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PubMed2005

Leptin stimulates the proliferation of human colon cancer cells in vitro but does not promote the growth of colon cancer xenografts in nude mice or intestinal tumorigenesis in Apc(Min/+) mice.

BACKGROUND AND AIMS: Leptin, the product of the ob gene, has been suggested to increase the risk of colon cancer. However, we have shown that although leptin stimulates epithelial cell proliferation it reduces the development of carcinogen induced preneoplastic lesions in the rat colon. Here, we explored the effect of leptin in vitro on proliferation of human colon cancer cells, and in vivo on the growth of HT-29 xenografts in nude mice and the development of intestinal tumours in Apc(Min/+) mice. METHODS: Proliferation of HT-29, LoVo, Caco2, and SW 480 cells was assessed in the absence or presence of leptin (20-500 ng/ml) by 3H-thymidine incorporation and cell count. Leptin (800 microg/kg/day) or its vehicle was delivered for four weeks to nude mice, inoculated with HT-29 cells on day 0, and for six weeks to Apc(Min/+) mice. RESULTS: Leptin dose dependently stimulated cell DNA synthesis and growth in all cell lines. In nude mice, leptin caused a 4.3-fold increase in plasma leptin levels compared with pair fed controls. This hyperleptinaemia, despite leptin receptor expression in tumours, did not induce significant variation in tumour volume or weight. Tumour Ki-67 index was even inhibited. In leptin treated Apc(Min/+) mice, a 2.4-fold increase in plasma leptin levels did not modify the number, size, or distribution of intestinal adenomas compared with pair fed controls. CONCLUSIONS: Leptin acts as a growth factor on colon cancer cells in vitro but does not promote tumour growth in vivo in the two models tested. These findings do not support a pivotal role for hyperleptinaemia in intestinal carcinogenesis.

Adenoma↗

PubMed1989

Comparative study of carcinoembryonic antigen and epithelial membrane antigen expression in normal colon, adenomas and adenocarcinomas of the colon and rectum.

The heterogeneous nature of tumour antigen expression may require selection of monoclonal antibodies on an individual patient or tumour basis to allow adequate tumour localisation. Carcinoembryonic antigen (CEA) and epithelial membrane antigen (EMA) expression has not previously been compared in colorectal cancer patients. Sections of cancer (n = 52), adjacent normal colon (n = 45), synchronous adenomas (n = 11) and nodal metastases (n = 49) were examined by indirect immunoperoxidase staining in 51 consecutive patients with colorectal cancer using monoclonal antibodies to CEA and EMA. The percentage of cells with positive staining in the primary tumours was graded 1: less than 25%, 2: 25-49%, 3: 50-75%, 4 greater than 75%. All primary colorectal cancers expressed CEA and 43 of 52 expressed EMA (83%). Grading showed CEA greater than EMA in 39, equal in 11 and less in two. Well differentiated cancers were more frequently graded three or four for CEA staining (23 of 27) than moderately differentiated cancers (11 of 22) (p less than 0.01). Equivalent figures for EMA were four of 27 and three of 22 (not significant) (NS) although the majority (86%) were graded 1 and 2. Grade 1 CEA expression was found in six of 15 proximal and only two of 37 distal lesions (p less than 0.01, chi 2 test) while for EMA equivalent figures were three of 15 and six of 37 (NS). Nodal deposits all expressed CEA and 45 of 49 expressed EMA (92%); 29 of 45 normal colon sections showed CEA expression (64%) as did all adenomas. EMA was not expressed by normal colon or adenomas. These results suggest that EMA expression is more specific but less sensitive than CEA for colonic cancer and is independent of tumour differentiation and site. Thus selecting monoclonal antibodies to CEA or EMA based on tumour biopsies may allow improved tumour localisation for imaging or therapy in patents with colorectal cancer.

Adenocarcinoma↗

PubMed1992

Quantification of pancreatic secretory trypsin inhibitor in colonic carcinoma and normal adjacent colonic mucosa.

AIMS: To measure the content of immunoreactive human pancreatic secretory trypsin inhibitor (irPSTI) in colonic carcinoma and adjacent normal colonic mucosa. METHODS: From a stable hybridoma cell line producing monoclonal antibodies specific for human PSTI, a specific enzyme linked immunosorbent assay (ELISA) for human PSTI was developed. In a precipitation assay system these antibodies bound human PSTI in a dose-dependent manner. The specimens were obtained from resectional surgery. RESULTS: The content of irPSTI was 19.9 micrograms/g protein (0.55 micrograms/g tissue wet weight) in colonic carcinoma. In adjacent normal colonic mucosa 43.6 micrograms/g protein (1.12 micrograms/g tissue wet weight) was shown. CONCLUSIONS: The enzymatic degradation of surrounding tissue necessary for tumour cell invasion could be facilitated by this relative deficit of the inhibitor in infiltrative carcinoma.

