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)

We have purified a protein from serum-free conditioned medium of the HT29 human colon adenocarcinoma cell line based on its ability to inhibit the proliferation of the same cell line. The purification procedure consisted of acid gel permeation, semipreparative, and analytical reversed-phase chromatographies. The high-pressure liquid chromatography-purified colon cancer cell growth inhibitor migrates as a single band of 27 and 34 kDa on sodium dodecyl sulfate/polyacrylamide gels under nonreducing and reducing conditions, respectively. NH2-terminal amino acid sequence analysis of the first 32 residues has demonstrated that this protein belongs to the insulin-like growth factor-binding protein (IGFBP) family. More precisely, this growth inhibitor appeared to be identical to the recently cloned human IGFBP-4. This IGFBP (HT29-IGFBP) has been characterized by performing ligand blotting and competitive binding experiments. The affinity of HT29-IGFBP for insulin-like growth factor (IGF) II (approximately 3.4 x 10(10) M-1) is slightly greater than its affinity for IGF-I (approximately 1.4 x 10(10) M-1). HT29 cells also produce two other isoforms (28 and 31 kDa, nonreduced) of the HT29-IGFBP having the same partial NH2-terminal amino acid sequence as the 27-kDa protein. The monoclonal antibody alpha IR-3 is known to block the mitogenic actions of IGFs. alpha IR-3 inhibited the growth of HT29 cells, thus suggesting that IGFs are required for the growth of these colon cancer cells.
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PMID:Purification of a colon cancer cell growth inhibitor and its identification as an insulin-like growth factor binding protein. 170 85

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

Between 1978 and 1983 we performed 19 ureterosigmoidostomies (25% of all urinary diversions). We try to realise a reevaluation of this technique by means of clinical data, laboratory findings, U.S.- and X-ray examinations. The mean follow-up time is 7.5 years. All patients mention a comfortable life-style. By routine administration of sodium bicarbonate, no electrolyte disturbances occur. Only 5 kidneys (on a total of 32 renal units) show major deformities. Colon carcinoma is not reported. Since the introduction of the ileal conduit by Bricker in 1950 (1), together with the repeatedly published higher incidence of colon carcinoma (2), a certain revulsion for the traditional Coffey-technique arose. Yet there are some important advantages in this peculiar surgical method. We think that, after a rather premature condemnation, the time is ripe for a reevaluation and a reevaluation of the ureterosigmoidostomy.
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PMID:Ureterosigmoidostomy: reevaluation of a "forgotten" continent urinary diversion. 181 95

Although many monoclonal antibodies have been made in human colon cancer, none of them are from the Chinese species. Recently, a colon cancer cell line CC-M2 established from a Chinese patient has been completely characterized and used as immunogen to produce monoclonal antibodies. Monoclonal antibodies were produced by standard hybridoma technique. The fusion rate was 95.8%. An isotype IgG1 of high proliferation named as Sam-2 was used in this study. The titers were measured around 10(4). Further studies on MoAb Sam-2 through indirect immunofluorescent and immunoperoxidase tests revealed its good specificity and sensitivity in colorectal cancer tissue. In CEA study, the result indicated that Sam-2 may react on a non-CEA related antigen. For further clinical application, the antigen was identified as a glycoprotein by chemical resistant test. In preliminary studies using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting techniques, Sam-2 could recognize two closed antigens or a dimer antigen with molecular weight 25.2 and 27 Kd respectively.
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PMID:[Production and characterization of monoclonal antibody against colon cancer associated antigen in Chinese]. 184 60

The effect of a number of drugs belonging to different therapeutic categories on cell proliferation in a human colon cancer cell line (HT 29) was studied. Generally, drugs classified as calcium antagonists had a moderate to strong inhibitory effect on cell growth. The EC50 value for prenylamine, perhexiline and bepridil was 10 microM. The so-called calcium channel blockers (verapamil, nifedipine, diltiazem) were less effective. With the exception of the sodium selective ionophore, monensin, which was extremely potent (EC50 less than 0.1 microM), calmodulin antagonism appeared to be a common feature of compounds inhibiting cell proliferation of human colon tumour cells.
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PMID:Effect of diverse categories of drugs on human colon tumour cell proliferation. 188 53

An experimental model is proposed to study suture line recurrence. By giving enemas with K12 colon carcinoma cells, derived from a 1,2-dimethylhydrazine-induced colon cancer in male syngeneic BDIX rats, we were able to obtain a suture implantation in about 30% of the control animals. Possible systemic and local factors which might influence this implantation rate could be studied using this model. Only local irrigations of the colon lumen with sodium hypochlorite 0.2% prior to anastomosis produced a significant decrease in implantation rate. Irrigations with chlorhexidine-cetrimide 2.5%, the use of iodized suture material and altering the cellular immune system of the hosts by ciclosporin or excessive surgical stress, had no significant effect on the implantation rate.
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PMID:Factors influencing the implantation of colon cancer cells on the colonic suture line in rats. 207 96

In a panel of eight cloned complementary DNA sequences whose level of expression characterize colon cells as transformed in vivo and in vitro, one which may also serve as a marker of risk in familial polyposis and familial colon cancer flat mucosa has been identified as mitochondrial cytochrome c oxidase subunit 3. Mean level of expression of cytochrome c oxidase subunit 3 decreases progressively in colon adenomas and carcinomas relative to normal mucosa in vivo, and returns to higher levels present in biopsies of normal mucosa when the HT29 human colonic adenocarcinoma cell line is induced to differentiate with sodium butyrate. Quantitation of cytochrome c oxidase subunit 3 DNA by dot blots indicated that these changes in expression were not associated with alterations in the number of mitochondrial genomes.
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PMID:Expression of mitochondrial cytochrome c oxidase in human colonic cell differentiation, transformation, and risk for colonic cancer. 215 29

