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PubMed2005

Risk of colorectal adenomas in a multiethnic Asian patient population: race does not matter.

BACKGROUND: Ethnic differences have been reported for colorectal polyps and large bowel cancer; although the supporting data is weak and insufficient to draw firm conclusions. AIM: We undertook this study to determine whether such racial disparity in colorectal adenomas exists in an ethnically mixed non-migrant population. The prevalence, histology and distribution of colonic polyps were documented as well as other known risk factors for colorectal malignancy. METHODS: In this prospective cross-sectional study, 311 consecutive referred and self-referred multiracial patients attending for colonoscopy over a 41-month period in a private endoscopy center were recruited. The mean age of the study population was 51.8 +/- 14 years (range 16-91). The male to female ratio was 1.1 and an ethnic breakdown as follows: 87 Malays, 115 Chinese and 109 Indians. RESULTS: Sixty-three adenomas were recorded in 36 patients: six Malays, 19 Chinese and 11 Indians. Of these adenomas, 59 were polypoid, three flat and one depressed. The majority of adenomas 42/63 (67%) were distal to the splenic flexure as were all (10/10) the Duke's A carcinomas and 6/8 (75%) of the advanced cancers. Patients with adenoma(s) compared with those without (controls) were significantly older (P = 0.005), more likely to have a family history of colorectal cancer (P = 0.005), and showed a trend towards significance for ethnic group (P = 0.09) on univariate analysis. Using logistic regression analysis, only family history (P = 0.05) and age > or = 50 years (P = 0.011) were found to be significantly associated with adenomas. CONCLUSION: Risk factors for colonic adenoma(s) in our cohort of symptomatic multiethnic patients attending for colonoscopy do not seem to differ from those reported elsewhere and, in particular, race does not appear to be a factor.

Adenoma↗

PubMed1997

Medium-large polyps of the colon: a contribution for their clinical profile and a proper surveillance.

A retrospective analysis of polypoid lesions of the colon larger than 1 cm was performed with the aim to study their characteristics and a proper surveillance schedule. We reviewed all colon polypoid lesions larger than 1 cm found and treated during the period January 1984- December 1993 that were not considered cancer macroscopically. The records of 361 patients with 391 polyps are the object of this report. The polyps were divided into subgroups according to size: A) less than 20 mm, B) between 21 and 30 mm, and C) larger than 30 mm. Out of 391 polypoid lesions 373 were adenomas: 60% were found in males. The age group distribution showed no differences among the subgroups. The pedunculated type showed a decrease from 69.1% to 43.3% with the increasing of size: inverse figures were observed for sessile polyps. The lesions were mainly located in left colon. Synchronous adenomas were found in 25.4% patients, and metachronous and previous adenomas respectively in 24.8% and 5.2%: no significant difference was present in the subgroups. Synchronous malignancy in the colon was found in 2% of the patients. Histological characteristics demonstrated a decrease of tubular adenoma from 46.5% to 22.6% from subgroup A to C, while villous adenomas increased inversely from 6.6% to 15.1%. The presence of severe dysplasia ranged from 20.9% to 56.1% in subgroups A and C, respectively, and adenomas with invasive cancer showed a significant increase from the subgroup A to C, respectively from 4.3% to 10.5%. During an average 36-month follow-up we observed 2 metachronous colon cancers, surgically treated in Dukes stage B, 84 metachronous adenomas, all less than 10 mm and without malignant alterations. Our data confirm other literature reports regarding the profile of colon adenomas with an increasing risk of malignancy with the increase of size and the presence of villous structure. In our opinion the assessment of a "clean colon" status is important when an adenoma is found in the colon. The proper follow-up for adenomas must be tailored for any individual patient when risk factors such as size, villous structure, personal and family history of neoplastic lesions of the colon are present. The follow-up schedule, presently recommended for colon adenomas, must be flexible according to these parameters.

Adenoma↗

PubMed1996

Sulindac increases the expression of APC mRNA in malignant colonic epithelial cells: an in vitro study.

