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)

The antigenic surface pattern of a continuous cell line (HT29) derived from a human primary carcinoma of the colon was studied by the immunofluorescence technique. Monovalent and polyvalent immune sera were used. The cells of this long-term culture kept the ability to synthesize the three principal colon tumor antigens: carcinoembryonic and nonspecific cross-reacting antigens, and the membrane-associated tissular autoantigen. On the HT29 cells, which still carry the original blood group of the tumor donor, no receptors for human Ig's were detected.
J Natl Cancer Inst 1975 Sep
PMID:Immunohistology of the antigenic pattern of a continuous cell line from a human colon tumor. 115 34

The relation between tumour spread, histological differentiation, and in-vitro antitumour immunoreactivity was studied in 132 cases of carcinoma of the large bowel. Positive correlations were found between blood lymphocyte antitumour cytotoxicity and both tumour differentiation and absence of recurrence or metastatic spread.
Br Med J 1975 Sep 27
PMID:Colonic carcinoma: clinicopathological correlation with immunoreactivity. 117 74

In approximately 80 per cent of cases the gallbladder is closely applied to the superior medial aspect of the right colic flexure. This intimate anatomic relationship provides pathways for direct extension of both inflammatory and neoplastic lesions of the gallbladder to involve the adjacent colon. The resultant secondary colonic abnormalities noted in 15 patients have been analyzed and correlated with surgical-pathologic findings. In acute cholecystitis, barium enema examination shows evidence of indentation by an enlarged gallbladder, spasm and mucosal edema in the anterior hepatic flexure. Chronic cholecystitis results in involvement of the adjacent colon by fibrous adhesions and inflammatory reaction. These may further lead to the development of pseudotumors simulating primary carcinoma of the colon. Similar findings including cholecysto-colic fistulae may be the initial manifestations of carcinoma of the gallbladder. The spectrum of pathologic-roentgenographic alterations in the cholecysto-colic interface is described and illustrated. Recognition of these features is of critical importance for the correct interpretation of barium enema findings and the subsequent management of patients with gallbladder disorders.
Am J Roentgenol Radium Ther Nucl Med 1975 Sep
PMID:The cholecysto-colic relationships. A roentgen-anatomic study of the colonic manifestations of gallbladder disorders. 120 Feb 12

We have examined the effects of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] on the phosphoinositol signal transduction pathway in the human colon cancer-derived cell line CaCo-2 and have studied the regulation of intracellular calcium ([Ca2+]i) and pH (pHi) by this secosteroid. CaCo-2 cells were prelabeled with [3H]myoinositol and treated with 10(-8) M 1,25-(OH)2D3 or vehicle for 90 sec. 1,25-(OH)2D3 caused a decrease in labeled phosphatidylinositol-4-5-bis-phosphate and an increase in labeled inositol 1,4,5-trisphosphate. Treatment with 10(-8) M 1,25-(OH)2D3 for 90 sec also raised the cellular content of diacylglycerol. In a dose-dependent manner, 1,25-(OH)2D3 caused the translocation of protein kinase-C activity from the cytosolic to the membrane fraction, which occurred after as little as 15 sec of exposure to the secosteroid, peaked at about 1-5 min, and then returned toward baseline values. In these CaCo-2 cells, baseline [Ca2+]i was 258 +/- 2 nM (mean +/- SE), as assessed using the fluorescent dye fura-2. After exposure to 10(-8) M 1,25-(OH)2D3, [Ca2+]i rapidly increased to 392 +/- 14 nM after 100 sec, fell, and then subsequently rose to a plateau of 350 +/- 3 nM after 400 sec. In Ca(2+)-free buffer, 1,25-(OH)2D3 caused only a transient rise in [Ca2+]i, indicating that 1,25-(OH)2D3 stimulated both the release of intracellular calcium stores and calcium influx. 1,25-(OH)2D3 caused a dose-dependent decrease in pHi in CaCo-2 cells, as assessed by the fluorescent dye BCECF, which was not observed in cells suspended in Na(+)-free buffer or pretreated with amiloride, indicating that the secosteroid inhibited Na(+)-H+ exchange. No effect of 1,25-(OH)2D3 on pHi was observed in cells in a Ca(2+)-free buffer or pretreated with the phospholipase-C inhibitor U-73,122, which also blocked the rise in [Ca2+]i, or in cells pretreated with the Ca2+/calmodulin inhibitor calmidazolium. Taken together, these studies indicate that 1,25-(OH)2D3 rapidly stimulates membrane phosphoinositide breakdown in CaCo-2 cells, generating the second messengers inositol 1,4,5-trisphosphate and diacylglycerol, causing translocation of protein kinase-C to the membrane, and increasing [Ca2+]i by both releasing calcium stores and promoting calcium influx. Secondary to the rise in [Ca2+]i, Na(+)-H+ exchange is inhibited by a calcium/calmodulin-dependent pathway.
Endocrinology 1992 Sep
PMID:1,25-dihydroxyvitamin D3 inhibits Na(+)-H+ exchange by stimulating membrane phosphoinositide turnover and increasing cytosolic calcium in CaCo-2 cells. 132 51