Antibodies, Monoclonal↗

PubMed2003

Anthocyanin-rich extract from Aronia meloncarpa E induces a cell cycle block in colon cancer but not normal colonic cells.

Anthocyanin-rich extracts, potent antioxidants and commercially available food coloring agents, have been reported to inhibit growth of various cancer cell lines. We investigated the effect of semipurified anthocyanin-rich extract from fruits of Aronia meloncarpa, on normal colon and colon cancer cell lines. A 24-h exposure to 50 mg monomeric anthocyanin/ml of Aronia extract resulted in 60% growth inhibition of human HT-29 colon cancer cells. The treated cells showed a blockage at G1/G0 and G2/M phases of the cell cycle. The cell cycle arrest coincided with an increased expression of the p21WAF1 and p27KIP1 genes and decreased expression of cyclin A and B genes. Prolonged exposure to the extract resulted in no further change in the cell number, indicating a cytostatic inhibition of cell growth. NCM460 normal colon cells demonstrated <10% growth inhibition at the highest concentration of 50 mg/ml extract. A 35% decrease in the cyclooxygenase-2 gene expression was observed within 24 h of exposure of HT-29 cells but did not translate into decreased protein levels or protein activity. These results support the need for further research to identify the specific component(s) in this extract that suppress cancer cell growth and the genes affected by these natural compounds.

Anthocyanins↗

PubMed1993

Colonic epithelial proliferation indices before and after colon cancer removal.

Rectal mucosal (epithelial) proliferation labeling indices (LI) have been widely used as a risk marker for colorectal cancer and as an intermediate end-point in chemoprevention studies. The purpose of this study was to determine whether the presence of cancer preoperatively altered the LI and whether these LI could be used over the long term as a marker for colon cancer. We studied 25 patients (18 with colorectal cancer and 7 with benign colonic diseases) who were admitted for colonic resection. Biopsies for thymidine LI were taken before, during, and 4 and 7 months after the operation. The preoperative LI of cancer patients was higher, but not significantly, than that of noncancer patients (5.22 +/- 3.54 and 4.11 +/- 1.34%, respectively, p = 0.28). The intraoperative LI was significantly higher than the preoperative LI (8.08 +/- 4.00 and 4.90 +/- 3.07%, respectively; p = 0.004). After 4 and 7 months, the LI was not significantly different from the preoperative LI (p = 0.60 and 0.89, respectively). Resection of a colonic segment did not affect the level of proliferation over time. Therefore, it is unlikely that LI can be used as a marker to predict local recurrence after curative resection of colorectal cancer.

Adult↗

PubMed2002

Detection of Enterobius vermicularis eggs in the submucosa of the transverse colon of a man presenting with colon carcinoma.

We report a case of a chronic infiltrate of the intestinal wall of the transverse colon by the eggs of Enterobius vermicularis in a man who had immigrated to Taiwan from mainland China 50 years ago. During surgery for suspected transverse colon carcinoma, histologic examination of the tumor mass revealed eggs of E. vermicularis embedded in granulation tissue in the submucosa of the transverse colon. Results of a stool examination were negative for eggs but strongly positive for occult blood. The mass in the transverse colon was completely removed during surgery. At the present time, the patient remains asymptomatic.

Aged↗

PubMed1997

[Preoperative colonic lavage and one-stage excision-anastomosis in obstruction of the left colon].

In a retrospective series of 95 patients requiring emergency surgery for distal colonic obstruction, primary bowel resection followed by immediate anastomosis after intraoperative colonic irrigation was performed. Carcinoma was the cause of obstruction in 81 cases (85%); 13 patients had diverticulitis, and 1 had sigmoid volvulus. The technique of on-table lavage was similar to that described by Dudley in 1980: a caecostomy tube was used in 86 patients (90%) and was removed on the tenth postoperative day. 4 patients died, none from complications of anastomotic leakage. There were three anastomotic leakages (3.1%) and 10 radiologic leaks were observed. 3 patients were reoperated. The mean hospital stay was 23 days. The results of this study suggest that intraoperative colonic irrigation is an effective method, enabling the surgeon to perform primary anastomosis with reasonable safety after emergency resection of selected distal colonic lesions.