BACKGROUND: Sulindac is a non-steroidal anti-inflammatory drug which induces regression of colonic polyps in patients with familial adenomatous polyposis. Animal and in vitro studies have shown that both the sulphide metabolite of sulindac, which is able to inhibit cyclo-oxygenase, and the sulphone metabolite, which lacks this ability, are able to inhibit the growth of colonic carcinoma cells. The exact mechanism by which these effects occurs is not known. AIMS: To examine the effect of sulindac sulphide and sulindac sulphone on the expression of APC messenger RNA (mRNA), and on the proliferation of colonic carcinoma cells in vitro. METHODS: The colonic carcinoma cell line LIM 1215 was treated with sulindac sulphide and sulindac sulphone (10 microM or 100 microM) for 24 hours. Total RNA was extracted and APC mRNA was quantitated using competitive reverse transcription polymerase chain reaction. Measurements of cell number, cell proliferation, and prostaglandin E2 concentrations were also made. RESULTS: A significant increase in APC mRNA was observed after treatment with 10 microM of both sulindac sulphide and sulindac sulphone (control: 37.2 (19.7); 10 microM sulindac sulphide: 129 (112.8); 10 microM sulindac sulphone: 207.7 (102.9) pg/(g total RNA) (p < 0.05). Prostaglandin E2 concentrations were significantly reduced after treatment with sulindac sulphide, but not after sulindac sulphone. Both agents produced a dose dependent reduction in cell numbers and cell proliferation, which was more noticeable after treatment with sulindac sulphide. CONCLUSIONS: Both sulindac sulphide and sulindac sulphone inhibit the growth of carcinoma cells in vitro and cause an increase in APC mRNA. The effect of these agents on colonic carcinogenesis is not mediated entirely by means of an inhibition of prostaglandin biosynthesis.

Adenomatous Polyposis Coli↗

PubMed2003

PMEPA1, a transforming growth factor-beta-induced marker of terminal colonocyte differentiation whose expression is maintained in primary and metastatic colon cancer.

To identify potential effectors of transforming growth factor (TGF)-beta-mediated suppression of colon cancer, we used GeneChip expression microarrays to identify TGF-beta-induced genes in VACO 330, a nontransformed TGF-beta-sensitive cell line derived from a human adenomatous colon polyp. PMEPA1 was identified as a gene highly up-regulated by TGF-beta treatment of VACO 330. Northern blot analysis confirmed TGF-beta induction of PMEPA1 in VACO 330, as well as a panel of three other TGF-beta-sensitive colon cell lines. PMEPA1 induction could be detected as early as 2 h after TGF-beta treatment and was not inhibited by pretreatment of cells with cycloheximide, suggesting that PMEPA1 is a direct target of TGF-beta signaling. Wild-type PMEPA1 and an alternative splice variant lacking the putative transmembrane domain were encoded by the PMEPA1 locus and were shown by epitope tagging to encode proteins with differing subcellular localization. Both variants were found to be expressed in normal colonic epithelium, and both were shown to be induced by TGF-beta. Consistent with TGF-beta playing a role in terminal differentiation of colonocytes, in situ hybridization of normal colonic epithelium localized PMEPA1 expression to nonproliferating, terminally differentiated epithelium located at the top of colonic crypts. Intriguingly, in situ hybridization and Northern blot analysis showed that the expression of PMEPA1 was well maintained both in colon cancer primary tumors and in colon cancer liver metastases. PMEPA1 is thus a novel TGF-beta-induced marker of a differentiated crypt cell population. Moreover, as PMEPA1 expression is maintained, presumptively in a TGF-beta-independent manner after malignant transformation and metastasis, it demonstrates that even late colon cancers retain a strong capacity to execute many steps of the normal colonic differentiation program.

Alternative Splicing↗

PubMed1986

[Epithelial tumors of the large intestine in short-term tissue culture (relation to biological behavior)].

Short term tissue cultures on space substrate were made from 13 samples of normal colonic mucosa and non-tumours colonic lesions as well as from 28 samples of epithelial colonic tumours. The growth and morphological features of cultivated tumours were mostly connected with their original histological structure and biological behaviour. Epithelial structures from adenoma and carcinoma survived longer than those from non-tumorous lesions. Epithelial cells from villous adenomas and from familiar polypous colonic adenomas showed increased proliferation on space substrate similar to the growth of carcinoma cells.

Adenoma↗

PubMed1978

Streptococcus bovis bacteremia and underlying gastrointestinal disease.

Twenty-six adults with Streptococcus bovis endocarditis and ten with bacteremia alone were studied to determine possible portals of entry. Of 36 patients (17 with endocarditis, eight with bacteremia alone), 25 had gastrointestinal lesions or manipulation. In 22, the gastrointestinal tract appeared to be the source of S bovis bacteremia. Four patients had either carcinoma of the colon (two) or potentially malignant villous adenomas (two) when first seen because of S bovis bacteremia. None of these, nor two other patients with benign colonic polyps, had bowel-related symptoms or signs prior to admission. Since S bovis is a normal intestinal tract inhabitant, bacteremia may frequently be associated with bowel lesions. Streptococcus bovis bacteremia may provide an early clue to the presence of serious and clinically unexpected gastrointestinal disease. Gastrointestinal tract evaluation should be part of S bovis bacteremia patient management, with or without endocarditis.