Two colon cancer cell lines, HT-29 (human) and DHD/K12/TRb (rat), were grown as monolayer cultures to various confluence degrees. The cytotoxic efficacies of doxorubicin and 4'-deoxydoxorubicin, evaluated by a survival assay, and the nuclear drug concentrations, measured by microspectrofluorometry, were shown to progressively decrease with the augmentation of confluence. This confluence dependent resistance (CDR) to anthracyclines was demonstrated independent of the multidrug resistance drug efflux mechanism. The cellular uptake of three compounds (sodium [51Cr]chromate, D-[14C]alanine, L-[14C]glucose) known to passively diffuse across the cell membrane as anthracyclines do was also reduced in confluent cells. After trypsin cell detachment, the kinetics of reversion of the sodium [51Cr]chromate uptake decrease and that of CDR were similar. Therefore, CDR may be attributed to a reduction of anthracycline cell intake due to a general alteration of passive diffusion across the cell membrane. However, CDR is only partly explained by this phenomenon since a reduced sensitivity of confluent cells was observed compared with nonconfluent cells for a similar amount of drug in their nuclei. CDR could explain the high resistance to anthracyclines of some solid tumors, such as colon tumors, in which cancer cells are tightly aggregated.
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PMID:Mechanisms of resistance of confluent human and rat colon cancer cells to anthracyclines: alteration of drug passive diffusion. 220 25

Spleen cells from inbred Biozzi mice, immunized against the human breast cancer cell line T47D, were fused with murine myeloma SP2O cells to generate monoclonal antibodies. One of these, 1BE12, of IgM isotype, reacted with five of six human breast tumor cell lines, while no binding was detectable with normal lymphocytes, RBC, or fibroblasts. The antigen recognized by monoclonal antibody 1BE12 was localized on the surface of T47D and MCF7 cells and was detected in cell-free supernatants of cultures. The antigen was found also on the surface of milk secretory cells. Immunohistochemical staining of frozen and paraffin-embedded sections of human tissues showed apical polarized reactivity in normal breast glands, while in all breast cancers staining was either cytoplasmic or membranous and heterogeneously distributed. Immunostaining was also observed in some other normal epithelia, including salivary gland, gastroduodenal mucosa, exocrine pancreas, and cervix. The antigen was not detectable in secretory endometrium, whereas proliferative endometrium was strongly stained. Colon carcinoma, and cancers of the bladder and endometrium were strongly reactive. No staining was detected in melanoma, lymphoma, mesothelioma, non-small cell lung carcinoma, and thyroid, renal, and ovarian carcinomas. Lectin absorption of MCF7 membrane extracts reduced 1BE12 binding. A large reduction in 1BE12 reactivity was observed after digestion of T47D and MCF7 membrane extracts with proteases. Treatment with sodium periodate resulted in complete loss of antigenicity, while neuraminidase treatment did not affect 1BE12 binding. These findings suggest that the 1BE12 epitope is expressed on the carbohydrate moiety of a glycoprotein and does not contain sialic acid. Immunoblotting of the perchloric acid-soluble fraction of MCF7 membrane extracts after electrophoresis in 1% agarose detected the antigen as a high molecular weight species (Mr greater than 900,000). The antigen was purified by perchloric acid extraction of MCF7 membrane preparations followed by affinity chromatography on 1BE12 antibody coupled to Sepharose-4B and gel exclusion fast protein liquid chromatography. No reactivity of the purified material was found with monoclonal antibodies directed against human milk fat globule membrane-associated mucins HMFG1 and DF3.
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PMID:Characterization and distribution in human tissues of a glycoproteic antigen defined by monoclonal antibody 1BE12 raised against the human breast cancer cell line T47D. 222 61

The purpose of this study was to examine the mechanism of specific antibody pretreatment for reduction of liver uptake of 111In-labeled monoclonal antibody (MAB). Previous work with an anti-carcinoembryonic antigen (CEA) MAB (T84.66) and LS174T human colon cancer xenografts in nude mice has shown that giving a high dose (0.2 mg) of unlabeled T84.66 in conjunction with the same MAB (T84.66) labeled with 111In (Indacea) significantly lowered the liver uptake of 111In. High performance liquid chromatography and sodium dodecyl sulfate-polyacrylamide gel electrophoresis were used to assess the radiolabeled components in serum and liver at different times following administration of Indacea in normal and tumor bearing mice. In serum the 111In remained associated with the IgG in both tumor bearing and non-tumor bearing mice. Liver uptake of 111In in mice without tumor was low (8-12% injected dose/g) and both IgG and a low molecular weight metabolite were found in the liver homogenates. Liver uptake in tumor bearing mice increased dramatically (15-40% injected dose/g) with size of tumor and in addition to the IgG and low molecular weight components, a high molecular weight compound was identified. Administration of CEA: Indacea complexes to non-tumor bearing mice produced the same high pressure liquid chromatography and gel patterns as those seen in mice with large (greater than 1 g) tumors. Liver homogenates from tumor bearing mice given specific antibody pretreatment showed the same patterns seen with non-tumor bearing mice (no high molecular weight peak). In conclusion, CEA:Indacea complexes are formed in tumor bearing mice and rapidly cleared by the liver. Specific antibody pretreatment results in the production of unlabeled CEA:MAB complexes causing a reduction in the formation of CEA:Indacea complexes and a lower liver uptake of 111In.
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PMID:Mechanism of decreasing liver uptake of 111In-labeled anti-carcinoembryonic antigen monoclonal antibody by specific antibody pretreatment in tumor bearing mice. 229 32


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