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

Selected biochemical parameters (serum protein, albumin, prealbumin, total retinol-binding protein, vitamins A and E, total carotenoids, and urinary urea and creatinine) were determined in healthy, free-living vegetarian and nonvegetarian subjects. The groups studied were composed of Seventh-day Adventist pure vegetarians, Seventh-day Adventist lacto-ovo vegetarians, Seventh-day Adventist nonvegetarians, and general population nonvegetarians. No values indicative of nutritional deficiencies were observed in any of the subjects. Serum carotenoid levels were significantly higher in Seventh-day Adventist pure vegetarians than in members of the other groups. Mean values for serum vitamin A showed no differences between the dietary groups, although 41% of general population nonvegetarian subjects (the group considered at highest risk for colon cancer) had serum vitamin A levels in the upper quartile of the distribution. From these data no conclusions can be drawn relating to the role of dietary habits as determinants of colon cancer risk.
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PMID:Diet, nutrition intake, and metabolism in populations at high and low risk for colon cancer. Selected biochemical parameters in blood and urine. 654 31

Urinary pseudouridine/creatinine ratio was determined in 74 patients with gastrointestinal tumours and 34 patients with no known malignant disease. The reproducibility of a single random urine sample was demonstrated. The mean ratio for control patients was 26.9 +/- 7.7 nmol/mumol and no control patient exceeded the mean by 2 standard deviations. There was no difference in the ratio between the sexes. Sixty-five per cent of colon cancer patients and 37.5 per cent of gastric and rectal cancer patients exceeded this upper limit of normality. There was no correlation between pseudouridine/creatinine ratio and histological differentiation, liver involvement or stage in either colorectal or gastric cancer patients. Urinary pseudouridine/creatinine ratio is one of the better non-specific cancer markers and may be particularly useful for detecting colonic cancer.
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PMID:Urinary pseudouridine/creatinine ratio as an indicator of gastrointestinal cancer. 717 69

The diet contains various mutagens and carcinogens that can be classified into three groups: naturally occurring chemicals, synthetic compounds and compounds produced by cooking. The first group includes mycotoxins and plant alkaloids while the second is exemplified by food additives and pesticides. The third includes polycyclic aromatic hydrocarbons and heterocyclic amines (HCAs). HCAs are mutagenic to microbes and eukaryotes and their precursors are creatine or creatinine, sugars, and amino acids in meat and fish. Among 10 HCAs so far examined for carcinogenicity in rodents, 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1), 2-aminodipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induced colon cancer in rats. PhIP is an especially interesting compound inducing colon tumors specifically in male F344 rats and only very rarely in females, which develop mammary carcinomas at high frequency instead. Since induced DNA adduct levels, determined by the 32P-postlabeling method, were found to be almost the same in male and female F344 rats adduct formation in itself is not directly responsible for carcinogenesis. We established, however, that PhIP causes increased cell proliferation in colon mucosa but not in the non-target liver or kidney of male rats. Induction of cell proliferation is therefore possibly an additional important factor determining carcinogenic organ specificity. In terms of molecular alteration ras family gene mutations are very rare and no mutations are evident in the p53 gene in colon tumors induced by HCAs. Their development due to HCAs can thus be considered an appropriate experimental model for human colon tumors in which ras or p53 gene activation is not involved. Since HCAs are genotoxic compounds, a causal role in some stage of human colon carcinogenesis is plausible. Exposure to HCAs should accordingly be avoided as far as possible.
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PMID:Carcinogenic factors in food with relevance to colon cancer development. 769 98

Urinary N1-acetylspermidine (N1SPD) and N8-acetylspermidine (N8SPD) were measured in 24-hr urine specimens from 42 patients with colon adenocarcinoma and 29 healthy controls to assess their use as markers for colon cancer screening. Serial spot urines in four controls demonstrated significant fluctuations in these polyamine levels throughout the day without a distinct circadian pattern and therefore all subsequent analyses were performed on 24-hr collections. Both N1SPD and N8SPD were significantly increased in colon cancer patients compared to controls. Neither test correlated with tumor stage or location, but N8SPD was elevated in patients with poorly differentiated adenocarcinoma when compared to moderate or well-differentiated tumors. Using receiver operator characteristic (ROC) analysis, N1SPD had a higher information content than N8SPD, N1SPD + N8SPD, or the ratio of N1SPD/N8SPD and at a normal cut-off value of 4.0 nmol/mg creatinine, yielded a 95% specificity and 50% sensitivity for colon cancer.
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PMID:Urinary N1-acetylspermidine and N8-acetylspermidine excretion in normal humans and in patients with colorectal cancer. 778 45