Aged↗

PubMed2000

Genetic reprogramming in pathways of colonic cell maturation induced by short chain fatty acids: comparison with trichostatin A, sulindac, and curcumin and implications for chemoprevention of colon cancer.

The short-chain fatty acid butyrate, produced by microbial fermentation of dietary fiber in the large intestine, is a physiological regulator of major pathways of colonic epithelial cell maturation: cell cycle arrest, lineage-specific differentiation, and apoptosis. Microarray analysis of 8,063 sequences demonstrated a complex cascade of reprogramming of SW620 colonic epithelial cells upon treatment with butyrate characterized by the progressive recruitment of gene sets as a function of time. Comparison with the effects of trichostatin A, in conjunction with differences in the kinetics of alteration of histone acetylation induced by butyrate and trichostatin A, identified subsets of induced and repressed genes likely coordinately regulated by altered histone acetylation. The butyrate response was also compared in detail with that of sulindac, a nonsteroidal anti-inflammatory drug with significant chemopreventive activity for colon cancer, and curcumin, a component of mustard and curry structurally and functionally related to sulindac that also has chemopreventive activity. Although gene clusters were identified that showed similar responses to butyrate and sulindac, the data were characterized by the extensive differences in the effects of the two agents. This was striking for functional classes of genes involved in signaling pathways and in cell cycle progression, although butyrate and sulindac induce a similar G0-G1 arrest, elevation of beta-catenin-Tcf signaling, and apoptotic cascade. As regards cell cycle arrest, the underlying mechanism in response to butyrate was most similar to that of the Caco-2 cell line that had spontaneously undergone a G0-G1 arrest and least similar to the G2-M arrest stimulated by curcumin. Thus, high-throughput microarray analysis of gene expression profiles can be used to characterize and distinguish the mechanisms of response of colonic epithelial cells to physiological and pharmacological inducers of cell maturation. This has important implications for characterization of chemopreventive agents and recognition of potential toxicity and synergies. The data bases, gene clusters, and analyses are available at http:// sequence.aecom.yu.edu/genome/.

Acetylation↗

PubMed2002

[Functional activity of ABC transporters (markers of multidrug resistance) in human colon adenocarcinoma and normal colonic mucosa].

Functional activity of multidrug resistance (MDR) markers (total activity of ABC-transporters, P-glycoprotein (Pgp) and multidrug resistance-associated protein (MRP) activities) in human colon adenocarcinoma and normal mucosa was examined. Functional activity of ABC-transporters was revealed in all colon tumors and in 70% of normal mucosa samples investigated. Expression of Pgp and MRP functional activity was determined in about 50% and 70% of colon tumors respectively. Pgp+MRP+ phenotype was determined in 36% of normal mucosa and adenocarcinoma samples. Expression of Pgp+MRP- phenotype was practically the same in normal mucosa and tumors (in 10 and 18% of samples respectively). Pgp-MRP+ phenotype was revealed two times more often in tumors than in mucosa--in 36 and 18% respectively. On the contrary, Pgp-MRP- phenotype was detected more rarely in tumors than in mucosa (in 10 and 36% of samples respectively). Transporters different from Pgp and MRP were also determined in some tumors and normal mucosa. At the patients with expression of Pgp function in normal mucosa the activity of the transporter was revealed in 25% of tumor samples only. On the contrary, at the patients with expression of MRP function in normal mucosa the activity of the transporter was revealed in 70% of tumor samples. At the patients with no expression of Pgp or MRP activity in normal mucosa the function of the transporters in tumors was determined in 60% and 70% of samples respectively. It is concluded that functional activity of various ABC-transporters (Pgp, MRP and other different from Pgp and MRP) is expressed in human colon adenocarcinoma; expression of ABC-transporters functional activity in normal mucosa does not predict MDR phenotype of the tumor.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMedDate not supplied

Growth effects of tamoxifen on Lovo colon carcinoma cells and cultured cells from normal colonic mucosa.

The growth effects of tamoxifen (TAM) were studied using normal and malignant colonic epithelial cells. Addition of TAM (0.8 to 10 microM) to cultured normal human colon epithelial cells and Lovo colon adenocarcinoma cells produced a dose response decrease in growth of 42 to 76%. Histamine (1 to 10 microM) did not affect cell growth and did not negate the TAM effect. Calmodulin (2 micrograms/ml) totally blocked growth inhibitory effects of a calmodulin antagonist, trifluoperazine (10 microM), but did not block the TAM inhibitory effect. These data suggest that antiestrogen binding sites (AEBS) may play an important role in the growth-inhibitory effects of TAM on colon cells. Competition with estrogen and antagonism with histamine or calmodulin do not appear to be significant in this regard.

