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At least 19 recordsLinked to original sources
PubMed1979

Cell population kinetics of 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse.

The parameters of cell population kinetics of symmetrical 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse were analyzed using the fraction labeled-mitoses curve method and compared with those of three groups of epithelial cells in the crypt of the descending colon of normal mouse. The analysis of three groups of epithelial cells in the crypt of normal mouse indicates that differentiation of epithelial cells was associated not only with a smaller proliferative pool of cells but also with a shortening of the duration of G2 phase and a prolongation of mitotic time. Other parameters of cell cycle did not change significantly. The mean cell cycle time of neoplastic cells in chemically induced colonic neoplasms was similar to that of epithelial cells in normal colon, but the variance was much greater in neoplastic cells. In neoplastic cells, the proliferative pool was greater, the G1 phase prlonged, and the S phase and the mitotic time became shorter as compared to epithelial cells in normal colon. The duration of G2 phase of neoplastic cells fell between the values of presumptive stem cells and differentiating cells in normal colon, compatible with the hypothesis that neoplastic cells are transformed stem cells defective in cellular differentiation. In the colonic mucosa immediately adjacent to neoplasms, the fraction-labeled-mitoses curve showed a flat second wave, indicating that the group of cells initially labeled by the pulse became a mixture of cells, some continuing the proliferative cycle normally, some going out of cycle, some slowing down in their passage from S through G2 to M, and some being arrested in mitotic phase. Such heterogeneous behavior of cells may be closely related to expansion of neoplasms. With some assumptions, however, cell cycle parameters of those normally cycling cells were estimated: the cell cycle time and the duration of G1 phase and mitotic phase were prolonged as compared to neoplastic cells and epithelial cells of normal colon.

Adenocarcinoma↗
PubMed1991

Induction of nm23 gene expression in human colonic neoplasms and equal expression in colon tumors of high and low metastatic potential.

Levels of expression of the murine nm23 gene inversely correlate with metastatic potential in several rodent tumor model systems. Expression of the human nm23 homologue also is lower in human breast cancers of high metastatic potential than in breast cancers of low metastatic potential. In the present study, we examined changes in nm23 expression during colon carcinogenesis as found in 18 matched pairs of normal and neoplastic human colon tissues. We found that a 0.8-kilo-base nm23 transcript was expressed in all samples of morphologically normal colon mucosa. In 16 of 18 colon neoplasms, nm23 expression was further increased in the neoplastic, compared with the morphologically normal, colon mucosa from the same individual. Expression of nm23 was elevated over normal mucosa in 3 of 3 polyps, in 2 of 3 nonmetastatic cancers, and in 11 of the 12 cancers that were metastatic at the initial presentation. The levels of nm23 expressed were similar in the 12 metastatic colon neoplasms and in the 6 colon neoplasms of lower clinical stage. In addition, nm23 expression was maintained in culture in each of 12 cell lines initiated from human colon neoplasms and did not differ between lines established from neoplasms of high or low metastatic capability. We concluded that nm23 was expressed in normal colon mucosa. Expression of nm23 increased during early stages of colon carcinogenesis and remained increased in metastatic colon cancer. Therefore, in the colon, tissue-specific events dissociate nm23 expression from loss of tumor metastatic competence.

Adenocarcinoma↗
PubMed1989

Is there an association between gastric polyps and colonic neoplasms?

The association between colonic neoplasms and gastric polyps (GP) was evaluated. Two hundred and sixty patients with known colonic neoplasms undergoing gastroduodenoscopy for abdominal symptoms, with or without anemia, were evaluated for the occurrence of synchronous GP. There were 100 patients with 1-4 colonic adenomas, 80 patients with multiple (5 or more) colonic adenomas and 80 patients with colorectal cancer. One hundred patients free from colonic neoplasms, investigated for abdominal pain or anemia, served as controls. The overall occurrence of GP in patients with colonic neoplasms was 18.8% compared to 1% in the control group. Hyperplastic GP were found in 4, 22.5, 18.7 and 1% of these patients, respectively, while gastric adenomas occurred in 2, 3.7, 3.5 and 0%, respectively. Patients with colorectal cancer or multiple colonic adenomas had significantly more GP than patients with 0-4 colonic adenomas. It is suggested that gastroduodenoscopic evaluation should be performed in patients with colorectal cancer or with 5 or more colonic adenomas.

Adenoma↗
PubMed1981

Resolution of radiographic-endoscopic discrepancies in colon neoplasms.