Adult↗

PubMed1998

Glutathione S-transferases--biomarkers of cancer risk and chemopreventive response.

The critical role of the glutathione S-transferase (GST) multigene family in cellular protection in combination with the large interindividual variability in the expression of these enzymes has prompted an investigation of their importance in cancer prevention and susceptibility. Previous preclinical and clinical studies from this laboratory have established an association between decreased GST activity and increased risk for colorectal cancer. Based upon the increased incidence of colon malignancies among patients with ulcerative colitis, GST activity has been examined in a mouse model of induced colitis. Significant decreases (50% of controls) in the GST activity of colon tissue were observed during the establishment and progression of colitis. These data suggested that depletion of cellular protection may be an important event in the carcinogenic progression of ulcerative colitis. The ability of the dithiolthione oltipraz to induce GST expression within the murine colon has been demonstrated. Use of chemopreventive regimens to induce phase 2 detoxication enzyme expression represents a promising strategy for the prevention of cancer. Clinical studies revealed that the GST activity of blood lymphocytes from individuals with either a personal or family history of colorectal cancer or a personal history of colon polyps was decreased significantly when compared to that of healthy controls. Phase 1 clinical evaluation of oltipraz has demonstrated its ability to induce GST activity as well as the level of transcripts encoding gamma-glutamylcysteine synthetase (gamma-GCS) and DT-diaphorase in the colon mucosa of individuals at increased risk for colorectal cancer. The observed correlation between the posttreatment response in blood lymphocytes and colon mucosa suggested that blood lymphocytes may be used in future trials as a surrogate biomarker of the responsiveness of colon tissue to chemopreventive regimens.

Animals↗

PubMed2006

Fibroblastic polyp of the colon: clinicopathological analysis of 10 cases with emphasis on its common association with serrated crypts.

AIMS: To describe the clinical and pathological features of 10 further cases of fibroblastic polyps (FP), a recently described, distinctive type of colorectal mucosal polyp. METHODS AND RESULTS: The patients were seven women and three men with ages ranging from 44 to 63 years. The lesions ranged in size from 2 to 4 mm. Eight of the polyps were located in the sigmoid colon. Five cases were associated with hyperplastic polyps. Histologically, FP displayed bland, plump spindle cells with oval nuclei arranged as bundles parallel to the surface or as haphazardly orientated sheets with a focal periglandular or perivascular concentric arrangement. Eight polyps represented mixed fibroblastic/hyperplastic polyps as they contained serrated (hyperplastic) crypts. Immunohistochemically, all cases were positive for vimentin and negative for desmin, smooth-muscle actin, h-caldesmon, S100 protein, c-Kit, epithelial membrane antigen, cytokeratin AE1/3, CD34, CD68, COX-2, and factor XIIIa. Ultrastructural examination supported the fibroblastic nature of the tumour cells. CONCLUSIONS: FP is a distinctive type of benign mucosal colorectal polyp characterized by its distal location, small size, frequent association with hyperplastic polyps, distinct morphological appearance and typical immunonegativity for markers of specific differentiation. FP with serrated crypts (mixed fibroblastic/hyperplastic polyp) represents a frequent variant of this lesion. Pathologists should recognize FP and discriminate it from other types of colorectal polyps.

Adult↗

PubMed2005

[Gardner-syndrome: case report].

The major symptoms of Gardner-syndrome are described by the authors (multiple osteomas, desmoid tumors, colon polyps with malignant tendency) with a case appearing in their department. The importance of early diagnosis is also emphasized.

Adenomatous Polyposis Coli↗

PubMed2001

Regulation of vascular endothelial growth factor by the Wnt and K-ras pathways in colonic neoplasia.

Angiogenesis is not restricted to advanced stages of tumor development but is also observed in benign precursor lesions. Vascular endothelial growth factor (VEGF) is a key regulator of tumor angiogenesis, but the genetic mechanisms controlling its expression in premalignant lesions are poorly described. The Wnt signaling pathway, which is commonly mutated in benign colonic adenomas, was found to strongly up-regulate VEGF. A T-cell factor-4-binding element at -805 bp in the VEGF promoter is an important mediator of this effect. Signaling through the K-ras oncogene, also frequently mutated in benign colonic polyps, up-regulated VEGF in a phosphatidylinositol 3-kinase-dependent manner. Furthermore, K-ras activation appeared to enhance Wnt signaling, which suggests a unique interaction between these two pathways. These studies thus identify VEGF as a novel target of the Wnt pathway in early colonic neoplasia and serve to underscore the importance of angiogenesis in premalignant disease.

