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At least 793 records · Page 44Linked to original sources
PubMed1993

Increase in activity and level of pp60c-src in progressive stages of human colorectal cancer.

Activation of the tyrosine kinase of the c-src gene product, pp60c-src, has been shown to occur in nearly every primary colorectal carcinoma, and is found as early as in polyps of high malignant potential. However, no studies have addressed potential pp60c-src changes which occur during progression. To examine this question, we have studied kinase activity and protein levels in 7 colonic polyps, 19 primary lesions, and 19 liver metastases relative to normal colonic mucosa. Significant increases in tyrosine kinase activity were seen as early as in colonic polyps of high malignant potential. Further increases were observed in activity and level in primary tumors. However, the greatest increases in activity and protein levels were observed in liver metastases. Additionally, six metastatic lesions were obtained in which synchronous primary tumor was resected. In each of these liver metastases, pp60c-src activity and level were significantly increased relative to the corresponding primary tumor, as well as to normal colonic mucosa. Our results demonstrate that progression of colon primary tumors to liver metastases correlates with increased pp60c-src kinase activity and protein level.

Adenocarcinoma↗
PubMed1993

Effect of bowel cleansing and colonoscopy on serum CEA levels.

A group of patients being investigated for various forms of colonic pathology showed an apparent rise in serum carcinoembryonic antigen (CEA) level following bowel cleansing at the time of colonoscopy, as compared with the 'resting' level. The rise was particularly marked in a small group of patients with colonic polyps or previous colonic resection for carcinoma, suggesting a need for careful timing in the taking of blood samples. The findings may also have diagnostic importance in identification of patients at higher risk of malignant disease of the colon.

Adult↗
PubMed1984

Colorectal polyps in Cowden's disease (multiple hamartoma syndrome).

Colorectal polyps are described in five patients with Cowden's disease. A brother-sister kindred and two unrelated patients had multiple colonic polyps 0.1-0.4 cm in diameter. Microscopical examination of seven polyps removed from these four patients showed distinctive lesions which were probably hamartomatous, and characterized by disorganization and proliferation of the muscularis mucosae with minimally abnormal overlying mucosa. The fifth patient had a solitary 2-cm epitheloid leiomyoma resected from the rectum. Review of all cases of Cowden's disease in the English literature suggests that gastrointestinal polyposis may be a frequent finding if it is specifically searched for. It does not appear that the previously reported association of Cowden's disease with gastrointestinal cancer is valid. The discovery of multiple colonic polyps 0.1-0.4 cm is diameter with a rectosigmoid distribution and a hamartomatous microscopical appearance is characteristic of Cowden's disease. Cowden's disease should be included in the differential diagnosis of gastrointestinal polyposis states.

Adult↗
PubMed1984

[Gastric mucosal polyps--an irrelevant finding? Studies on the incidence and clinical significance].

Among about 20.000 patients who had a gastroscopy in a period of 6 years, 92 had gastric mucosal polyposis, diagnosed by endoscopy and histology, an incidence of 0.46%. Eight patients with an age average of 38 years had familial gastrointestinal adenomatosis, in six of them the criteria of Gardner's disease were fulfilled. The remaining 84 patients had an average age of 62 years. In patients with more than ten polyps the sex ratio (female to male) was 3.9:1. In 56 patients without familial gastrointestinal adenomatosis, coloscopy and(or) proctosigmoidoscopy was performed. In 18 there were polyps in the colon, in three an invasive carcinoma in an adenoma. In three further patients extensive carcinoma of the colon (in two with stenosis) was found. These observations suggest that patients with gastric mucosal polyposis have a higher incidence of colon polyps and carcinoma.

Adult↗
PubMed1977

[Eight years of gardner's syndrome in a family (author's transl)].

In all affected members of a family with Gardner's syndrome the complete triad of skin tumours, osteomas and polyps of the colon has developed since 1968 when examination revealed an apparently bisymptomatic variant of Gardner's syndrome. In this family bony changes consisting of circumscript osteomas, diffuse sclerosing zones within certain bones, and ridge-like widening of the corticalis were noted, having developed during puberty but remaining constant thereafter. Similarly, no significant new skin tumours appeared after puberty. Most colonic polyps however, occurred in adolescence or thereafter, with malignant transformation after a variable interval of several years. The necessity of long-term observation of the colon, also in patients presenting with a bi- or monosymptomatic form, is stressed. Coloscopy has proven to be more useful diagnostically than radiological methods.

Adult↗
PubMed1997

Follow-up of patients with hyperplastic polyps of the large bowel.

