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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological data from different populations have suggested positive relationships between the incidence of colon cancer and meat and fat intake and a negative relationship with dietary fiber consumption. Within population comparisons have been less clearcut. Current theories on colonic carcinogenesis in man involve increased concentrations of bile acids and their metabolites, alterations in colonic pH, low Ca++, raised NH3 and long chain fatty acid levels, and alterations in bacterial numbers, type, and metabolic capabilities. The many laboratory studies in rats have been difficult to interpret since powerful initiators of carcinogenesis are always required and this rather than the promotion of spontaneous neoplastic change is the sine qua non for tumor growth in this situation. The current dilemma highlights the lack of knowledge of most aspects of human colonic physiology. Until these issues are more clearly resolved the epidemiological leads would point to low fat diets rich in less processed starchy foods with increased fiber as possible protection. Such advice is in common with the pronouncements of heart foundations, diabetes associations, and recommendations of official bodies to the general public.
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PMID:Cancer risk: possible protective role of high carbohydrate high fiber diets. 302 Sep 71

The present study was designed to predict the clinical effect of UFT and FT-207 in short-term administration using a nude mouse-xenograft system. Five human tumor xenografts transplanted into nude mice were used. UFT and FT-207 were administered with the LD10 doses orally for seven consecutive days. Tumor size was measured on day 7, 14 and 21 after the administrations. No significant differences in antiproliferative effects were observed between the measurements of tumor size made on day 7 and day 21. UFT inhibited significantly the tumor growth of CH-I established from colon cancer in which the prolongation of life span has been obtained by clinical long-term administration of UFT. These results suggest that this chemosensitivity test system using nude mice is useful for prediction of clinical response at 7 days after final administration of UFT and FT-207.
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PMID:[In vivo chemosensitivity test for UFT and FT-207. II. Chemosensitivity test on human tumor xenografts transplanted in nude mice]. 310 79

A synergistic antitumor effect of natural human tumor necrosis factor-beta (TNF-beta) in combination with hyperthermia was found, in comparison with that of TNF-alpha, using an in vitro antiproliferative assay on a human colon cancer cell line (RPMI4788) and an in vivo tumor growth inhibition assay on Meth A sarcoma cells. In vitro combined treatment with TNF-beta (10,000 U/ml) and hyperthermia (at 43 degrees for 60 min) synergistically inhibited the proliferation of the cells. Combined effects of TNF-alpha or natural human interferon-alpha or -gamma (IFN-alpha, -gamma) and hyperthermia were also examined, and furthermore, the combinations of TNFs and IFNs were examined in combination with hyperthermia at 42 degrees; their antiproliferative effects were further augmented by hyperthermia. In vivo growth of Meth A sarcoma cells (5 x 10(5)), transplanted subcutaneously into BALB/c mice, was inhibited significantly (P less than 0.05) with the combination of TNF-alpha or -beta (2 x 10(5) U/mouse) and hyperthermia (at 43 degrees for 60 min) as compared to either a single intravenous injection of TNF-alpha or -beta alone or the hyperthermia alone. The influence of TNF-beta and hyperthermia on the cell cycle was examined. Flow cytometric analysis showed that RPMI4788 cells treated with TNF-alpha or -beta accumulated in the S phase of the cell cycle, and that hyperthermia (at 42 degrees for 60 min) alone had no influence on the cell cycle and did not augment the S phase accumulation of the cells treated with TNF-alpha or -beta.
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PMID:Hyperthermic enhancement of the antitumor effect of natural human tumor necrosis factor-alpha and -beta: an in vitro and in vivo study. 314 36

We have previously reported that the in vitro growth of MC-26 mouse colon cancer and H2T hamster pancreatic cancer cells are inhibited by cyclosporine (CsA) and alpha-difluoromethylornithine (DFMO). The present study was designed to investigate the effects of these two drugs on the two experimental tumors (MC-26 and H2T) growing in vivo. Forty-eight male Balb/c mice or Syrian golden hamsters were inoculated with MC-26 (250,000) or H2T (500,000) cells, respectively, and then were randomized into four groups of 12 each: group I was control; group II received CsA; group III received DFMO; group IV received a combination of CsA and DFMO. MC-26 tumors were significantly more sensitive than H2T tumors to the effects of CsA and DFMO. MC-26 tumor growth and tumor weight, as well as the tumor content of DNA, RNA, and protein were all significantly more reduced by CsA and DFMO than were the H2T tumors. Our present study shows that both CsA and DFMO are potent inhibitors of MC-26 colon carcinoma growth in vivo, though DFMO is more than twice as effective as CsA. DFMO also produced greater reductions in the tumor content of DNA, RNA, and protein than did CsA. DFMO significantly decreased the concentrations of polyamines in both H2T and MC-26 tumors; the MC-26 tumors were affected to a greater degree.
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PMID:Differential sensitivity of pancreatic and colon cancer to cyclosporine and alpha-difluoromethylornithine in vivo. 314 68