Androstadienes↗

PubMed1990

[Protease activities in gastric and colon cancer tissues].

Activities of cathepsin B, cathepsin L, and plasminogen activators (urinary type plasminogen activator and tissue type plasminogen activator) were assayed in homogenates of cancer tissue, normal tissue closely surrounding the cancer tissue, and normal tissue distant from the cancer tissue from 30 patients undergoing surgery for gastric cancers and 10 patients undergoing surgery for colon cancers. Activities of those proteases were also assayed in homogenates of adenoma tissue from 10 patients undergoing polypectomy for colon polyps. In the gastric cancer tissue homogenates, the activities of cathepsin B, cathepsin L and tissue type plasminogen activator were significantly higher than in normal tissues. By contrast, the activities of urinary type plasminogen activator of gastric cancer tissues were significantly lower than normal tissues. In the colon cancer tissue homogenates, the activities of cathepsin, B, cathepsin L, and urinary type plasminogen activator were significantly higher than in normal tissues. On the other hand, the activities of tissue type plasminogen activator of cancer tissues were significantly lower than normal tissues. But there were no significant differences in the activities of plasminogen activators between the cancer tissues and adenoma tissues. These results suggest that cathepsin B and cathepsin L play an important role in gastric and colon cancer proliferation and evolution, although the roles of plasminogen activators in gastric and colon cancer proliferation and evolution and in the colon adenoma-carcinoma sequence are still unknown.

Cathepsin B↗

PubMed1996

Three secretory phospholipase A(2) genes that map to human chromosome 1P35-36 are not mutated in individuals with attenuated adenomatous polyposis coli.

Mutation of Pla2g2a, a secretory phospholipase A(2) gene, dramatically increases the number of intestinal polyps that develop in the multiple intestinal neoplasia (Min) mouse, a murine model for adenomatous polyposis coli in humans. We tested the hypothesis that mutation of the human homologue(s) of this gene might be responsible for the more severe phenotype (hundreds of polyps) seen in a subset of individuals with attenuated adenomatous polyposis coli (AAPC). DNA sequence analysis demonstrated that alterations of PLA2G2A, as well as related genes PLA2G2C and PLA2G5, were evenly distributed between three classes of AAPC subjects: those with small, intermediate, and large numbers of adenomatous colonic polyps. Among 67 additional unrelated AAPC subjects, a stop mutation in PLA2G2C did not correlate with an increased burden of adenomatous polyps. Therefore, mutation of the human homologue(s) of murine Pla2g2a does not appear to be responsible for phenotypic variation among subjects with AAPC.

Adenomatous Polyposis Coli↗

PubMed2001

Magnetic resonance colonography for colorectal cancer screening.

Colorectal cancer screening has vast potential. Beyond considerations of cost and diagnostic accuracy, the effectiveness of any colorectal screening strategy will be dependent on the degree of patient acceptance. Magnetic resonance (MR) colonography has been shown to be accurate regarding the detection of clinically relevant colonic polyps exceeding 10 mm in size, with reported sensitivity and specificity values exceeding 95%. To further enhance patient acceptance, strategies for fecal tagging have recently been developed. By modulating the signal of fecal material to be identical to the signal characteristics of the enema applied to distend the colon, fecal tagging in conjunction with MR colonography obviates the need for bowel cleansing. This article will describe the techniques underlying MR colonography and early clinical experience with fecal tagging techniques.

Colonography, Computed Tomographic↗

PubMed1998

Screening endoscopy and risk of colorectal cancer in United States men.