BACKGROUND: Adenomatous colonic polyps are accepted as premalignant lesions. There is controversy regarding the significance of the hyperplastic polyp. The aim of this study was to determine the incidence of further polyps in patients with only hyperplastic polyps on a first colonoscopy in comparison with patients without polyps and with adenomatous polyps. METHODS: Ninety patients had only hyperplastic polyps (group I). These patients were paired according to age and sex with subjects having no polyps (group II) and with patients having adenomas (group III). RESULTS: Fifty-six patients in group I had at least one follow-up examination. New polyps were found in 46.4% in group I versus 15.5% in group II (p < 0.001) and 50% in group III (NS). In group I, 30.7% of new polyps were hyperplastic and 69.3% were adenomas. In fact, 32.2% of group I patients developed further adenomas (mean 1.5 +/- 0.8 adenomas). These adenomas occurred 1 to 4 years after the first polypectomy (mean 2.4 +/- 0.8 years). Most of these adenomas were small and tubular, but 16.6% were villous or had severe dysplasia. CONCLUSION: Patients with hyperplastic polyps were 2.4 times more likely to have further adenomas than were those without polyps.

Adenoma, Villous↗
PubMed2002

Endoscopic evaluation of patients with partial gastrectomy and iron deficiency.

Endoscopy is indicated for the evaluation of unexplained iron deficiency to rule out neoplasia. Iron deficiency is common in postgastrectomy patients. The endoscopic yield for significant pathology in these patients is unknown but is expected to be lower than for other iron-deficient groups. A retrospective case-control study with 2:1 matching was performed comparing iron-deficient patients (ferritin < or = 50 microg/liter) having prior Billroth I or Billroth II gastrectomy to matched iron-deficient controls with normal gastric anatomy. There were 52 postgastrectomy patients and 113 controls. There were no significant differences between postgastrectomy patient and controls in age, gender ratio, or laboratory test results, with the exception of MCV (88.9 +/- -1.1 vs 86.0 +/- -0.8, mean +/- SEM, P = 0.048) There were no significant differences in the prevalence of upper gastrointestinal pathology (24.5% vs 29.2%), large (>1 cm) colon polyps (8.3% vs 5.2%), or the presence of any adenomatous colon polyp (28.6% vs 18.9%). There were no malignancies. In conclusion, prevalence of clinically significant pathology is similar for postgastrectomy and nonpostgastrectomy iron-deficient patients. Endoscopic evaluation of iron deficiency should not differ in postgastrectomy patients.

Aged↗
PubMed1975

Proliferative patterns in colonic mucosa in familial polyposis.

Microautoradiographic measurements of TdR3H incorporation into epithelial cells of colonic biopsies were compared in normal and eight index cases with familial polyposis, an inherited trait characterized by the development of colonic polyps and carcinomas. Colonic epithelial cells normally synthesized DNA synthesis was proliferated in the deeper two-thirds of the crypts, while DNA synthesis was repressed in the upper one-third. Patients with familial polyposis and patients with isolated single polyps incorporated TdR into epithelial cells lining the surfaces of polyps and occasionally into surface cells of intervening flat mucosa. Symptom-free members of polyposis families also demonstrated TdR3H incorporation into surface epithelial cells in biopsies of morphologically flat mucosa. The findings indicate similar proliferative behavior of epithelial cells in the formation of all adenomas, be they single isolated polyps or multiple familial adenomatous polyps. A sequence of changes occurs involving a loss of the cells' ability to repress DNA synthesis and the appearance of cells with persistent DNA synthesis at the surface and along the upper portion of colonic crypts. These defects are focal and widespread in the colonic mucosa of those with familial polyposis and are expressed at early age.

Adolescent↗
PubMed1976

Familial juvenile adenomatous polyposis.

Most colonic polyps in children are of the juvenile type and occur either as single or scattered colonic polyps. The peak incidence occurs between 4 and 6 yr of age, with a spontaneous decline from 12 to 15 yr. Significant clinical symptoms are rare, and operative therapy is rarely indicated. Diffuse colonic juvenile polyposis, however, varies with different clinical, prognostic, and genetic implications. In infancy, colonic polyposis may be associated with diffuse gastrointestinal involvement leading to fatal complications unless treated aggressively. In childhood, colonic polyposis can occur with a genetic variance with an increased incidence of familial intestinal malignancies. Colonic polyposis in childhood, both familial and nonfamilial, can present with a mixed form of juvenile and adenomatous polyposis. In children with colonic polyposis, the biopsy of a single polyp that reveals the histologic appearance of a juvenile polyp does not rule out the simultaneous existence of adenomatous polyps.

Adolescent↗
PubMed2003

Dose-dependent suppression of hyperlipidemia and intestinal polyp formation in Min mice by pioglitazone, a PPAR gamma ligand.