Fifty-one colon neoplasms larger than 1 cm were diagnosed by double-contrast barium enema (DC), but were not confirmed by initial endoscopy. Seventeen lesions were shown to be radiographic false-positive diagnoses by careful review of the original radiographs (10 cases) or repeat DC (7 cases). The presence of a neoplasm was confirmed in 21 cases (41%) by repeat endoscopy or surgery (15 cases) or by repeat DC alone (6 cases). Seven (47%) of 15 resected lesions were malignant. The results emphasize the complementary nature of the DC and endoscopy in detection of colon neoplasms. When discrepancies between the radiographic and endoscopic diagnoses cannot be explained by careful review of the DC, repeat radiographic or endoscopic examination should be performed.

Adenocarcinoma↗
PubMed1987

Perforation of colonic neoplasms. A review of 36 cases.

Colonic perforation is the second most common complication of colonic neoplasms and is associated with an elevated morbidity and mortality. We undertook a two-centre retrospective analysis of 378 colonic neoplasms seen from 1978 to 1985. Thirty-six patients (9.5%) presented with a perforated colonic carcinoma. Two-thirds had a past history suggesting colonic disease while in the remaining one-third, the perforation was the first manifestation of the disease. Resection was carried out initially in 33 cases (21 Hartmann's procedure, 9 primary anastomosis, 2 mucous fistula and 1 abdominoperineal excision). Two patients had a proximal colostomy only and 1 an exploratory laparotomy only because of disseminated disease. Postoperative mortality was 14% (five cases). Actuarial survival rate was 52% at 1 year and 40% at 2 years. Eleven patients are still alive after a mean follow-up of 43 months.

Aged↗
PubMed1990

Association of human papillomavirus and colon neoplasms.

Human papillomavirus has been shown to be associated with squamous carcinomas. We evaluated benign and malignant colon tissues for the presence of human papillomavirus infection to determine if a similar relationship exists between human papillomavirus and colon neoplasms. Colon tissues were screened using an immunohistochemical technique to detect human papillomavirus antigen. In situ DNA hybridization was then performed on those tissues that yielded positive results by immunohistochemistry. Groups were compared using chi 2 analysis. Human papillomavirus antigen was present in 23% of normal colon specimens, 60% of benign tumors, and 97% of carcinomas. Human papilloma viral genome was demonstrated in 27% of benign tumors and in nearly 43% of all carcinomas tested. These data indicate that human papillomavirus infects the columnar mucosa of the colon, and that an association exists between human papillomavirus and colon neoplasia.

Adenoma↗
PubMed1990

[Studies on the microcirculatory architecture in five colonic neoplasms].

The microcirculatory architecture of colonic neoplasms was prepared with methylmethacrylate cast. Scanning electron microscopy showed that microcirculation was deficient in the central area of neoplasms, but increased markedly and become claw, sinus and sphere patterns in appearance at the periphery of neoplasms. The microcirculation of the transitional mucosa lost its typical hexagon structure, becoming larger in diameter and showing increase of branches. These results suggest that the technique described in this article can be used to show the morphologic changes of neoplastic microcirculation, which may be worthy for the future investigation of neoplasm development.

Colonic Neoplasms↗
PubMed1976

Production of intestinal and other tumours by 1,2-dimethylhydrazine dihydrochloride in mice. II. Scanning electron microscopic and cytochemical study of colonic neoplasms.

Thum of colon induced by repeated subcutaneous injections of 1,2-dimethyl-hydrazine dihydrochloride in mice were studied by scanning electron microscopy. In addition, the surface composition of normal and malignant colonic epithelial cells were investigated by ultrastructural cytochemistry. The neoplastic, nodular tumour masses which protruded into the lumen of colon displayed an asymmetrical, irregular growth pattern and surface contour. In contrast to the normal surface structure, the shape of crypt openings in malignant areas was distorted and they were irregularly spaced. Cells varying in size and shape in the intercrypt regions often formed random patterns of elevations and depressions. Microvilli on neoplastic cells were larger, more club-shaped and showed more disorderly arrangement than their normal counterparts. The distribution and quantity of surface acid mucopolysaccharide content and adenosine triphosphatase activity varied considerably from cell to cell in the neoplastic epithelium while they were more uniform in the normal colonic surface cells.

Adenocarcinoma↗
PubMed2000

Decreased expression of CD44, alpha-catenin, and deleted colon carcinoma and altered expression of beta-catenin in ulcerative colitis-associated dysplasia and carcinoma, as compared with sporadic colon neoplasms.