OBJECTIVES: The purpose of this study was to describe the effect of screening endoscopy (sigmoidoscopy or colonoscopy) on colorectal cancer incidence and mortality. METHODS: We used data from a prospective cohort study of 24,744 men aged 40 to 75 years in 1986, free from cancer and colon polyps, followed until 1994. The outcomes are diagnosis of colorectal cancer and death from colorectal cancer. RESULTS: Screening endoscopy in 1986-87 was associated with a lower risk of all colorectal cancer (multivariate relative risk [RR] = 0.58, 95 percent confidence interval [CI] = 0.36-0.96); cancer in the distal colon or rectum (multivariate RR = 0.40, CI = 0.19-0.84); Dukes stage A&B (multivariate RR = 0.66, CI = 0.35-1.25); and Dukes stage C&D (multivariate RR = 0.50, CI = 0.20-1.26) colorectal cancer; and death from colorectal cancer (multivariate RR = 0.56, CI = 0.20-1.60), after adjusting for age and a wide range of colon cancer risk factors. Screening endoscopy in 1988-87 appeared to provide strong protection against distal stage C&D cancers (age-adjusted RR = 0.16, CI = 0.02-1.23) but no protection against proximal stage C&D cancers (age-adjusted RR = 0.96, CI = 0.32-2.91). CONCLUSIONS: This study provides strong evidence for a protective effect of screening sigmoidoscopy on colorectal cancer incidence and mortality and supports recommendations for screening sigmoidoscopy as an approach to colon cancer prevention.

Adult↗

PubMed1997

Peutz-Jeghers polyps, dysplasia, and K-ras codon 12 mutations.

BACKGROUND: Peutz-Jeghers syndrome (PJS) is a rare, autosomal dominant, polyposis syndrome, associated with an increased risk of gastrointestinal and extragastrointestinal malignancy. Occasionally dysplasia occurs in PJS polyps. AIMS: In colorectal carcinomas, mutations in codon 12 of the K-ras oncogene are common and are found at similar frequency in precursor adenomas. Therefore, K-ras codon 12 point mutations in PJS polyps, were evaluated. MATERIALS AND METHODS: Fifty two PJS polyps, including four with dysplasia, collected from 19 patients with PJS, were analysed for mutations in the K-ras codon 12 by a mutant enriched polymerase chain reaction procedure, followed by allele specific oligodeoxynucleotide hybridisation. RESULTS: A K-ras codon 12 mutation was identified, in one colonic polyp with dysplasia. The mutation was found in the non-neoplasmic epithelial cells and not in the dysplastic component of the polyp. CONCLUSIONS: K-ras codon 12 point mutations are very rare in PJS polyps, by contrast with colorectal adenomas. The findings support previous evidence that there seems to be no intrinsic relation between K-ras codon 12 mutation and dysplasia.

Autoradiography↗

PubMed2003

Virtual magnetic resonance colonography.

Colorectal cancer screening has vast potential. Beyond considerations for cost and diagnostic accuracy, the effectiveness of any colorectal screening strategy will be dependent on the degree of patient acceptance. Magnetic resonance (MR) colonography has been shown to be accurate regarding the detection of clinically relevant colonic polyps exceeding 10 mm in size, with reported sensitivity and specificity values exceeding 95%. To further increase patient acceptance, strategies for fecal tagging have recently been developed. By modulating the signal of fecal material to be identical to the signal characteristics of the enema applied to distend the colon, fecal tagging in conjunction with MR colonography obviates the need for bowel cleansing. The review will describe the techniques underlying MR colonography and describe early clinical experience with fecal tagging techniques.

Colorectal Neoplasms↗

PubMed1996

Apoptosis of crypt epithelial cells in ulcerative colitis.

In the colon of ulcerative colitis (UC) patients, apoptotic bodies have been recognized in routine histopathological preparations. To investigate the extent of the apoptosis, colonic biopsies were examined from involved and uninvolved areas of untreated active UC and from normal areas in patients with colonic polyps, utilizing various markers of apoptosis. The markers included DNA breaks detected by TUNEL, Fas (CD95/APO-1) and Fas ligand (Fas-L) localized by immunohistochemistry, electron microscopic features of apoptosis, and laddering of extracted DNA. Apoptosis marker positive cells were found mainly on the luminal epithelium of the normal colon and were present in active UC in crypts of involved and uninvolved areas of the colon, in addition to the luminal epithelium. The DNA extracted from active UC colon electrophoresed as a ladder. These findings suggest that the loss of epithelial cells in active UC occurs mainly by apoptosis in crypts of involved and adjacent uninvolved areas and that the Fas/Fas-L interaction is a mediator of the apoptosis.

Apoptosis↗

PubMed1983

Submucous lipoma of the transverse colon: report of one case.

A case of submucous lipoma of the transverse colon is reported. The patient, a man aged 61, complained of recurrent crampy periumbilical pain. A plain x-ray of the abdomen was negative, while a barium enema showed an intramural filling defect of the transverse colon which was interpreted as a probably degenerated colonic polyp. Laparotomy did not clarify the diagnosis which was readily clear when the lesion was cut, and confirmed by histology.

Barium Sulfate↗