Adenocarcinoma↗

PubMed1990

Immunohistochemical localization of sodium-potassium-stimulated adenosine triphosphatase and carbonic anhydrase in human colon and colonic neoplasms.

Sodium-potassium-stimulated adenosine triphosphatase and carbonic anhydrase isozymes I and II were localized immunocytochemically in adenomas, adenocarcinomas, and normal epithelium of human colon harboring non-neoplastic lesions. Non-neoplastic control colon showed carbonic anhydrase I and II in the cytoplasm of the columnar cells lining the upper half of the crypts. Antiserum to sodium-potassium-stimulated adenosine triphosphatase bound to the basolateral but not the apical plasmalemma of columnar epithelial cells. Staining was most intense in the superficial cells, which also contained carbonic anhydrase, but was also evident to a lesser degree in cells deep in the crypts. Adenomas and adenocarcinomas failed to stain for content of carbonic anhydrase but retained basolateral sodium-potassium adenosine triphosphatase positivity. The staining characteristics of colonic neoplasms for the two enzymes involved in the transport function of colonic epithelium thus resembled those of the less mature cells lining the base of normal crypts.

Adenocarcinoma↗

PubMed1990

Expression of mitochondrial cytochrome c oxidase in human colonic cell differentiation, transformation, and risk for colonic cancer.

In a panel of eight cloned complementary DNA sequences whose level of expression characterize colon cells as transformed in vivo and in vitro, one which may also serve as a marker of risk in familial polyposis and familial colon cancer flat mucosa has been identified as mitochondrial cytochrome c oxidase subunit 3. Mean level of expression of cytochrome c oxidase subunit 3 decreases progressively in colon adenomas and carcinomas relative to normal mucosa in vivo, and returns to higher levels present in biopsies of normal mucosa when the HT29 human colonic adenocarcinoma cell line is induced to differentiate with sodium butyrate. Quantitation of cytochrome c oxidase subunit 3 DNA by dot blots indicated that these changes in expression were not associated with alterations in the number of mitochondrial genomes.

Adenomatous Polyposis Coli↗

PubMed1989

[Colonic motility and irritable colon].

The importance of colonic motility disorders in the irritable bowel syndrome is now well accepted, but an accurate description of these abnormalities is still wanting. The insufficiency of investigational methods and, mainly, the heterogeneity of the disorders can explain this need. Twenty-four hour recordings of colonic myoelectrical activity can now provide a better knowledge of motor disturbances. No evidence of a specific basic disorder has been presented, and the effects of stress produce contradictory results depending on the method used. In contrast, motility patterns recorded during sleep and after a meal show segmental hyperactivity in painful constipation, abnormalities of the colonic response to feeding in painful abdominal distension, propulsive hyperactivity with absence or reduction of the "sigmoidal brake" in painless diarrhea. However, it appears clearly that myoelectrical activity disturbances can only be observed in two thirds of the patients presenting with functional digestive disorders. "Sensitivity" or personality disorders and disturbances of other organs can explain the physiopathology of "irritable bowels" where no evidence can be found that the colon is involved.

Animals↗

PubMed1979

Isoenzymes of beta-hexosaminidase from normal rat colon and colonic carcinoma.

N-Acetyl-beta-D-hexosaminidase isolated from normal rat colon was compared to that obtained from a transplantable rat colonic carcinoma. Levels of total hexosaminidase from purified epithelial cells of normal colon were similar to those from purified malignant cells from the transplantable tumor. Cultured malignant cells had significantly higher levels of activity than did freshly purified tumor cells. Isoelectric focusing of hexosaminidase from normal rat colon indicated approximately equal amounts of A (pI 5.0 ) and B (pI 8.1) isoenzyme activity. The B isoenzyme (normal cell) was more stable to heat inactivation than was the A isoenzyme and had significantly higher activity at low pH's. In contrast, the B isoenzyme from the tumor was relatively unstable to heat and low pH.

Animals↗

PubMedDate not supplied

[Correlation between colonoscopy and histopathology of the colon in diverticular disease and the irritable colon syndrome].

