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)

Patients with cancer may display taste abnormalities. In this study, abnormalities observed before treatment involved decreased salt and sweet sensitivity. For some thresholds, greater abnormalities were observed among men and women, among patients with colon cancer than among those with breast cancer, and among those with a greater extent of disease. Observations of slight increases in thresholds for sour detection and bitter recognition during the early treatment period and normalization of high sweet recognition thresholds after two weeks of treatment suggest that additional changes in taste acuity may accompany short-term treatment with 5'fluorouracil. However, absence of a correlation of taste changes with changes in food preferences points to the role of other factors in determining patients' food preferences during such treatment. Consideration of the incidence of taste abnormalities in these groups of patients with cancer and observation of altered food attitudes among patients receiving 5-fluorouracil does provide a basis for general recommendations for serving foods which will appeal to these patients.
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PMID:Taste acuity and food attitudes of selected patients with cancer. 84 47

Two bile salts, sodium chenodeoxycholate and sodium deoxycholate, induced a DNA repair response in the bacterium Escherichia coli. Similarly, a bile acid and a bile salt, chenodeoxycholic acid and sodium deoxycholate, induced DNA repair (indicated by unscheduled DNA synthesis) in human foreskin fibroblasts. Also, DNA repair-deficient Chinese hamster ovary (CHO) cells were found to be more sensitive than normal cells to killing by bile salts. In particular, mutant UV4 CHO cells, defective in DNA excision repair and DNA cross-link removal, were more sensitive to sodium chenodeoxycholate, and mutant EM9 CHO cells, defective in strand-break rejoining, were more sensitive to sodium deoxycholate than wild-type cells. These results indicate that bile salts/acid damage DNA of both bacterial and mammalian cells in vivo. Previous epidemiological studies have shown that colon cancer incidence correlates with fecal bile acid levels. The findings reported here support the hypothesis that bile salts/acids have an etiologic role in colon cancer by causing DNA damage.
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PMID:Bile salt/acid induction of DNA damage in bacterial and mammalian cells: implications for colon cancer. 177 85

Butyrate has induced differentiation in neoplastic cells grown in vitro, among them being colon cancer cell lines. In vivo, only one major study used sodium butyrate in the drinking water and showed an elevation in 1,2-dimethylhydrazine induced colon cancer in rats. Seeking to show that it was the sodium and not the butyrate which was responsible for the enhancement, we fed tributyrin at a 5% level to mice for 48 weeks. Mice experienced normal growth and development at this dose. Analysis of short chain fatty acids in the feces after 6 months in tributyrin feeding showed a 10-fold increase in butyric acid. However no difference in AOM induced focal areas of dysplasia or colonic tumor incidence was observed between tributyrin fed and control mice. At least two conclusions have been reached by this study, (1) that the dietary use of a sodium salt can contribute to the enhancement of chemically induced colon neoplasia and (2) butyrate may be discounted as providing any major therapeutic benefit against colonic tumorigenesis.
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PMID:Dietary butyrate (tributyrin) does not enhance AOM-induced colon tumorigenesis. 235 22

This study reports on the taste for salt among patients with gastric, colon, or rectal cancers and among population controls, within the scope of an investigation on those cancers in two Belgian provinces. Among people who systematically added salt to their food, the relative risks observed were as follows: 1.78 for gastric cancer, 1.53 for colon cancer, and 1.74 for rectal cancer. Even though all three were statistically significant, these increases are moderate and may be due to interaction with other, as yet unknown casual factors.
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PMID:Salt and gastrointestinal cancer. 321 61

