without familial polyposis but at increased risk for colon cancer because of previous colonic neoplasms or familial association; in cells from three of four asymptomatic individuals in familial polyposis families at risk for that disease; and in cells of three of ten patients symptomatic with familial polyposis. Growth of tubular adenoma cells from two of seven familial polyposis patients was also inhibited by calcium. Growth inhibition was not observed in more advanced colon tumors including eight adenomas, either villotubular or villous, and five carcinomas. These findings indicate heterogeneity within the familial polyposis phenotype for the normal cellular response to growth inhibition by calcium, and a further loss of response to calcium as these cells progress toward malignancy.

Adenoma↗
PubMed2004

Colonic adenocarcinomas rapidly induced by the combined treatment with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine and dextran sodium sulfate in male ICR mice possess beta-catenin gene mutations and increases immunoreactivity for beta-catenin, cyclooxygenase-2 and inducible nitric oxide synthase.

Heterocyclic amines are known to be important environmental carcinogens in several organs including the colon. The aim of this study was to induce colonic epithelial malignancies within a short-term period and analyze the expression of cycooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) and beta-catenin, and mutations of beta-catenin gene in induced tumors. Male Crj: CD-1 mice were given a single i.g. administration (200 mg/kg body wt) of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) or 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) followed by 2% dextran sodium sulfate (DSS) in the drinking water for a week. The expression of beta-catenin, COX-2 and iNOS was immunohistochemically assessed in colonic epithelial lesions and the beta-catenin gene mutations in colonic adenocarcinomas induced were analyzed by the single strand conformation polymorphism method, restriction enzyme fragment length polymorphism and direct sequencing. At week 16, a high incidence of colonic neoplasms with dysplastic lesions developed in mice that received PhIP and DSS, but only a few developed in those given MeIQx and DSS. Immunohistochemically, the adenocarcinomas induced were all positive for three proteins. All seven adenocarcinomas induced by PhIP and DSS have mutations. The findings suggest that DSS exerts powerful tumor-promoting effects on PhIP-initiated colon carcinogenesis in mice and this mouse model is useful for investigating environment-related colon carcinogenesis within a short-term period.

Adenocarcinoma↗
PubMed1989

1,2-Dimethylhydrazine-induced carcinogenesis influenced by different colonic anastomoses in rats.

Dispensing subcutaneously 1,2-dimethylhydrazine, intestinal carcinogenesis was investigated in male Fisher rats with different surgical colonic anastomoses, producing blind gut loops of isoperistaltic high (fecal stasis) and anisoperistaltic low fecal contact. One hundred and eight rats, except 1 rat of the control group, developed colonic neoplasms. In contrast to the control group, mainly in anastomotic areas and in isoperistaltic blind gut loops with intensive fecal contact huge adenocarcinomas of exophytic growth appeared with a mean tumor diameter (MTD) of 1.9 +/- 0.7 to 2.2 +/- 0.8 cm. Even in the control group, where rats only underwent laparotomy, we observed small polypoid adenocarcinomas mainly located in the distal colon (MTD: 0.7 +/- 0.3 cm). Anastomotic areas and isoperistaltic blind loops with intensive fecal contact proved to be regions with a higher risk for carcinoma formation.

1,2-Dimethylhydrazine↗
PubMed1993

The effect of the fiber components cellulose and lignin on experimental colon neoplasia.

Sixty Sprague-Dawley rats were pair-fed one of three nutritionally identical diets. One diet contained "low-fiber" (3.8% crude fiber); the others contained "high fiber" (28.7% crude fiber) composed of either cellulose or lignin. Although both "high fiber" diets had similar stool bulking effects, only the cellulose diet was associated with a reduction in 1,2-dimethylhydrazine (DMH)-induced colon neoplasms. The cellulose diet was also associated with distinct changes in the gut bacterial profile and with a lowered serum cholesterol.

1,2-Dimethylhydrazine↗
PubMed2000

Significance of a normal surveillance colonoscopy in patients with a history of adenomatous polyps.

PURPOSE: The aim of this study was to determine the appropriate surveillance for patients with a history of adenomatous polyps whose last colonoscopic examination was normal. METHODS: This was a retrospective review of a database of 7,677 colonoscopies (1990 to 1996). In patients under colonoscopic surveillance, we reviewed cases of patients who had received three colonoscopies (an index (initial) colonoscopy positive for adenomas and 2 follow-up colonoscopies (interim and final)). The risk of adenomas and cancers at final follow-up colonoscopy was compared between patients having a normal interim colonoscopy and those with a positive interim colonoscopy. The risk at final colonoscopy was also stratified by time interval and the size and number of adenomas at the initial index colonoscopy. RESULTS: Two hundred four patients undergoing surveillance for adenomas met inclusion criteria. At index colonoscopy the median polyp size was 1 cm and median frequency was three polyps. At all follow-up colonoscopies, we detected 493 adenomas and one cancer (median follow-up, 55 months). At 36 months patients with a normal interim colonoscopy (n = 91) had significantly fewer polyps than patients with a positive interim colonoscopy (n = 113; 15 vs. 40 percent; P = 0.0001). By 40 months, adenomas were detected in more than 40 percent of patients in both groups. The risk after a normal interim colonoscopy was not affected by time interval or number or size of polyps. Adenomas found subsequent to a normal interim colonoscopy were dispersed throughout the colon in 28 patients and isolated to the rectosigmoid in 6 patients. CONCLUSIONS: In patients with a history of adenomas, a normal follow-up colonoscopy is associated with a statistically but not clinically significant reduction in the risk of subsequent colonic neoplasms. These patients require follow-up surveillance colonoscopy at a four-year to five-year interval.

