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PubMedDate not supplied

Effect of tumour size on the in vivo growth inhibition of human colon carcinoma cells (HT-29) by colon mitosis inhibitor.

We have previously shown that the colon mitosis inhibitor (CMI) suppresses the growth of transplanted HT-29 human colon carcinoma cells by approximately 40%. However, this effect declined along the time-course, as the inoculums progressively grew larger. In the present work we designed a test to assess the effectiveness of CMI as a function of tumour size. After ranking the terminal tumours by ascending size in the control group and the CMI group the growth inhibition was calculated at each rank position. The observed negative correlation between control tumour size and CMI inhibition (r = -0.94, p < 0.001) clearly demonstrated decreased growth inhibition with increased tumour size. Consequently, a retrospective analysis of the smallest and slowest growing tumours showed a profound growth inhibition (72-81%, p < 0.008), whereas a similar analysis of the large and fast growing tumours revealed no significant CMI effect. The increased CMI effect among slow growing tumours was apparently not associated with increased susceptibility to CMI in a subset of slow growing cells because the slow growing subclone HT-29A4 did not show increased CMI effect. Furthermore, HT-29A4 displayed a similar tendency of decreased CMI effect with increased tumour size (r = -0.70, p < 0.001). Interestingly, the same tendency of increased growth inhibitory effect on smaller tumours was also seen with retinoic acid and difluoromethylornithine (r = -0.96, p < 0.001). The apparent enhanced responsiveness among small tumours underlines the importance of early chemoprevention and chemotherapy.

Adenocarcinoma↗
PubMedDate not supplied

Pyroglutamyl-histidyl-glycine, the endogenous colon mitosis inhibitor, regulates cyclic AMP level in non-tumorigenic colonic epithelial cells.

BACKGROUND: We have proposed that the mitosis inhibiting peptide, pyroGlu-His-Gly (pEHG), a colon-specific negative feedback regulator of cell proliferation, works through a G protein-coupled receptor (GPCR), as do many other pyroglutamyl-peptides. MATERIALS AND METHODS: Non-tumorigenic YAMC (colon mucosa of Immorto mice), IMCE (Immorto-Min mouse hybrid) and human hepatoma (HepG2) cell lines were exposed to pEHG. cAMP concentrations were measured with a protein binding assay, mRNA levels with real-time PCR and Ca2+ concentration with an inverted fluorescence microscope on Fura-2/AM-loaded cells. RESULTS: pEHG (1 nM) increased the intracellular concentration of cAMP after 5-10 min in YAMC cells, but not in HepG2 cells. No effect was seen on cytosolic Ca2+, or in the expression of the proliferation and differentiation regulatory genes c-fos, egr-1 or fosB in YAMC or IMCE cells. CONCLUSION: pEHG stimulates the second messenger cAMP, but has no effect on intracellular Ca2+ or the gene expression of c-fos, egr-1 or fosB.

Animals↗
PubMed1979

Scanning electron microscopy of interaction of peripheral blood lymphocytes from colonic cancer patients with human colonic cancer-derived cells; P-4788.

Peripheral blood lymphocytes and the various lymphocyte fractions from patients with cancer of the colon were cultivated with target cells (P-4788) derived from the colon cancer. Changes in the surface ultrastructure during tumor cell destruction were studied by scanning electron microscopy (SEM). P-4788 cells adhering to the coverslip showed various surface activity. The surfaces of some cells were relatively flat; others were smooth or had fine granules. Still other cells were villous, round or had marked blebs. When host lymphocytes were added to the target cells, adhesion of the two cell groups began by many fine projections. After incubation for 6 h, some lymphocytes had adhered to the target cells. Many lymphocytes had adhered to the target tumor cells by 24--48 h incubation. Ultimately the tumor cells became swollen and disrupted. Most lymphocytes adherent to the target cells had few microvilli. Lymphocytes after elimination of phagocytes by carbonyl iron treatment also adhered readily. Some target cells showed adhesion with lymphocytes passed through nylon-wool columns, although the number of lymphocytes adhering was fewer than in the case of lymphocytes not passed through nylon-wool columns. T cells were collected from lymphocytes that form rosettes with SRBC by isolation with NH4Cl. They had markedly elongated microvilli which in places were sparsely scattered and tended to be localized on the side, a finding which suggests loss of cell activity by the time of SEM. Only a few T cells adhered to target cells and they seemed to be T cells without activity. It was thought that there are cytotoxic cells among T cells and that the co-existence of T cells, non-T cells and monocytes caused target cell destruction.