In our previous study, a peroxisome proliferator-activated receptor gamma (PPAR gamma) agonist, pioglitazone, suppressed both hyperlipidemia and intestinal polyp formation in Apc(1309) mice at doses of 100 and 200 ppm in the diet. In contrast, it has been reported that doses of 1500 or 2000 ppm of another PPAR gamma agonist, troglitazone, enhanced colon polyp development in Min mice. In the present study, we therefore investigated the effects of a wide range of pioglitazone doses on both hyperlipidemia and intestinal polyp formation in Min mice. Serum triglycerides and very low density lipoprotein (VLDL) cholesterol in the basal diet group were elevated to levels 13-15 times higher than those in the wild-type counterparts at 20 weeks of age. They were reduced dose-dependently by treatment with 100, 200, 400 and 1600 ppm pioglitazone from 6-20 weeks of age with suppression to almost the wild-type level at the highest dose. Moreover, up-regulation of the liver mRNA levels for lipoprotein lipase (LPL) was evident in the pioglitazone-treated animals. Dose-dependent reduction of intestinal polyps was observed in Min mice given 100-1600 ppm for 14 weeks, total numbers being decreased to 63-9% of the control value. A suppressive effect of pioglitazone on colon polyp formation was also found. The PPAR gamma agonist, pioglitazone, may thus be a promising candidate chemopreventive agent for colon cancer.

Animals↗
PubMed1983

Aberration of poly(adenosine diphosphate-ribose) metabolism in human colon adenomatous polyps and cancers.

The activities of three principal enzymes engaged in the biosynthesis and degradation of poly(adenosine diphosphate-ribose) [poly(ADP-ribose)] were examined in cell nuclei isolated from adenomatous polyps (tubular adenomas of familial polyposis coli, villous adenoma, and tubulovillous adenoma), cancers, and normal mucosa of human colon. The activities of poly(ADP-ribose) synthetase in adenomatous polyps [161 +/- 46 (S.E.) pmol/min/mg DNA] and cancers (114 +/- 32 pmol/min/mg DNA) were, on an average, about 3 and 2 times, respectively, higher than those in normal mucosa (52 +/- 24 pmol/min/mg DNA); the difference was statistically significant (p less than 0.001). The activity of poly(ADP-ribose) glycohydrolase was also significantly high in adenomatous polyps (13.0 +/- 3.4 nmol/min/mg DNA), but not in cancers (10.1 +/- 2.5 nmol/min/mg DNA), compared with normal mucosa (5.2 +/- 1.4 nmol/min/mg DNA) (p less than 0.001). The activity of ADP-ribosyl protein lyase, in contrast, was lower in adenomatous polyps (152 +/- 40 pmol/min/mg DNA) than in normal mucosa (345 +/- 111 pmol/min/mg DNA) and cancers (288 +/- 80 pmol/min/mg DNA) (p less than 0.001). Analyses of reaction products with snake venom phosphodiesterase digestion revealed that poly(ADP-ribose) synthesized in nuclei of normal mucosa, adenomatous polyps, and cancers had the average chain lengths of 2.9, 1.7, and 9.7 ADP-ribose units, respectively. Based upon these values and total amounts of ADP-ribose incorporated, the amount of poly(ADP-ribose) synthesized per mg DNA in 30 min was calculated as 308, 1510, and 106 pmol in the above three types of colon tissues, respectively. These results suggested that a larger amount of monomers and short oligomers of ADP-ribose was synthesized in adenomatous polyps, while a smaller number of longer polymers was produced in cancers as compared with normal mucosa. Immunohistochemical analysis of these tissues using anti-poly(ADP-ribose) antibody supported this view.

Adenoma↗
PubMed2006

Accuracy of high-resolution chromoendoscopy in prediction of histologic findings in diminutive lesions of the rectosigmoid.

BACKGROUND: The ability to differentiate adenomatous from nonadenomatous colonic polyps by using chromoendoscopy would obviate the need to remove hyperplastic lesions. The aim of this study was to define the accuracy of high-resolution chromoendoscopy for the determination of colonic polyp histology. METHODS: In 158 patients, 273 polyps (<5 mm) in the rectosigmoid were estimated for their histology. The endoscopists, in two steps, predicted the histopathology of each lesion on the basis of its surface characteristics by using high-resolution colonoscope without any staining and after indigo carmine dye according to the Kudo classification. RESULTS: The resected polyps included 48 adenomatous and 225 nonadenomatous polyps. When histologically confirmed hyperplastic polyps were compared with adenomatous polyps, the prediction of hyperplastic polyps based on endoscopic findings had a sensitivity of 93%, a specificity of 60%, and an overall accuracy of 81%. The corresponding sensitivity, specificity, and overall accuracy after indigo carmine dye were 94%, 64%, and 83%, respectively. CONCLUSIONS: The results suggest that the chromoendoscopy only marginally improves the determination between hyperplastic and adenomatous polyps when using high-resolution colonoscopes. The overall accuracy rate increased after dyeing, from 81% to 83%. The omission of histopathologic analysis cannot yet be achieved by chromoendoscopy.