BACKGROUND: To clarify the cell adhesion status in ulcerative colitis (UC)-associated colon neoplasm, expression of cell adhesion molecules were investigated and compared with that of sporadic colon neoplasm. METHODS: A total of 14 low grade dysplasias, 16 high grade dysplasias, and 8 adenocarcinomas associated with UC and 17 sporadic adenomas with mild to moderate dysplasia, 22 adenomas with severe dysplasia, and 15 invasive adenocarcinomas were immunohistochemically examined using monoclonal antibodies against CD44, E-cadherin, alpha- and beta-catenin, and deleted colon carcinoma (DCC). RESULTS: CD44, especially its standard form, and DCC expression was stronger in the sporadic colon neoplasms than in the UC-associated lesions. Although E-cadherin did not show significant differences between the two cases, alpha-catenin was more expressed in sporadic colon adenomas with severe dysplasia and carcinomas than in their UC-associated counterparts. Membranous beta-catenin staining was stronger in UC-associated neoplasms, whereas sporadic lesions had greater cytoplasmic and nuclear expression. CONCLUSIONS: The differences in cell adhesion molecule expression suggests that UC-associated and sporadic colon neoplasms arise from different pathways of tumorigenesis.

Cadherins↗
PubMed1995

Adenomatous polyposis coli gene mutations in ulcerative colitis-associated dysplasias and cancers versus sporadic colon neoplasms.

Adenomatous polyposis coli (APC) gene mutations occur in most sporadic colonic adenomas and carcinomas. Precursor lesions of ulcerative colitis (UC)-associated colon carcinomas, although morphologically similar to sporadic adenomas, may be biologically distinct from them and are, in fact, managed differently. Since sporadic adenomas may also occur in UC, a method of discriminating between these forms of neoplasia could have clinical utility. We examined 33 patients with UC-associated dysplasias and cancers and 23 sporadic colon neoplasms in a side-by-side comparison for APC mutations. Codons 686-1693, containing 64% of all reported APC mutations (the mutation cluster region), were screened for truncating mutations using an in vitro synthesized protein assay. Two of thirty-three patients (6%) with UC-associated dysplasias and cancers had a total of three truncating APC mutations, all in frank carcinomas, while 17 of 23 (74%) with sporadic colonic neoplasms had mutations. DNA sequencing confirmed two mutations in codon 1460, replacing arginine with a stop codon, as well as one 2-base pair deletion, resulting in a frameshift and a stop at codon 1477. One specimen contained one each of these APC mutations. This apparent contrast in mutation rates at the mutation cluster region of APC is consistent with other biological characteristics separating sporadic colon neoplasms from UC-associated dysplasias and cancers. These data raise the possibility that nonadenomatous UC dysplasias may arise by a molecular pathway distinct from that prevailing in sporadic colon carcinogenesis, and they suggest a molecular assay to discriminate between sporadic adenomas and dysplasias occurring in UC.

Base Sequence↗
PubMed1988

Ultrasonographic diagnosis of clinically non-palpable primary colonic neoplasms.

Over a 2-year period, more than 1700 abdominal ultrasound scans were performed which included a search for bowel disease in the scanning routine. Features consistent with a primary colonic neoplasm were reported in 35 patients. In 14 patients, ultrasound indicated the possibility of a colonic neoplasm in the absence of a clinically palpable mass. An intraabdominal mass was confirmed in 12 patients (86%), and was a primary colonic neoplasm in 11 patients (79%). In one patient a metastatic malignant mass had been misinterpreted as arising from the colon. In two patients no lesion could be demonstrated to account for the ultrasonographic abnormality. In a further 21 patients in which an abdominal mass had been evident on clinical examination, ultrasound was performed for further elucidation and indicated the mass to be arising from the colon. In this group, a primary colonic neoplasm was the cause in 11 patients (52%), while other primary or metastatic malignancy was found in six patients (29%) and benign disease in four patients (19%). We conclude that ultrasound is a useful primary diagnostic technique for colonic neoplasms, with a predictive value of 79% in detecting clinically non-palpable lesions. In our experience, false positive results due to scanning artefacts are rare. We consider that examination of the bowel is a worthwhile addition to the routine scan in patients with non-specific abdominal complaints.

Adolescent↗
PubMed1998

Proliferative patterns of rectal mucosa as predictors of advanced colonic neoplasms in routinely processed rectal biopsies.