Adenocarcinoma↗
PubMed2006

Colonic amoebic abscess mimicking carcinoma of the colon.

Amoebiasis is an uncommon disease in developed countries. Its clinical presentation can be variable and non-specific, and the diagnosis can be easily overlooked. We report a case of colonic amoebic abscess mimicking advanced colonic cancer with acute intestinal obstruction and liver metastasis. The presentation, diagnosis, and treatment of amoebiasis are also reviewed.

Animals↗
PubMed1990

[Extend of colonic excision in the curative treatment of cancers of the left colon. Left or segmental hemicolectomy? A controlled prospective multicenter study].

The ideal extent of colic excision in the curative treatment of left colic cancers has not yet been defined. The aim of this study is to compare the survival rates following left hemicolectomy and segmental colectomy. Over a period of 5 years from 1980 to 1985, 270 consecutive patients with cancer of the left colon without visceral metastases nor invasion of neighboring organs were included in the study. Survival at 5 years was the main criterion of assessment, with mortality and morbidity being the secondary criteria. 10 patients were excluded a posteriori. Out of the remaining 260 patients, 131 were operated with left hemicolectomy and 129 with segmental colectomy. Both groups were comparable as regards age; sex, risk factors (diabetes, renal failure), radiation therapy, antimitotics, procedure of anastomosis (hand or machine), protective colostomy, size of the tumor, and Dukes' stage. Only the length of the colon resected proximel to the tumor was greater in left hemicolectomy. 16% of the patients had a Dukes A adenocarcinoma. Postoperative mortality was higher after left hemicolectomy (6.1%) than after segmental colectomy (2.3%), but not significantly. Morbidity was similar. The survival rate at 5 years, including immediate deaths, was 64.8% after left hemicolectomy and 65.8% after segmental colectomy. Both survival charts could be strictly superimposed without significant differences. Left hemicolectomy therefore produced results that were comparable to those of segmental colectomy.

Colectomy↗
PubMed1990

[Fecal intestinal flora in patients with colon adenoma and colon cancer].

Fecal intestinal flora in patients with colon adenoma showed significant decrease of Bifidobacterium. A tendency of decrease of Bifidobacterium and increase of Clostridium-other was shown in adenomas with higher degree atypia, but no definite tendency could be found concerning its size. Compared with the control group, patients with colon cancer showed significant increase of Clostridium-other and decrease tendency of Bifidobacterium which was not relevant to its percentage of total circum ference involved by the cancer. From the above findings, it is suggested that tumor growth or malignant transformation has relation to Bifidobacterium and Clostridium-other.

Adenoma↗
PubMed1982

Patterns for normal colon mucosa and colon adenocarcinoma compared by two-dimensional gel electrophoresis.

A two-dimensional gel "map" of the proteins in normal cells and transformed cells may well help establish the presence of putative tumor-specific protein antigens, which can be isolated and used as antigens. We so examined normal colon mucosa and colon adenocarcinoma, using a sensitive silver stain. Samples were promptly prepared after excision by rapidly trimming the tissue to a small, grossly homogeneous piece, which was frozen on solid CO2. Frozen histological sections and permanent mounts were also prepared for several areas, to document the cellular constitution and to grade the carcinoma. Sample preparation for electrophoresis is described. The DNA was pelleted by centrifugation (108 000 x g x 1.5 h). Little or no pellet was observed, indicating complete solubilization. Many of the tumors contained proteases, liberated during sample preparation, so protease inhibitors were included. A highly reproducible pattern was observed for normal mucosa. Comparison of the gels from paired samples with histological data allows many of the spots to be tentatively assigned to the different cell types present in the mucosa (epithelium, connective tissue, or muscularis mucosa) and, in most tumors analyzed, detection of a series of spots that are not detectable in the pattern for normal tissue. These apparently tumor-associated proteins may be of epithelial cell or stromal origin.