Polyunsaturated n-3 fatty acids, abundant in sea fish, can inhibit the growth of chemoinduced or transplanted mammary tumours in the rat. Since mammary and colonic cancers have both been linked to a high fat consumption, we studied the effect of 2 diets moderately (7% fish meal) or strongly (9% fish oil) enriched in fish fatty acids on the growth of colon cancer cells subcutaneously inoculated into syngeneic rats. The diets had no effect on the in vivo tumor growth and on the in vitro tumouricidal activity of peritoneal macrophages or splenic lymphocytes.
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PMID:In vivo and in vitro effects of fish-containing diets on colon tumour cells in rats. 336 34

The effect of 13-cis-retinoic acid (13-cis-RA) on 1,2-dimethylhydrazine (DMH)-induced colon cancer in male, random bred, Sprague-Dawley (S-D) and inbred Wister/Furth (W/Fu) rats and on isograft tumor growth and metastases in a Brown Norwegian (BN) X W/Fu F1 rat was studied. 13-cis-RA (300 mg/kg diet) was administered to S-D rats 1 week before commencing DMH injections and for the duration of the experiment. W/Fu rats received 13-cis-RA (10 mg/kg weight X 5 days) 6 weeks after DMH injection had begun and monthly thereafter. Primary tumors were detected by serial laparotomy under ether anesthesia in both strains. The time to tumor onset was significantly delayed in treated groups, S-D and W/Fu, P = 0.0339 and 0.0322, respectively (Mantel-Haenszel test), compared with placebo-treated controls. 13-cis-RA (15 mg/kg weight) administered 2 days before and for the duration of isograft tumor growth (DMH 2054, a well-differentiated mucin-producing colon adenocarcinoma that spontaneously metastasized to lung) had no effect on tumor growth or metastasis in the BN X W/Fu F1 rat. The findings suggest that the role of 13-cis-RA is in colon cancer prevention and not in its treatment either in an adjuvant or established setting.
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PMID:Effect of 13-cis-retinoic acid on tumor prevention, tumor growth, and metastasis in experimental colon cancer. 348 Mar 91

This review summarizes selected information about the influence of proteins, protein-fat interactions, and calorie intake on carcinogenesis. Most of the definitive studies concerning protein and cancer have utilized protein underfeeding and feed restriction. Optimal or less than optimal protein intakes have generally inhibited spontaneous and chemically induced tumor growth as well as the growth of transplantable tumors. Studies have focused on the quantity of protein and its amino acid supply rather than its source. Raising protein intake increases carcinogen metabolizing capacity, and the incidence of tumors depends upon the biologic activity of the metabolites that are formed. The few published studies dealing with the effects of protein on chemically induced colon, mammary, and liver cancers show that the incidence varied with the carcinogen and the level of protein fed at the time of carcinogen administration. With 1,2-dimethylhydrazine, a colon cancer-inducing agent, the toxic and tumorigenic responses have varied with the route of administration, the level of protein fed, and the level and duration of exposure to the carcinogen. In some instances, high protein diets may have led to a lower incidence of tumors because of depressed feed intake, a known confounding factor. The existing data about the relation of protein to cancer make generalizations about mechanisms hazardous because experimental models and protocols have varied widely. Some early studies undoubtedly used diets that lacked nutrients now known to be essential. Unfortunately, some recent studies have overlooked established nutritional principles and the known nutritional requirements appropriate for the age and species of animals used as models.
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PMID:Dietary protein and experimental carcinogenesis. 359 18