Twenty patients with either unresectable primary hepatocellular carcinoma or hepatic metastases were entered into a chemoembolization program with cisplatin and lipiodol; 19 patients were evaluable for response. Doses of cisplatin ranged from 40 to 100 mg/m2. Toxicity was tolerable and reversible and included abdominal pain, transient elevation in serum creatinine, serum bilirubin, and serum transaminases. Less common side effects include fever, ascites or pleural effusion, and hiccups. Two of four patients with ocular melanoma had partial responses. Duration of response was 10 and 11 months. Among 8 patients with unresectable hepatoma, 2 patients had partial response for 10+ and 13 months, 2 had minor response for 2 months and 4+ months, 1 patient had stable disease for 5+ months, and 3 patients failed to respond. Of the six colon cancer patients treated, one had a partial response in the liver, but developed progressive nodal disease, and another patient had a partial response for 3 months. Chemoembolization of the liver with cisplatin and lipiodol is feasible and doses of cisplatin at least 100 mg/m2 are tolerable. Antitumor activity in metastatic ocular melanoma is encouraging but requires further study.
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PMID:A phase I study of chemoembolization with cisplatin and lipiodol for primary and metastatic liver cancer. 809 12

We report a patient known to have an enterovesical fistula who presented severe acute metabolic acidosis during an episode of urinary retention. The enterovesical fistula which had been intermittently symptomatic for 4 years, had developed after several intestinal surgical procedures and related intraperitoneal sepsis following resection of colon cancer 21 years previously. The patient who had a total colectomy and ileostomy, was admitted for hip replacement with the routine placement of a Foley bladder catheter. Three weeks post-operatively, the patient developed acute urinary retention following removal of the urinary catheter. The output from his ileostomy was immediately markedly increased, presumably from bladder urine diverted into the intestines through the enterovesical fistula. Within a few days he presented a normal anion gap metabolic acidosis with raised urea and stable creatinine; his clinical status deteriorated markedly with profound obtundation. These metabolic abnormalities were readily corrected by re-insertion of the Foley catheter with restoration of normal urine flow and immediate corresponding fall in the ileostomy output. Radiographic studies showed the presence of the enterovesical fistula originating from the jejunum. This is the first report of acute metabolic acidosis in association with an enterovesical fistula; the severe metabolic disturbances were triggered by the development of urinary retention resulting in the diversion of urine into the small bowel through the fistula.
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PMID:Metabolic acidosis during urinary retention in a patient with an enterovesical fistula. 1093 61

To assess the effects of a macromolecular prodrug in reducing the nephrotoxicity of cisplatin (CDDP), chondroitin sulfate A (CSA) with a mean molecular weight of 23,000 Da was used to form a complex with CDDP, and the pharmacokinetics and toxicology of the resulting complex were examined in rats in comparison with those of CDDP. The total plasma platinum levels and urinary accumulation were determined up to 3 h following a bolus injection of 2 mg/kg. The results of the pharmacokinetic analysis showed that the complex suppressed the rapid distribution of CDDP, decreased the renal clearance and resulted in over fivefold higher AUC values within 3 h in comparison with CDDP treatment. In addition, the plasma levels of the drug following administration of the complex decreased greatly with time throughout the experimental period (3-24 h), whereas a slow elimination was observed following CDDP administration, which was due to the irreversible protein binding of CDDP. The tissue-to-plasma partition ratio at 10 min also indicated that the CDDP-CSA complex controlled the perfusion of CDDP to tissues, especially to the kidney. The accumulation in various tissues was evaluated at 3 h and 24 h following the injection of 5 mg/kg. Marked differences in renal accumulation were found within 3 h. Significant reductions in accumulation in the kidney, lung, muscle and whole blood were found within 24 h of administration of the complex. The renal toxicity of the CDDP-CSA complex was evaluated by measuring blood urea nitrogen (BUN), serum creatinine (Cr) and the ratio of terminal kidney weight to body weight at doses of 2 mg/kg and 5 mg/kg. The complex displayed a much lower nephrotoxicity at 5 mg/kg in comparison to CDDP, and similar results were obtained at 2 mg/kg. This suggests that the complex changed the toxicodynamics of CDDP. Moreover, the anticancer activity of the CDDP-CSA complex, tested against SW 4800 human colon cancer cells and HeLa human cervix cancer cells in vitro, showed no decrease as compared with that of free CDDP. We conclude that the CDDP-CSA complex had the same activity as the parent drug but showed reduced nephrotoxicity at high doses of CDDP through an improvement in the pharmacokinetics of CDDP, which resulted from both the minimization of entry into normal tissues and renal clearance. In addition, it is also possible that different intracellular interactions in renal cells play a role in protection against the nephrotoxicity of high doses of CDDP.
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PMID:Effects of a cisplatin-chondroitin sulfate A complex in reducing the nephrotoxicity of cisplatin. 1100 75

