Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TNF, a cytokine produced by macrophages, is able either to exert an antitumor activity, or to determine severe clinical complications, such as cachexia and septic shock. Increased blood levels of TNF have been described in cancer patients. The present study was performed to better define TNF secretion in patients with solid tumors. The study included 48 cancer patients (lung cancer: 22; colon cancer: 11; breast cancer: 10; renal cancer: 5), and among them 27 showed distant organ metastases. TNF serum levels were measured by IRMA method. The control group comprised 40 healthy subjects. TNF levels were also evaluated in relation to those of SIL-2R, whose increase seems to be associated with an unfavorable prognosis in cancer. High levels of TNF were seen in 27/48 (56%) patients. Mean levels of TNF were significantly higher in cancer patients than in controls. Moreover, within the cancer group, TNF mean values were significantly higher in metastatic patients than in those without metastases; the highest levels were observed in patients with visceral lesions as dominant metastasis sites. Finally, patients with high TNF concentrations showed significantly higher mean levels of SIL-2R than those with normal values. This study shows that the neoplastic metastatic disease is associated with an exaggerated TNF secretion.
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PMID:Tumor necrosis factor in solid tumors: increased blood levels in the metastatic disease. 149 96

Anorexia and cachexia are common clinical problems of many patients with advanced cancer. Approximately 20 years ago, a controlled, clinical study demonstrated that dexamethasone could stimulate appetites of patients with advanced gastrointestinal cancer without causing any apparent effect on patient weight or survival. More recently, two double-blind, placebo-controlled trials investigated cyproheptadine and megestrol acetate in patients with cancer anorexia/cachexia. The first of these studies suggested that cyproheptadine could mildly stimulate appetite without causing any discernible effect on patient weight. Megestrol acetate, on the other hand, can clearly cause an increase in patient-perceived appetite and food intake and can also lead to substantial nonfluid weight gain in a proportion of patients with cancer anorexia/cachexia. Ongoing studies have been designed to better study the appetite-enhancing effects of megestrol acetate. In addition, current studies are evaluating the effect of the drug hydrazine sulfate on the appetite and weight status of patients with advanced lung or colon cancer.
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PMID:Alleviation of cancer anorexia and cachexia: studies of the Mayo Clinic and the North Central Cancer Treatment Group. 225 30

We have established four lines of transplantable gastric carcinoma in WF Osaka rats. They were derived from adenocarcinomas of the glandular stomach, which were developed along with the lesser curvature, measuring less than 1.0 square centimeter. Morphology of these four lines of the transplantable tumor showed essentially an identical figure in their respective generations. Histology in the early generation of transplanted tumors showed well differentiated tubular adenocarcinoma similar to the primary lesion of the stomach. Later the histological appearance of these four lines of the transplanted tumor altered from glandular structure to keratinizing squamous cell metaplasia of cancer cells. The lines of S4 and S5 transplantable tumor were recently established, but the lines of S1 and S3 transplantable tumor have been transplanted as far as more than the 60th generation, and changed their histological appearance to scirrhous carcinoma in the line of S1 and medullary carcinoma in the line of S3. The growth speed of S1 line became slow in the later generations compared to the former ones, and that of S3 line became extremely rapid and recipient rats died with cachexia within two weeks. Effectual activities of tumor enhancement for the gastric and the colon cancer, previously reported elsewhere, recently decreased, and gastric carcinoma was rarely induced by these two lines. Lately established S4 and S5 transplantable tumor lines showed vigorous flourish of inducing gastric and colon cancers.
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PMID:Morphology on the transplantable gastric carcinoma in WF Osaka rat strain. 248 93

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

The MAC 16 is a transplantable murine carcinoma of the colon producing extensive weight loss in tumour-bearing animals. The weight loss is proportional to the size of the tumour and occurs without a reduction in food intake when compared with non tumour-bearing control mice. Weight loss produced by the MAC 16 tumour is accompanied by hypoglycaemia which becomes more extensive as the tumour mass increases. In order to understand the mechanism of the cachexia produced by the MAC 16 tumour the rate of substrate utilization and CO2 formation from both glucose and palmitate has been compared in vitro, with other colon carcinoma cell lines known not to produce cachexia as well as a range of murine and human tumour cell lines. The rate of glucose consumption, lactate production and CO2 formation from both glucose and palmitate is much higher for the MAC 16 than for the other tumour cells. For all cell lines in vitro the consumption of glucose exceeds that of palmitate by a factor of 10(3). Excessive consumption of glucose by the MAC 16 tumour may account for the hypoglycaemic effect on the host. The level of 3 oxo acid CoA transferase, an initiator of ketone body utilization, was found to be much lower in the MAC 16 tumour than non-involved colon. This suggests that the tumour may not be able to metabolize ketone bodies effectively.
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PMID:Metabolic substrate utilization by a tumour cell line which induces cachexia in vivo. 377 4

A review of the current status of research on n-3 polyunsaturated fatty acids, eicosapentaenoic and docosahexaenoic, indicates that these fatty acids exhibit protective effects on: (i) the development of carcinogen-induced tumors, the growth of solid tumors, cachexia, and metastatic diseases in experimental models; and (ii) accelerated proliferation of flat human rectal mucosal epithelial cells in individuals at risk for colon cancer, and two biomarkers of risk for breast cancer--leukocyte adenosine diphosphate ribosyl transferase activity and 16-alphahydroxylated estrogen--in women at risk for breast cancer. These research findings, along with epidemiological evidence of an inverse relationship between n-3 fatty acid intake and incidence of some cancers, warrant clinical investigation in the potential benefit of n-3 fatty acids in the prevention and therapy of cachexia in cancer patients.
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PMID:Historical perspective and potential use of n-3 fatty acids in therapy of cancer cachexia. 885 Feb 10