Evidence has been presented to suggest that the patient with an obstructed carcinoma of the colon may have a more malignant form of the disease independent of lymph node status or tumor encirclement of the bowel. Rate of tumor growth is never consistent in patients with this disease. Patients who develop colon obstruction early in the course of the disease seem to have more aggressive tumors with rapid growth and a much poorer long-term prognosis. Perforations frequently accompany obstructions of the colon. Patients in this group have a dismal prognosis. Individuals with obstructed carcinoma of the colon have a higher operative mortality and morbidity and a shorter long-term survival. The higher operative mortality and morbidity may depend entirely on the choice of operative procedures. Tumor location affects prognosis. Obstructing tumors in the left colon have a more favorable prognosis than those in the right colon. Obstructing right colon tumors have a much poorer survival (three times worse) than nonobstructing carcinomas of the right colon. Obstructing tumors in the rectum have a very poor prognosis. Evidence exists that resection of the tumor without preliminary proximal decompression may reduce hospital mortality and morbidity and increase long-term survival. In selected cases, primary resection can be done as safely as staged operative procedures. Primary anastomosis with resection of the left colon carries a higher operative mortality because of anastomotic leaks. Resection without anastomosis is much safer. Primary resection with anastomosis is the procedure of choice in obstructing lesions of the right colon. This has a lower operative mortality and morbidity than a staged procedure. This primary resection with anastomosis is certainly as safe as an ileotransverse colostomy. It is important not to abandon the time-honored surgical principle of never suturing obstructed bowel. Primary resection without anastomosis confirms this surgical principle. Meticulous preoperative and postoperative care employing physiological monitoring, multiple antibiotics, total parenteral hyperalimentation, and respiratory and circulatory support will further reduce the hospital mortality and morbidity. Patients who initially appear to be obstructed on barium enema, but who in truth are only partially obstructed, can be properly managed so that an elective primary resection with anastomosis can be done with the same operative mortality and morbidity as in other elective colon cancer patients.
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PMID:Obstructing malignant lesions of the colon. 373 1

Enhancement of tumor growth by operation is a concern often expressed by surgeons and patients anticipating cancer surgery. Two series of experiments were performed in which Fischer 344 rats and a carcinogen-induced transplantable rat colon cancer were used to test whether anesthesia and operation facilitate tumor implantation and growth. In the first experiments two groups of rats were given intraperitoneal tumor cells. One group underwent sham laparotomy; the second did not undergo surgery. In the second set of experiments rats were injected subcutaneously with tumor cells and then divided into four groups. The first group did not undergo laparotomy. The second underwent laparotomy on day 1, the third on day 15, and the fourth on days 15 and 29 after tumor implantation. Animals were followed for the incidence and growth rate of tumors that developed. The initial experiments demonstrated that 89% of the operated versus 49% of the nonoperated animals developed a tumor (p less than 0.001). The second experiment demonstrated that: animals undergoing multiple operations have a higher incidence of subcutaneous tumor nodules than nonoperated animals (p less than 0.05); animals undergoing multiple operations have a higher incidence of subcutaneous tumor nodules than animals undergoing a single operation (p less than 0.05); animals undergoing multiple operations had larger size tumor masses than the nonoperated animals (p less than 0.05) and than animals undergoing only one operation (p less than 0.04). This study supports the hypothesis that multiple operations and anesthesia may enhance tumor implantation and growth of metastases. This should be considered when designing therapy for patients with cancer.
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PMID:Do operations facilitate tumor growth? An experimental model in rats. 373 55

Cancer bearing is frequently accompanied by weight loss, yet the factors causing cancer cachexia remain unclear. This study compares how tumor type and tumor burden affect host carcass fat depletion. Nude mice were inoculated with human malignant melanoma, human colon adenocarcinoma, or murine sarcoma cells, or were noninjected controls. Body weights, tumor burdens, and carcass lipid contents were measured. Carcass weights of melanoma-bearing mice were significantly lower than those of sarcoma-bearing mice, mice exposed to colon cancer antigens but without tumor growth, or control mice (all p less than 0.02). The degree of carcass lipid loss in melanoma-bearing mice (mean tumor burden 3.5% of total body weight [TBW]) was almost three times that of sarcoma-bearing mice (p less than 0.05), which had more than twice the tumor burden (mean tumor burden 7.8% TBW). Exposure to colon cancer antigens without tumor growth resulted in essentially no carcass lipid depletion compared with control mice. These findings argue against a mass effect of tumor as being solely responsible for host fat mobilization and suggest that carcass lipid depletion in tumor-bearing nude mice is more a function of tumor type than of tumor burden.
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PMID:Effects of tumor type and burden on carcass lipid depletion in mice. 373 56


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