Adenocarcinoma↗
PubMedDate not supplied

Prolonged monitoring of colonic spike activity by a computerized system: application to the rabbit colon.

In the present paper, we describe and validate a computerized system for the quantitative analysis of colonic spike activity in the conscious rabbit. This system allowed data acquisition at 160 Hz on 8 channels simultaneously during the recording session. Data analysis at the end of the recording session took approximately 10 min for each hour of recording. The spike recognition procedure was carried out on the basis of a discriminant function which discarded artifactual fast events. Data could be presented as histograms or be transferred into an ASCII file for later statistical analysis. Reliability tests showed that the misrecognition rate was only 3.88%. In conclusion, this computerized system is a reliable, timesaving tool for the quantitative analysis of colonic spike activity.

Action Potentials↗
PubMed1994

Focal polypoid ischemia of the colon: atheroemboli presenting as a colonic polyp.

Cholesterol emboli are known to imitate a variety of disease processes, thereby leading to delayed diagnosis. We describe a patient with a localized polypoid mass of the colon without endoscopic evidence of generalized ischemic colitis. Histologic evaluation revealed this polyp to be the result of localized ischemia with identifiable submucosal atheroemboli. Localized polyp formation appears to be a rare manifestation of atheroemboli; consequently, focal ischemia, caused by atheroemboli, should be added to the differential diagnosis of polyps of the colon.

Colitis, Ischemic↗
PubMed1993

T cell retargeting using bispecific monoclonal antibodies in a rat colon carcinoma model. II. Syngeneic colon carcinoma CC531 is efficiently killed by retargeted cytotoxic T lymphocytes in vitro despite limited lysis in 51Cr release assays.

We have previously described the generation of bispecific anti-TCR*anti-tumor mAb, intended for in vivo analysis of T cell retargeting in a syngeneic rat colon carcinoma model. Colon carcinoma CC531 proved to be markedly resistant to lysis by polyclonally activated, retargeted rat T lymphocytes, if measured in short term or overnight prolonged 51Cr release assays. Using cocultivation, we have now focused on another, biologically more relevant aspect of retargeted interaction: the effect on the capacity of CC531 tumor cells to survive and grow. Tumor neutralization was scored after 3 days of coculture, using a tetrazolium salt to quantify viable adherent tumor cells. Compared to 51Cr release assays, we found cocultivation to be more sensitive and more informative, as it revealed tumor cell killing at low E:T ratios, synergism of bispecific antibodies and exogenous IL-2, and free bispecific antibody-dependent recycling of effector cells. Apart from providing valuable information for future in vivo studies in this model, these data support the notion of tumor neutralization as a useful alternative for 51Cr release assays.

Animals↗
PubMed1997

Suppression of experimental lung colonization of mouse colon adenocarcinoma 26 in vivo by an anti-idiotype monoclonal antibody recognizing a platelet surface molecule.