OBJECTIVES: We sought to determine whether the evaluation of rectal cell proliferation in routinely processed rectal biopsies of apparently normal mucosa can predict the presence of advanced colonic neoplasms. METHODS: Fifty consecutive patients, who did not meet any of the following exclusion criteria, underwent total colonoscopy. Patients with nonadvanced adenomas, inflammatory bowel disease, hereditary predisposition to colonic cancer, or a history of colonic neoplasms were excluded. Patients with neoplasms in the distal 40 cm of the large bowel were also excluded. An adenoma was considered advanced if it had a diameter > 1 cm, or villous or severe dysplasia histology were present. In 26 of the 50 patients (Group A: 16 men, 10 women; mean age, 65 yr) advanced colonic neoplasms (advanced adenomas or cancer) were detected; in the remaining 24 (Group B: 13 men, 11 women; mean age, 66 yr) the large bowel was free of neoplasms. In all patients the proliferative patterns of apparently normal rectal mucosa were evaluated using the monoclonal antibody MIB-1 to assess the expression of Ki-67 antigen in routinely processed tissues. Proliferation index for the entire crypt, as well as proliferation indices for each of the five equal compartments, into which the crypt had been divided longitudinally, were calculated for each patient. RESULTS: The mean proliferation indices were similar between the two groups compared. The mean proliferation index for the upper crypt compartments (4 + 5) in the Group A patients was significantly higher than for those of the Group B patients (p < 0.01). Multivariate stepwise logistic regression analysis revealed that among gender, age, and proliferative parameters, the pattern of cell proliferation in the upper rectal crypt (4 + 5) compartment was the only predictor of advanced colonic neoplasms (beta = 11.01, p < 0.001). CONCLUSIONS: Our data suggest that the evaluation of the upward expansion of the rectal crypt proliferative zone in routinely processed rectal biopsies of apparently normal mucosa appears to predict the presence of advanced colonic neoplasms. These preliminary results should be confirmed in larger studies.

Adenoma↗
PubMed1998

Colonic chicken skin mucosa: an endoscopic and histological abnormality adjacent to colonic neoplasms.

OBJECTIVES: We recently described an endoscopic finding of pale yellow-speckled mucosa adjacent to colonic neoplasms. This resembled the appearance of chicken skin and was named chicken skin mucosa (CSM). CSM differs from previously reported gastrointestinal xanthelasmas in that this entity always occurs in association with colonic neoplasms. The prevalence, endoscopic characteristics, clinical significance, and possible etiology were investigated. METHODS: Eight hundred fifty-two consecutive colonoscopies were prospectively evaluated for the presence of CSM associated with either cancer or adenomas > or = 1 cm. Electron microscopy and histopathology using hemotoxylin and eosin, mucicarmine, and oil red O stains were performed. Twelve consecutive colon cancer resection specimens were prospectively examined to determine the presence of histologic CSM. RESULTS: CSM was adjacent to eight of 10 distal colorectal cancers, one of four proximal colon cancers, 16 of 42 distal adenomas, and three of 44 proximal adenomas. Four of seven resected distal cancers demonstrated histological evidence of CSM. Biopsies of the CSM revealed that lipid-filled macrophages in the lamina propria were responsible for this endoscopic appearance. Electron microscopy showed that the surface epithelial cells had small intestine-like microvilli. CSM was not seen with other colonic conditions and was not associated with the laxative preparation. In four instances, identification of the CSM alerted the endoscopist to the presence of polyps in locations difficult to visualize. CONCLUSIONS: CSM is an endoscopic entity that occurs as a result of fat accumulation in macrophages in the lamina propria of the mucosa adjacent to colonic neoplasms. Small intestine-like microvilli were present in CSM and the pathophysiological implications remain to be elucidated.

Adenoma↗
PubMed1985

Inhibitory effects of secretin on gastrin-stimulated rat colon neoplasms.

A study was done to determine if continuous administration of exogenous secretin would inhibit the trophic effect of elevated endogenous gastrin on colon neoplasms in rats. Colon tumors were induced in 37 Fisher rats by subcutaneous injection of 1,2-symdimethylhydrazine, 20 mg/kg, weekly for 18 weeks. Elevation of endogenous gastrin was achieved by antral exclusion surgery. Control rats received a sham operation. Subcutaneous osmotic minipumps delivered 35.5 U/kg/day of secretin for 7 days before the rats were killed. Rats receiving antral exclusion had significantly elevated serum gastrin levels and increased 3H-thymidine incorporation into tumor DNA compared with sham rats (P less than 0.05). There was a significant decrease in tumor DNA uptake in antral exclusion rats that received secretin as compared with antral exclusion rats without secretin (P less than 0.05). Therefore it appears that gastrin does have a trophic effect on rat colon neoplasms and that secretin does inhibit this effect, in a dose-related manner. The results of this study imply that hormonal manipulation of colon cancer may eventually become a viable therapeutic modality.

Animals↗