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

Cisplatin is one of the most effective chemotherapeutic agents and plays a major role in the treatment of a variety of human solid tumors. However, its toxicity limits the clinical use. Recently, the administration of antioxidants has been suggested to protect against cisplatin-induced nephrotoxicity. The present study was designed to estimate the antitumor activity of the licorice extract alone and in combination with cisplatin, and its protective potential against cisplatin-induced toxicity in a mouse xenograft model. The administration of the licorice extract significantly inhibited tumor growth in BALB/C mice inoculated with CT-26 colon cancer cells. The combination of the licorice extract and cisplatin diminished the therapeutic efficacy of cisplatin but promoted considerably antitumor activity of the licorice extract. In mice with cisplatin treatment for 15 d, the serum levels of blood urea nitrogen and creatinine remarkably were increased by kidney damage, and the serum alanine aminotransferase and aspartate aminotransferase levels were elevated by liver damage. The administration of the licorice extract plus cisplatin recovered these functional indices in the kidney and liver to almost the control levels. In addition, the administration of the licorice extract significantly reduced the cisplatin-induced oxidative stress. Taken together, the administration of the licorice extract inhibits the growth of mouse colon carcinoma without any adverse effects, and reduces the cisplatin-induced toxicity. Therefore, the licorice extract may be a candidate for an anticancer and chemopreventive agent. However, cancer patients with cisplatin therapy should avoid the supplementation of the licorice extract.
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PMID:Effects of the licorice extract against tumor growth and cisplatin-induced toxicity in a mouse xenograft model of colon cancer. 1797 99

A growing amount of attention has been focused on the investigation of the effects of chemopreventive agents on the inhibition of cancer cell growth and toxicity in combination with chemotherapeutics. The objective of this study was to determine whether isoliquiritigenin (ISL) has the potential to serve as a beneficial supplement during cisplatin chemotherapy. We found that the administration of ISL alone significantly reduced the size of the solid tumors in CT-26 cell-inoculated BALB/c mice, without any detectable induction of nephrotoxicity, hepatotoxicity, and oxidative stress, and ISL reduced the viability and DNA synthesis of CT-26 murine colon cancer cells in a dose-dependent manner. ISL did not affect the therapeutic efficacy of cisplatin. Furthermore, ISL suppressed cisplatin-induced kidney damage characterized by increases in serum creatinine and blood urea nitrogen, as well as cisplatin-induced liver damage characterized by increases in serum alanine aminotransferase and aspartate aminotransferase. The repeated oral administration of ISL prior to cisplatin treatment exerted a preventive effect on cisplatin-mediated increases in serum nitric oxide and tissue lipid peroxidation levels, and it recovered depleted GSH levels in the tissues. Therefore, supplementation with ISL may be an effective approach to counteracting the side effects of cisplatin therapy in cancer patients.
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PMID:Isoliquiritigenin inhibits tumor growth and protects the kidney and liver against chemotherapy-induced toxicity in a mouse xenograft model of colon carcinoma. 1836 95


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