The interaction between platelets and tumor cells is important in the formation of pulmonary metastasis. We previously established the 8F11 monoclonal antibody (mAb) by immunizing rats with the NL-17 cell line, a highly metastatic variant of mouse colon adenocarcinoma 26. 8F11 could inhibit the platelet aggregation in vitro and suppress the pulmonary metastasis in vivo by NL-17 cells. 8F11 recognized the Mr 44,000 sialoglycoprotein (gp44) on NL-17 cells, and the affinity-purified gp44 alone could induce platelet aggregation. Therefore, 8F11 might inhibit gp44-induced platelet aggregation by masking the epitope of gp44 that interacted with unknown molecule(s) on the platelet surface. To identify the platelet antigen that interacted with gp44, we generated anti-idiotype mAbs by immunizing rats with 8F11. Two of the established mAbs, AIP1 and AIP4, recognized not only 8F11 but also the Mr 160,000 platelet surface protein. AIP4 mAb could also inhibit the NL-17 cell-induced platelet aggregation in a dose-dependent manner. Furthermore, pretreatment of mice with AIP4 mAb suppressed the pulmonary metastasis of NL-17 cells in vivo. These results suggest that the Mr 160,000 platelet antigen participates in the NL-17 cell-induced platelet aggregation and colonization of NL-17 cells in the lung by interacting with the gp44 of NL-17 cells.

Adenocarcinoma↗
PubMed1984

Distribution of histocompatibility and leucocyte differentiation antigens in normal human colon and in benign and malignant colonic neoplasms.

Monoclonal antibodies (McAbs) directed against the framework determinants of Class I and Class II products of the major histocompatibility complex (MHC) and against leucocyte differentiation antigens were used in an indirect immunoperoxidase technique to study their expression in normal, benign (adenomatous polyps) and malignant disease of the colon. Class I products (detected by the McAb 2A1) were strongly expressed on all cell types in normal and benign tissues but some carcinomas exhibited a heterogenous pattern of epithelial cell staining and 4/15 were completely negative. Class II products (detected by TDR31.1) were strongly expressed on cells (mainly B lymphocytes) within the lamina propria. In carcinomas TDR31.1 staining was mainly interstitial, but in 2/15, DR + epithelial cells were also detected. In normal and benign tissues, leucocytes (reactive with 2D1) found predominantly in the lamina propria, comprised T cells mainly of the helper/inducer (OKT4) subset, DR + cells in approx. equivalent proportion and a few OKM1+ cells mostly of macrophage morphology. Occasional intraepithelial lymphocytes were of cytotoxic/suppressor (OKT8) phenotype. In malignant neoplasms, there was wide inter and intra-tumour variation in the proportion of leucocytes which were heterogeneous with respect to cell type and confined mainly to the stroma. T cells were consistently predominant, but B cells and macrophages were also present. Two neoplasms showed unequivocal evidence of a shift (relative to peripheral blood) in favour of the OKT8+ subset, but in the majority of tumours OKT4+; and OKT8+ cells were present in roughly similar proportions. Natural killer cells (monitored with Leu7, HNK1) were virtually undetectable in both normal and malignant tissues. There were no apparent correlations between the extent and type of leucocyte infiltration, tumour differentiation or expression of MHC products. Some implications for the extrapolation of in vitro data on leucocyte function to the in vivo situation are discussed.

Adenocarcinoma↗
PubMed1987

DNA in situ sensitivity to denaturation: a new parameter for flow cytometry of normal human colonic epithelium and colon carcinoma.

Modal DNA (ploidy) and sensitivity of DNA in situ to denaturation by acid have been analyzed by flow cytometry of 10 colorectal adenomas and 35 adenocarcinomas; 39 normal mucosa samples served as controls. A new method was developed to denature DNA in chromatin of the freshly isolated, intact, and unfixed individual cell nuclei from surgically resected material. The sensitivity of DNA denaturation (T alpha) was assayed by metachromatic staining with acridine orange and calculated as a ratio of the alpha t index of the tumor sample to the alpha t index of normal mucosa; the alpha t index is that fraction of DNA, following treatment at pH 1.4, that stains metachromatically with acridine orange at pH 2.6. All adenomas were diploid and in nine of 10 the T alpha value was close to 1.00, indicating no difference from control specimens in DNA sensitivity to denaturation. Forty-nine% of adenocarcinomas were aneuploid. Forty-six% of adenocarcinomas differed from normal in sensitivity of DNA to denaturation; the T alpha value was lower than 0.90 indicating that chromatin of the tumor cells was more resistant to denaturation than control cells. There was no correlation between sensitivity to denaturation of DNA and incidence of aneuploidy. However, there was a correlation between T alpha and the pathologically determined stage of disease. There was increased resistance to denaturation in 58% of tumors classified as Dukes' C/D stage, in 36% of tumors classified as Dukes' B, and in 20% classified as Dukes' A stage of the disease. Statistical analysis of these results revealed significant differences between distributions of T alpha in noninvasive (Adenomas and Dukes' A) versus invasive (Dukes' B and C/D) tumors with level of significance at P = 0.02. The data suggest that acid denaturation of DNA in situ may be a valuable adjunct in assessing the biology of colon cancer. The molecular basis for this phenomenon is discussed.