In this study 29 patients were carriers of diverticular disease of the colons (DDC) and 29 patients with irritable bowel syndrome (IBS). The patients were diagnosed by means of a directed anamnesis standardized by the radiologic study of the colons. The methodology included, radiologic study of the colons, endoscopic examination of the colon (colonoscopy with biopsy) and anatomic pathologic examination of the fragments obtained in the endoscopy. It was tried, by means of colonoscopy with biopsy and anatomic pathological examination, to demonstrate, classify and relate, in agreement with pre-established criterion, the degree of intensity of the inflammatory process in the colic mucosa. According to the results we may conclude that: 1) colonoscopy in the studied inflammatory diseases is important for diagnosis, evaluation of the inflammatory process, identification of associated illness and material obtention for the anatomic pathological examination; 2) there is always a chronic inflammatory process, in variable degrees, of the colic mucosa in DDC and in IBS; 3) colonoscopy with biopsy and the anatomic pathological examination are adequate to diagnose with precision the degree of intensity of the chronic inflammatory process of the colic mucosa and the presence of associated disease in DDC and in IBS.

Adult↗

PubMed1983

[ Pathology of the colon associated with diverticulosis of the descending colon and the sigmoid. Instrumental clinical study ].

A retrospective survey was carried out on 87 patients with diverticulosis and 223 control subjects with a view to studying the incidence of colon pathology in association with diverticulosis of the colon. All subjects were given colonoscopies of the distal section of the colon. The survey revealed that the group of diverticulosis patients was, on average, older than the control group (72 v. 59 years). There was no significant difference in the performance or totality of the endoscopic examination. Subjective and objective symptomatology revealed no a priori evidence of pathology associated with diverticulosis. There was no statistically significant difference in the incidence of polyps, neoplasias, haemorrhoids or colon melanosis in the two groups.

Aged↗

PubMed1984

12-O-Tetradecanoylphorbol-13-acetate stimulation of DNA synthesis in cultured preneoplastic familial polyposis colonic epithelial cells but not in normal colonic epithelial cells.

We have developed a method for the routine primary culture of human colonic epithelial cells. Cultured cells exhibited characteristic epithelial structures, including a brush border and junctional complexes. Flask-like goblet cells containing mucus were also seen within the epithelial monolayer. [3H]Thymidine labeling indices were used to distinguish between cultured cells from familial polyposis patients, other patients at high risk to develop colon cancer, and low-risk control subjects. 12-O-Tetradecanoylphorbol-13-acetate (TPA) at 10 ng/ml enhanced DNA synthesis an average of 8-fold when assayed by labeling index in colonic epithelial cells from five of six familial polyposis patients. No such stimulation by TPA was seen in cells from 13 high-risk patients without familial polyposis or in cells from five low-risk subjects. Hundreds of benign polyps can be found in the colons of familial polyposis patients. One such benign tubular adenoma exhibited the same enhancement of DNA synthesis by TPA as normal-appearing epithelial cells from a biopsy adjacent to that polyp. Mitogenic response to TPA had been seen earlier in cells from each of four tubular adenomas (Friedman, E. Cancer Res., 41: 4588-4599, 1981). Both familial polyposis epithelial cells and adenoma cells are considered preneoplastic, but they are not identical because their patterns of actin cytoskeletal organization differ. These results imply that familial polyposis epithelial cells are precursors of tubular adenoma cells, and their transition to the more advanced preneoplastic cells of this benign tumor is influenced by endogeneous tumor promoters.

Cells, Cultured↗

PubMed1978

Immune responses in human colon cancer. I. Microcytotoxicity assay for measuring killing of adherent human colon cancer cell lines.

A short term microcytotoxicity assay system using radioisotope release as an index of target cell damage has been developed to evaluate immune killing of cultured adherent human colon cancer cell lines. Using this assay system, complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and spontaneous cell-mediated cytoxicity of adherent human colon cancer cell lines can be assessed in 4 hr or less. An essential step in the development of this system was the successful 51Cr-labeling of human colon cancer target cells with subsequent low spontaneous release. This was achieved through careful attention to cellular growth phase and medium pH during the labeling and assay period. In this microsystem, labeled colon cancer cells spontaneously released 51Cr at a mean rate of 2% per hr during the assay, a level low enough not to obscure specific cytotoxic responses. Complement-dependent cytoxicity was measured most conveniently over a 2-hr period, whereas antibody-dependent cell-mediated cytotoxicity and spontaneous cell-mediated cytotoxicity were optimal when measured over a 4-hr period.

Animals↗