An inhibitor of soft agar colony formation by a human breast carcinoma-derived cell line was found to be present in latent form in the majority of cytology-positive human malignant effusions. Prior to dialysis, addition of human malignant effusions resulted in less than 10% alteration in efficiency of colony formation by the BT-20 human breast carcinoma cell line (mean efficiency 1 colony/4.3 cells plated at 14 days; mean colony diameter greater than 0.8 mm). After dialysis (membrane cutoff of 3500 molecular weight), 58 of 70 malignant effusions from patients with a variety of epithelial cell carcinomas resulted in 71% mean inhibition of colony formation (range 19.1-98% inhibition). Similar inhibition of anchorage-independent growth was observed for a human colon cancer-derived cell line (HCT-15) but not for polyoma and murine sarcoma virus-transformed rodent fibroblast lines. The malignant effusion-related transformed cell growth-inhibiting factor (TGIF) was sensitive to heat, sulfhydryl reduction, and protease treatment. TGIF-containing effusion resulted in parallel inhibition of thymidine incorporation in sensitive cell types in vitro. TGIF was precipitable in 28-34% ammonium sulfate with reconstitution of activity after resolubilization. TGIF was partially purified by chromatography on Biogel A-0.5 and Biogel P-100 which yielded two peaks of inhibitory activity. The predominant species had an approximate molecular weight of 110,000 and could be recovered as a single species from DEAE-cellulose at relatively high salt concentrations (0.4 M NaCl). A smaller amount of inhibitory activity was recovered from Biogel P-100 or Biogel P-60 with an apparent molecular weight of 55,000. The higher molecular-weight TGIF which appears to be a dimer of the Mr 55,000 protein is distinguishable from previously described growth-promoting and -inhibiting factors.
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PMID:Latent transformed growth-inhibiting factor in human malignant effusions. 325 64

A novel, substituted 4-quinolinecarboxylic acid (NSC 339768) demonstrated antitumor activity against L1210 leukemia and B16 melanoma in the National Cancer Institute's Developmental Therapeutics Program. An extensive analogue synthesis program was initiated; over 200 derivatives were synthesized and tested for anticancer activity. One of these compounds, 6-fluoro-2-(2'-fluoro-1,1'-biphenyl-4-yl)-3-methyl-4-quinolinecarboxylic acid sodium salt, NSC 368390 (DuP-785), was selected for further investigation because of its efficacy against a spectrum of human solid tumors and its water solubility. In initial studies with L1210 leukemia, the compound caused an increase in life span of greater than 80%. The activity was schedule dependent, and the compound was equally efficacious when administered i.p., i.v., s.c., or p.o. In tests against human tumors xenografted under the renal capsule of nude mice, NSC 368390 when injected i.p. in doses of 20-40 mg/kg daily for 9 days inhibited the growth of the MX-1 breast, LX-1 lung, BL/STX-1 stomach, and CX-1 colon carcinomas by greater than 90%. NSC 368390 also inhibited the growth of three distinct human colon carcinomas, the HCT-15, clone A, and DLD-2 tumors, growing s.c. in nude mice. An i.p. dose of 25 mg/kg given daily for 9 days inhibited the growth of the DLD-2 colon cancer by 98%. 1-beta-D-Arabinofuranosylcytosine and Adriamycin were ineffective, and fluorouracil was only moderately effective against these colon tumors. Because of its good activity against human colon tumors and other human carcinomas and its water solubility, NSC 368390 (DuP-785) is being developed as a Phase 1 anticancer agent.
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PMID:Activity of a novel 4-quinolinecarboxylic acid, NSC 368390 [6-fluoro-2-(2'-fluoro-1,1'-biphenyl-4-yl)-3-methyl-4-quinolinecarb oxylic acid sodium salt], against experimental tumors. 405 30

The relationships between areal differences in mortality from six digestive-tract cancers and consumption of selected foods in 46 of the 47 Japanese prefectures (Okinawa being excluded) were analyzed. Statistical analyses disclosed that the groups of foods positively associated with cancer death were as follows: for esophageal cancer, pork, oil, popular-grade sake, and green tea; for stomach cancer, fresh fish, salted or dried fish, salt, and special-grade sake; for colon cancer, bread, milk, butter, margarine, ketchup, beer, and salted or dried fish; for rectal cancer, fresh fish, salted or dried fish, salt, and popular-grade sake; for cancer of the biliary passages, pork, popular-grade sake, and green tea; and for pancreatic cancer, oil, mayonnaise, fresh fish, and salted or dried fish. These results are based on statistical analyses. Further epidemiological analyses are required to find a biological causal relationship.
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PMID:Statistical analyses on the pattern of food consumption and digestive-tract cancers in Japan. 654 78