Adenomatous Polyposis Coli↗
PubMed1997

Chemoprevention of azoxymethane-induced rat colon carcinogenesis by a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate.

In our studies to find natural compounds with chemopreventive efficacy in foods, using azoxymethane (AOM)-induced colonic aberrant crypt foci and colonic mucosal cell proliferation as biomarkers, a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate (ACA), present in the edible plant Languas galanga from Thailand was found to be effective. This study was conducted to test the ability of ACA to inhibit AOM-induced colon tumorigenesis when it was fed to rats during the initiation or post-initiation phase. Male F344 rats were given three weekly s.c. injections of AOM (15 mg/kg body weight) to induce colonic neoplasms. They were fed diet containing 100 or 500 ppm ACA for 4 weeks, starting one week before the first dosing of AOM (the initiation feeding). The other groups were fed the ACA diet for 34 weeks, starting one week after the last AOM injection (the post-initiation feeding). At the termination of the study (week 38), AOM had induced 71% incidence of colonic adenocarcinoma (12/17 rats). The initiation feeding with ACA caused significant reduction in the incidence of colon carcinoma (54% inhibition by 100 ppm ACA feeding and 77% inhibition by 500 ppm ACA feeding, P = 0.03 and P = 0.001, respectively). The post-initiation feeding with ACA also suppressed the incidence of colonic carcinoma (45% inhibition by 100 ppm ACA feeding and 93% inhibition by 500 ppm ACA feeding, P = 0.06 and P = 0.00003, respectively). Such inhibition was dose-dependent and was associated with suppression of proliferation biomarkers, such as ornithine decarboxylase activity in the colonic mucosa, and blood and colonic mucosal polyamine contents. ACA also elevated the activities of phase II enzymes, glutathione S-transferase (GST) and quinone reductase (QR), in the liver and colon. These results indicate that ACA could inhibit the development of AOM-induced colon tumorigenesis through its suppression of cell proliferation in the colonic mucosa and its induction of GST and QR. The results confirm our previous finding that ACA feeding effectively suppressed the development of colonic aberrant crypt foci. These findings suggest possible chemopreventive ability of ACA against colon tumorigenesis.

Animal Feed↗
PubMed1990

[Benign coloduodenal fistula caused by inflammatory pseudotumor of the colon].

We present a case of benign coloduodenal fistula, due to an inflammatory pseudotumor of the hepatic flexure of the colon, that was found included in a calcified hepatic cavity, presumably hydatic, that opened through a large fistulous orifice into the second duodenal portion. A barium enema satisfactorily demonstrated the colonic lesion and a fistulous tract. Although the preoperative diagnosis was of colonic neoplasm fistulized into the duodenum, the histopathological study of the surgical specimen did not demonstrate malignancy.

Aged↗
PubMed1983

Carcinogenic effects of intracolonic benzo[a]pyrene in beta-naphthoflavone-induced mice.

Benzo[a]pyrene (BP) was administered intracolonically to ICR/Ha and C57Bl/6 female mice, 1 mg/mouse, once weekly for 14 weeks. Half of the mice received beta-naphthoflavone (beta-NF, a mixed-function oxygenase inducer) i.p. 24 h prior to the BP. No colonic neoplasms were found in any of the mice after 18 months. However, the BP treatment did cause a significant increase in numbers of primary lung tumors, forestomach papillomas, mammary carcinomas, and sarcomas in one or both strains, relative to controls, and the incidence of all of these except for the sarcomas was significantly reduced by treatment with beta-NF prior to BP. Overall, the beta-NF pretreatment reduced total incidence of neoplasms by about 30% in the ICR/Ha mice and by about 60% in the C57Bl/6 mice, and did not potentiate the action of the carcinogen in any organ.

Animals↗
PubMed1987

Cell culture of human colon adenomas and carcinomas.

Cell lines were established from colon adenomas, including tubular and villous polyps, primary adenocarcinomas, and metastases arising in patients with colon adenocarcinomas. The protocol for cultivating these diverse tissues includes primary cultivation of tissue explants on a type I collagen gel followed by nonenzymatic subculture of the epithelial outgrowth. All early passages were accomplished using low subculture ratios. Cultured cells elaborate morphological structures which are similar to features present in the tissues from which they were cultivated. Specifically, all structural features of colon epithelial cells were identified, including junction formation, prominent microvilli, and mucin secretion, in several cell lines. Five cell lines cultured from colonic neoplasms at different stages of cancer progression were selected for detailed characterization. Cells grown from two tubular polyps had normal human karyotypes. Cells from a villous polyp and all adenocarcinomas were aneuploid with stable marker chromosomes. The established cell lines exhibit distinct phenotypes based on growth characteristics in vitro and in athymic mice; and it is suggested that these cell lines represent useful models for studying the evolution of colon cancer from a benign to an aggressive cell type.

Adenocarcinoma↗