Adenoma↗
PubMed1992

Benign colorectal neoplasms undetected by colonoscopy.

This retrospective investigation assessed the sensitivity of colonoscopy for the detection of colonic polyps seen previously at barium enema examination. Included in the study were 77 patients with 106 polypoid lesions. Films showing lesions not subsequently seen at colonoscopy were reviewed and only those lesions with a visible point of attachment, exhibiting no movement in response to filling or change in position of the patient, and confidently diagnosed as a polyp by both reviewing radiologists were included among the 106 lesions. Sixteen lesions (15%) seen radiologically were not located colonoscopically, indicating an endoscopic sensitivity of 85%. Contrary to previous reports, most of the lesions missed endoscopically were in the left colon in regions thought to have been traversed by the instrument. The 15% false-negative rate found for colonoscopy is consistent with existing reports on colonoscopic errors and is approximately the same as the false-negative error rate for radiologic detection of colonic polyps.

Adult↗
PubMed2002

Peroxisome proliferator activated receptor gamma expression is reduced in the colonic mucosa of acromegalic patients.

UNLABELLED: Acromegalic patients have an increased prevalence of colonic polyps, due to the elevated serum insulin like growth factor (IGF)-I levels. The mechanisms underlying this process are poorly understood. Peroxisome proliferator activated receptor (PPAR)gamma, a nuclear receptor that regulates adipocyte differentiation, is highly expressed in the human colonic mucosa, where it induces growth inhibition and cell differentiation. In the present study we evaluated the expression of PPARgamma in the bioptic samples of colonic mucosa from 22 patients with acromegaly (Acro) and 13 normal subjects (CONTROLS) matched for age and sex. Among Acro patients, 10 had active, untreated disease (AcroUntr), 6 were in remission after surgery (AcroRem), and 6 had active disease under treatment with somatostatin analogs (AcroSMSa). Serum GH and IGF-I (mean +/- SD) levels were as follows: AcroUntr: GH, 36 +/- 40 microg/l; IGF-I, 769 +/- 298 microg/l; AcroRem: GH, 1.0 +/- 1.3 microg/l; IGF-I, 248 +/- 96 microg/l; AcroSMSa: GH, 7.8 +/- 12 microg/l; IGF-I, 429 +/- 221 microg/l; CONTROLS: GH, 0.8 +/- 0.7 microg/l; IGF-I, 203 +/- 67 microg/l. In the CONTROLS the level of expression of PPARgamma mRNA was 15230 +/- 891 transcripts. Patients with AcroUntr had 2750 +/- 688 transcripts of PPARgamma. (p < 0.0001) vs. CONTROLS); patients AcroSMSa had 4629 +/- 1286 transcripts of PPARgamma. (p = NS vs AcroUntr, p = 0.0002 vs. CONTROLS); patients with AcroRem had 8261 +/- 2481 transcripts of PPARgamma (p = 0.008 vs. AcroUntr, p = NS vs. AcroSMSa, p = 0.007 vs. CONTROLS). A significant inverse correlation was found between serum IGF-I concentrations and the level of expression of PPARgamma (r = 0.43, p = 0.03). In conclusion, patients with active Acro have a reduced expression of PPARgamma in the colonic mucosa, which appears be related to the increased serum IGF-I levels and might lead to an increased prevalence of colonic polyps.

Acromegaly↗
PubMed1999

Polyps as biomarkers for colorectal neoplasia.

Current understanding of colorectal carcinogenesis suggests a series of genetic changes occurring pari passu with morphological changes ultimately resulting in a cancerous lesion. The adenomatous polyp was originally the prototype of the preneoplastic lesion but recently, other colonic polyps, primarily the hamartomas, have been clinically characterized as colorectal cancer biomarkers with genetic changes found mainly in the mesenchymal component as opposed to the ectodermal, or epithelial element. This, with the current interest in angiogenesis playing a role in the propagation of neoplastic lesions, has now encompassed every tissue element and opened the way for an understanding of the oncogenic process. This has suggested that considerable interaction occurs between all tissue elements, including what was previously described as epithelial-matrix interactions. While hyperplastic polyps are thought not to confer risk for cancer, they may offer clues as to the first steps of the overall process. Microadenomas have introduced new clinical as well as biological considerations, as unique risk factors. Investigation of these lesions has moved from purely morphological correlations to mechanistic dissections of important biological pathways using both genetic and protein chemistry tools. This review explores the microcosm of the colonic polyp and its relation to cancer as the quintessential premalignant biomarker.

Adenoma↗