The theory that bile salts may be colon tumour promoters was tested in the dimethylhydrazine (DMH)-induced rat colon cancer model. Fifty Wistar rats were randomly allocated to one of five experimental group (n = 10), all fed the same standard diet. One group served as saline-injected controls, while the other four groups received DMH (20 mg/kg body weight/rat/week s.c.) for 20 weeks. In addition, each of the DMH-injected groups concurrently received 20 weekly i.g. instillations of one of the following: cholic acid (a bile acid); cholestyramine or aluminium hydroxide (both bile acid binding agents), or water. After a years observation period, all the controls were alive and tumour-free, while all the DMH-injected rats had died of histologically proven colon cancer. Irrespective of the type of gastric instillate, there were no significant differences between the groups in terms of time to tumour presentation, survival, in the necropsy incidence of primary or metastatic colon cancer, or in the numbers of colon tumours per group. The data suggest that bile salts and bile salt binding agents are not colon tumour promoters in the rat. The bile salt theory of colon carcinogenesis may need reappraisal.
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PMID:The effects of cholic acid and bile salt binding agents on 1,2-dimethylhydrazine-induced colon carcinogenesis in the rat. 727 24

According to the bile salt theory of colon carcinogenesis, therapeutic agents which increase the delivery of bile salts to the large intestine may promote colon cancer. The possibility that aluminium hydroxide (Aludrox), a bile salt binding agent, might facilitate colon carcinogenesis in vivo was tested experimentally, using the dimethylhydrazine (DMH)-induced rat colon cancer model. 48 Wistar rats were randomly allocated to 1 of 3 groups, all fed the same standard diet. Two groups received a course of ten weekly DMH injections. One was allowed fresh drinking water ad libitum whilst the other received Aludrox in their drinking water. A third group received weekly saline injections plus Aludrox in their drinking water. After 1 year's observation, there were no significant differences between the groups of DMH-injected rats given drinking water with or without Aludrox in respect of survival, necropsy incidence of primary or metastatic colon cancer, or in the total number of colon tumours per group. The results provide reassurance that Aludrox does not promote colon cancer and tend to contradict the bile salt theory of colon carcinogenesis.
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PMID:Experimental evidence against the bile salt theory of colon carcinogenesis. 729 76

The overview of apoptosis presented here emphasizes cell deletion in the immune system, with particular reference to T- and B-lymphocyte development, and the in vivo and in vitro senescence of human neutrophils. Some biochemical criteria that are used to identify apoptotic cells are described. Pitfalls in using agarose gel electrophoresis as the sole method for the identification of apoptotic cells are discussed. There are multiple modes of cell death that can be identified at the morphologic level. Thus the central role of microscopic methods, and in particular, electron microscopy, as an important tool in the study of cell death mechanisms, is presented. Apoptosis has a protective role against disease and could, a priori, have an important role in either the initiation or progression of cancer. Two paradoxes concerning the relationship of tumor aggressiveness at the clinical level to mitotic activity have been explained by an evaluation of apoptotic index. In the first case, basal cell carcinomas grow slowly but show a high rate of mitosis. Here, the apoptotic rate is quite high, but just below the mitotic rate, thereby accounting for the slow rate of growth. A second instance is follicular lymphoma, which has a low rate of mitosis that is less than that described for reactive germinal centers. However, apoptosis is markedly reduced in follicular lymphomas compared with that seen in reactive germinal centers, thus providing an explanation for the progressive growth of the follicle. We present a brief description of recent work from our laboratory that indicates that apoptosis may play an important role in colon carcinogenesis. We have shown that sodium deoxycholate, the particular bile salt present in highest concentration in the colon, induces apoptosis in the goblet cells of the human colonic mucosa in an in vitro assay. The intriguing finding is that cells of the normal-appearing mucosa of colon cancer patients are resistant to bile salt-induced apoptosis. This suggests a novel hypothesis about the etiologic role of bile salts in colon cancer. The chronic presence of bile salts that accompany a high-fat diet could select for apoptosis-resistant epithelial cells in the colon over time. Thus, a resistance-to-apoptosis bioassay may prove useful as an intermediate biomarker for determining which individuals are at high risk for colon cancer.
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PMID:Role of apoptosis in biology and pathology: resistance to apoptosis in colon carcinogenesis. 757 Oct 81


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