Free radical-induced damage to DNA in vivo is implicated to play a role in carcinogenesis. Evidence exists that DNA damage by endogenous free radicals occurs in vivo, and there is a steady-state level of free radical-modified bases in cellular DNA. We have investigated endogenous levels of typical free radical-induced DNA base modifications in chromatin of various human cancerous tissues and their cancer-free surrounding tissues. Five different types of surgically removed tissues were used, namely colon, stomach, ovary, brain and lung tissues. In chromatin samples isolated from these tissues, five pyrimidine-derived and six purine-derived modified DNA bases were identified and quantitated by gas chromatography/mass spectrometry with selected-ion monitoring. These were 5-hydroxy-5-methylhydantoin, 5-hydroxyhydantoin, 5-(hydroxymethyl)uracil, 5-hydroxycytosine, 5,6-dihydroxycytosine, 4,6-diamino-5-formamidopyrimidine, 8-hydroxyadenine, xanthine, 2-hydroxyadenine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine, and 8-hydroxyguanine. These compounds are known to be formed typically by hydroxyl radical attack on DNA bases. In all cases, elevated amounts over control levels of modified DNA bases were found in cancerous tissues. The amounts of modified bases depended on the tissue type. Lung tissues removed from smokers had the highest increases of modified bases above the control levels, and the highest overall amounts. Colon cancer tissue samples had the lowest increases of modified bases over the control levels. The results clearly indicate higher steady-state levels of modified DNA bases in cancerous tissues than in their cancer-free surrounding tissues. Some of these lesions are known to be promutagenic, although others have not been investigated for their mutagenicity. Identified DNA lesions may play a causative role in carcinogenesis.
FEBS Lett 1992 Sep 07
PMID:DNA base modifications in chromatin of human cancerous tissues. 132 97

Because colorectal cancer is the second leading cause of cancer death in the United States and many developed countries, its primary prevention is of extreme importance. Environmental and dietary factors are considered responsible for 85-90% of all cases. Epidemiologic, animal, and biochemical studies suggest that diets high in total calories and fat and low in various dietary fibers, vegetables, and micronutrients are associated with an increased incidence. Of these factors, calcium and wheat bran have been used most extensively in recent trials. It has been reported that 1.5-2.0 g/day of calcium significantly decreases DNA synthesizing cells of high-risk patients. However, chronic wheat bran supplementation appears to decrease both rectal mucosal DNA synthesis and polyp recurrence. Several clinical trials currently are underway to evaluate the diet-colon cancer link. The results of these studies will help to determine the importance of dietary intervention in the reduction of the colorectal cancer risk.
Cancer 1992 Sep 01
PMID:Primary prevention of colorectal cancer through dietary modification. 132 81

The effects of 12 weeks of omega-3 fatty acid supplementation on rectal mucosal proliferation were assessed with [3H]thymidine autoradiography in a double-blind, placebo-controlled study of 20 patients with sporadic adenomatous colorectal polyps. In the group of 10 that received fish oil containing eicosapentaenoic acid (4.1 g/day) and docosahexaenoic acid (3.6 g/day), the mean percentage of replicative "S"-phase cells in the upper part of colonic crypts (considered a reliable marker of colon cancer risk) significantly dropped from the baseline level after only 2 weeks of treatment and remained lower throughout the study period; no change in upper-crypt labeling was observed in the 10 placebo patients. Rectal mucosal eicosapentaenoic acid content increased in fish oil patients, whereas arachidonic acid levels decreased. The fish oil-induced kinetic changes represent contraction of the proliferative compartment to the levels of a low-risk population and may be related to omega-3 fatty acid effects on the arachidonic prostaglandin pathway. In this short-term trial, fish oil appeared to exert a rapid effect that may protect high-risk subjects from colon cancer.
Gastroenterology 1992 Sep
PMID:Effect of omega-3 fatty acids on rectal mucosal cell proliferation in subjects at risk for colon cancer. 846 20