It is well documented that proteoglycans are involved in a wide range of pathological conditions. Recently published results in international journals provide new information on the role of proteoglycans in such conditions. A mutation in the gene encoding for a cell surface proteoglycan has been demonstrated in overgrowth syndromes. A proteoglycan has been isolated from urine and shown to induce cachexia in cancer patients. Furthermore, in both achondrogenesis and colon cancer, the reduced ability to sulphate proteoglycans is due to genetic defects in cellular sulfate transporters. Finally, fibrosis has been inhibited in glomerulonephritic mice by transferring the gene for decorin, a transforming growth factor beta-1 binding proteoglycan, into muscle tissue.
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PMID:[Proteoglycans and pathology--new aspects]. 910 6

The effects of omega-3 polyunsaturated fatty acids (PUFAs) and omega-6 PUFAs on the development of experimentally induced colon carcinoma metastasis in rat liver were investigated quantitatively in vivo. Rats were kept on either a low-fat diet or on a fish oil (omega-3 PUFAs) or safflower oil (omega-6 PUFAs) diet for 3 weeks before the administration of colon cancer cells to the portal vein, until they were sacrificed at 1 or 3 weeks after tumor transplantation. At 1 week after transplantation, the fish oil diet had induced 7-fold more metastases (in terms of number and size) than had the low-fat diet, whereas the safflower oil diet had not affected the number and total volume of metastases. At 3 weeks after tumor transplantation, the fish oil diet and the safflower oil diet had induced, respectively, 10- and 4-fold more metastases (number) and over 1000- and 500-fold more metastases (size) than were found in the livers of rats on the low-fat diet. These differences were sex independent. Immunohistochemical analysis revealed that the immune system in the liver (Kupffer cells, pit cells, T cells, newly recruited macrophages, and the activation state of macrophages) did not play a significant role in this diet-dependent outgrowth of tumors. In conclusion, omega-3 and omega-6 PUFAs promote colon cancer metastasis in the liver without down-regulating the immune system. This finding has serious implications for the treatment of cancer patients with fish oil diet to fight cachexia.
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PMID:Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver. 969 61

Epidemiological evidence has revealed an inverse relationship such that increased physical activity as measured directly subjective recall, job classification, former athletic status, or indirectly by physical fitness is associated with decreased incidence and (or) mortality rates for various cancers. The relationship appears strongest for colon cancer and female estrogen-dependent cancers of the breast, ovary, and endometrium. While some epidemiological studies have controlled for numerous confounding variables such as smoking, body mass index, and percent body fat, it is still difficult to ascertain whether physical activity exerts an independent effect on cancer above and beyond that associated with an improved lifestyle and numerous other potential confounding variables. Experimental studies performed in animals suggests that chronic exercise, especially when performed prior to tumorigenesis, can retard, delay, or prevent the incidence, progression, or spread of experimental tumors. There is also limited animal evidence suggesting that exercise may help ameliorate cancer cachexia. Exercise or physical activity may contribute to a reduction in site-specific cancers by different physiological mechanisms. Some purported mechanisms include decreased lifetime exposure to estrogen or other hormones, reduced body fat, enhanced gut motility, improved anti-oxidant defenses, and stimulation of anti-tumor immune defenses. Unfortunately, most animal studies have failed to account for plausible biological mechanisms as to how exercise might influence cancer. In addition, the exercise or activity dosage required to provide optimal protection from cancer is unclear. Interpretation of epidemiological studies is hampered by the numerous and sometimes inaccurate assessments of physical activity. Likewise, many animal studies have utilized unrealistic exercise protocols. Clearly, more research is needed to define appropriate activity or exercise dosages definitively and to explore the mechanism(s) by which exercise helps protect against cancer. Nevertheless, moderate exercise appears to be a safe and effective means of aiding in the prevention of cancer and should be adopted by the public in addition to other prudent behavioral practices such as proper diet. More research needs to be performed regarding the effects of exercise or physical activity on those who already have cancer to determine if exercise improves their prognosis.
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PMID:Exercise and resistance to neoplasia. 983 85

We report herein an unusual case of metachronous triple cancers of the sigmoid colon, stomach, and esophagus. A 60-year-old man was initially admitted to our hospital for investigation of occult fecal blood. This was found to be caused by sigmoid colon cancer which was resected in July 1985 (T3, N0, M0; Stage II). A follow-up endoscopy performed in 1990 showed early gastric cancer, and a gastrectomy was performed in August 1990 (Tis, N0, M0; Stage 0). Another endoscopic examination performed as follow-up in 1993 revealed early cancer of the remnant stomach, and all the remnant stomach was surgically resected in March 1993 (Tis, N0, M0; Stage 0). He presented again in December 1996, complaining of discomfort in the chest which was found to be caused by cancer of the middle thoracic esophagus. Although surgery was considered necessary, the patient refused to undergo any further operations. Instead, radiation was administered from January 1997. An endoscopy after the completion of radiotherapy confirmed that the cancer had almost disappeared; however, it started to grow again from the beginning of 1998. He was hospitalized due to esophageal stenosis in April 1998, and died of carcinomatous cachexia in September of the same year.
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PMID:Metachronous triple cancers of the sigmoid colon, stomach, and esophagus: report of a case. 1079 71


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