Acridine Orange↗
PubMed1986

Antigen expression in normal and neoplastic colonic mucosa: three tissue-specific antigens using monoclonal antibodies to isolated colonic glands.

Monoclonal antibodies to normal colonic glands were used to localize three tissue-specific antigens in sections of 40 hyperplastic polyps, 29 adenomas, 43 colorectal adenocarcinomas, and blocks or rolls of histologically normal large bowel mucosa. Two antibodies identified antigens (designated 3NM and 17NM) associated with the mucin vacuole of goblet cells and the third antibody identified a cell membrane antigen (designated 6NM). Antigen 3NM was absent from virtually all carcinoma cells and from all, or most, cells of hyperplastic polyps. Antigen 17NM was absent from 21 carcinomas, with some antigen-positive cells present in the others. Antigen 6NM content was unchanged compared to normal mucosa in 12 carcinomas, decreased somewhat in another 20, and either absent or markedly depleted in 11. Antigen 6NM increased in 22 hyperplastic polyps. Three cancer patients synthesized 6NM in their normal mucosa but the cellular distribution was abnormal. Antigens decreased in most adenomas, with heterogeneity of expression seen in glands and cells of some adenomas. Low concentrations of one or more antigens in normal mucosa were significantly more frequent (P less than 0.05) in patients with metastases than in those with stage A or B tumors.

Adenoma↗
PubMed1985

[Cancer of the colon following ureterosigmoidostomy or following bladder enlargement using a colonic graft].

The role of carcinogenic factors following urinary diversion are here studied on the basis of three very different cases. In the first, an adenocarcinoma developed at the site of a ureterocolic anastomosis thirty one years after Coffey's operation for bladder exstrophy. In the second, the tumor had developed, 31 years after uretero-sigmoidostomy, for ureteral trauma. The anastomosis had moreover ceased to function ten years previously. In the third case, the patient had undergone a right nephrectomy for urinary tuberculosis and a colocystoplasty to enlarge the bladder with re-implantation of the left ureter in the graft. Twenty one years later, an adenocarcinoma developed at the site of the anastomosis between the colonic graft and the bladder. This was an exceptional case (possibly the first) of a cryptal tumor developing out of contact with material. It thus runs counter to the alleged role of facies in the development of adenocarcinomas following urinary diversion.

Adenocarcinoma↗
PubMed1993

[Colonic ileus. Treatment of colonic ileus, a 10-year patient material].

Morbidity and mortality have been evaluated in 238 patients with acute large bowel obstruction admitted over a ten year period. In two thirds, the cause of obstruction was a primary colonic carcinoma. Most of these patients (61%) had advanced disease and were over 70 years of age. Volvulus and cancer recurrences each accounted for 10%, and diverticulitis for eight percent. An overall mortality of 24% was found. Of 115 patients who had the obstructing lesion--primary carcinoma or diverticulitis--resected, a mortality of 8.7 was seen, higher for primary (14.9%) than for staged (4.4%) resections, in contrast the latter had a significantly longer hospital stay, 30 days as against 17 days when a primary resection was performed. Six non-lethal anastomotic leaks occurred. It is concluded, that patients with large bowel obstruction, most often caused by a colorectal carcinoma, are a high-risk group. In this retrospective study staged procedure compared with primary resection had lowest morbidity and mortality.

Adult↗