Aberrant crypts are putative preneoplastic lesions that have been proposed as intermediate biomarkers for colon cancer. The goals of these studies were to determine (i) if the colon cancer chemopreventive agent, sodium phytate, when started 1 week after a single dose of carcinogen, has any effect on the development of aberrant crypt foci (ACF) in treated rats; and (ii) if ACF at an early time period under these conditions correlate with the later formation of tumors in similarly treated animals. The number of ACF with four or more crypts was greater (P = 0.02, Mann-Whitney test) in rats with tumors compared with rats without tumors killed at 36 weeks after the injection of azoxymethane (AOM); the total number of ACF was not significantly different in these two groups. The incidence of tumors in F344 rats treated with AOM without phytate was 83% (10/12) compared to 25% (3/12) in rats treated with AOM plus phytate (P = 0.0045, two-tail Fisher's exact test). The finding of more (P = 0.005, Mann-Whitney test) ACF with four or more crypts in rats without phytate than in rats with phytate at 12 weeks after the injection of AOM is consistent with the hypothesis that the development of larger ACF (with four or more crypts) is predictive of the tumor incidence. These results validate the use of this parameter, i.e. ACF with four or more crypts, as an intermediate biomarker for tumor incidence in this system.
Carcinogenesis 1992 Sep
PMID:Aberrant crypts correlate with tumor incidence in F344 rats treated with azoxymethane and phytate. 139 32

For investigations involving monoclonal antibodies (mAbs) against cellular antigens cell binding assays are routinely used to determine the immunoreactive fraction after radiolabeling. In general, surface antigens are targets for radioimmunodetection, but recent studies indicate that intracellular determinants may also prove useful for this purpose. Thus, there is a need to adapt the regular cell binding assay for use with antibodies directed against cytoplasmic antigens. Here we describe a fixation method which permits such mAbs to bind to cell surfaces as well as to intracellular determinants. Moreover, the procedure may be used for antigens that are sensitive to the commonly used aldehyde fixatives. The method is illustrated with two human IgM mAbs 16.88 and 28A32, which recognize cytoplasmic antigens. Human colon cancer cells in suspension were fixed with either acetone or glutaraldehyde. Intracellular antigens appeared to be best exposed for antibody binding after fixation with acetone as determined by immunofluorescent staining and flow cytometry. An antibody directed against the cell surface antigen HLA class I showed similar binding with both live cells and acetone-fixed cells. Double-inverse plots of the binding of radiolabeled 16.88 or 28A32 antibody with acetone-fixed cells gave reliable immunoreactive fraction values. Acetone-fixed cells stored at 4 degrees C could be used for immunoreactivity assays for at least 6 months without loss of performance.
J Immunol Methods 1992 Sep 18
PMID:Determination of the immunoreactive fraction of radiolabeled monoclonal antibodies directed against intracellular antigens. 140 43

Malignant neoplasms are responsible for more than half a million deaths annually and 22.5% of all deaths in the United States. Cancer is the second leading cause of death overall and the leading cause of death among Americans aged 35-64. Within the next decade it may become the leading cause of death. Cancers of digestive and respiratory organs are responsible for 53% of all cancer deaths. Certain subgroups are at elevated risk for various cancers. For example, sun-sensitive or excessively sun-exposed young white adults, young black women, and elderly patients are at increased risk for cutaneous melanoma, breast cancer, and colon cancer, respectively. Black men have the greatest risk for both lung cancer and cancer of the prostate. Acute lymphoblastic leukemia and solid tumors of the brain and nervous system are the most frequent forms of malignancy occurring among children less than or equal to 14 years. Office screening is the traditional method for identifying cancer victims as early as possible. A suitable screening test should be rapid, simple, inexpensive, and impose minimal discomfort. There must be a window of opportunity available to identify the cancer during a detectable preclinical phase, and therapeutic modalities must be available to alter progression. An office screening test for cancer may have any one of four outcomes, and three of them are bad. False negatives are the worst adverse outcome because cancer remains undetected despite screening. An epidemic of lung cancer, caused by cigarette smoking, is occurring in all race and sex groups. If Americans stopped smoking, 87% of lung cancer deaths could be prevented. Tobacco abuse also is a major risk factor for cancer of the esophagus, larynx, and oral cavity. Cigarette smoking is a contributing factor for cancer of the bladder, kidney, and pancreas, and it has been associated with both cervical cancer and cancer of the stomach. Smoking and smokeless tobacco cessation endorsements, messages, and programs must be part of routine disease prevention and health promotion activities in every primary care practice. More than 1 million Americans became new cancer victims last year, and more than 1 million additional cases will be detected this year. Because of the striking variability in state and regional patterns of various forms of cancer, geographic location of a practice may influence the frequency of cancers seen. Four sites (breast, prostate, lung, colon, and rectum) were responsible for 55% of cancer mortality and 56% of all new cases of cancer detected during 1991.(ABSTRACT TRUNCATED AT 400 WORDS)
Prim Care 1992 Sep
PMID:Epidemiology of cancer in the United States. 141 56


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