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)

Given the increasing incidence of colon cancer in recent years, it is important to establish a diagnostic system for early detection and introduce it into clinical practice. A double contrast examination that uses a disposable tip and tube with an enema reservoir filled with 200 ml of 60 w/v% barium sulfate, known as SCG (screening colonography) was used in this study. In order to assess its utility SCG was performed on 1,554 patients, and 2,004 patients were examined by a within 24 hours combination of sigmoidoscopy and SCG by way of screening for colon cancer. Given the brief duration of SCG, which ranged from 10 to 13 min in most patients in the study, the efficiency of the examinations was considered to be rather high. Furthermore, the barium reached the cecum in as many as 98.7% of the patients. Overall, SCG proved to have an excellent diagnostic capability. Sigmoidoscopy-SCG, on the other hand, detected colon cancer in 114 patients (5.7%) and colon polyps in 658 patients (32.8%). The rates of detection of colon cancers and polyps were higher in the patients who tested positive in immunological fecal examinations for occult blood. Judging from our results, it may be said that for many patients receiving thorough physical checkups to screen for colon cancer, our system will provide for efficient screening whereby patients are first examined for fecal occult blood and those who test positive undergo sigmoidoscopy and SCG within the same day.
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PMID:[Utility of SCG (screening colonography) and combined sigmoidoscopy-SCG in thorough physical checkups]. 140 Sep 8

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

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

Control of colon cancer depends, in part, on intact immune defense mechanisms. Since opiates are known to affect some components of immune function, this study was conducted to determine the effect of high-dose subcutaneous morphine sulfate and of low-dose intrathecal morphine on the postoperative growth of metastatic colon cancer. Five groups of 15 Fischer 344 rats were given intraportal injections of colon cancer cells as follows: group 1, control; group 2, daily subcutaneous injections of 20-mg/kg morphine the day before and for 2 days after colon cancer cell inoculation; group 3, daily subcutaneous injections of saline; group 4, daily intrathecal injections of 20 micrograms of morphine; and group 5, daily intrathecal injections of saline. There was a significant decrease in the hepatic tumor burden in group 2 compared with groups 1 and 3 and a significant increase in the hepatic tumor burden in groups 4 and 5 compared with group 1. This study demonstrates that intermittent injections of a narcotic may decrease the growth of tumor cells that gain access to the circulation during a surgical procedure. In addition, the results support the concept that tumor cells entering the circulation during a vulnerable period of postoperative immunosuppression are more likely to survive as metastatic tumor.
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PMID:Effect of morphine on growth of metastatic colon cancer in vivo. 200 60

Isotopically labeled [( 3H]serine, [3H]proline, and [35S]sulfate) subendothelial cell basement membranes were used to determine the role of urokinase plasminogen activator (uPA) and its specific inhibitor plasminogen activator inhibitor 2 (PAI-2) in colon cancer cell extracellular matrix degradation. Recombinant PAI-2 irreversibly inhibited low and high molecular weight purified human uPA in addition to both colon cancer cell-associated and secreted uPA, particularly if pro-uPA had been preactivated. Two selected lines (COLO394 and LIM1215) preferentially degraded differently labeled matrices in a time- and plasminogen-dependent manner. This process was inhibitable by PAI-2 in the medium at levels which suggested that some degree of "shielding" of cell surface uPA from inhibitor occurred. The ability of PAI-2 to regulate the invasive phenotype of cells which express cell surface or receptor-bound uPA is discussed.
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PMID:Inhibition of cancer cell urokinase plasminogen activator by its specific inhibitor PAI-2 and subsequent effects on extracellular matrix degradation. 211 45

The connective tissue stroma of malignant tumors is a newly formed tissue that supports the growth and progression of neoplastic cells. Proteoglycans are intrinsic components of this complex structure and molecular changes in this class of macromolecules can significantly affect behavioral properties of transformed cells. We report that human colon carcinoma contained increased levels of a chondroitin sulfate proteoglycan that exhibited an altered glycosaminoglycan structure in which 0- and 6-sulfated units, as detected by specific monoclonal antibodies, predominated. Proteoglycans with such epitopes were localized primarily to the connective tissue stroma surrounding the tumor cells but not to the tumor cells themselves or the native, non-cancerous connective tissue. Analysis of mRNA encoding PG-40, the main chondroitin sulfate proteoglycan of colon tissue, revealed a 7-fold increase in the two transcripts encoding this gene product. This increase was evident whether the data were normalized to total RNA content or beta-actin mRNA levels. The altered steady state levels of PG-40 mRNA did not correlate with any significant gene amplification or rearrangement of PG-40 in human colon cancer. However, when genomic DNA was tested for degree of methylation, the colon carcinoma tissue showed a marked hypomethylation of PG-40 gene locus, a finding that has been associated with increased gene activation. Interestingly, PG-40 gene was also hypomethylated in cultured colon fibroblasts, which express PG-40, but not in colon carcinoma cells which do not express this gene. These results indicate that specific proteoglycan changes occur in colon carcinoma and that these alterations are the product of stromal cells that are topologically associated with and functionally respondent to the growing malignant cells. This is the first evidence that enhanced PG-40 expression in a human malignant tissue is associated with a hypomethylated gene and suggests that the control of PG-40 gene expression may represent an important factor in the progression of colon carcinoma.
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PMID:Altered expression of chondroitin sulfate proteoglycan in the stroma of human colon carcinoma. Hypomethylation of PG-40 gene correlates with increased PG-40 content and mRNA levels. 216 45

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

Tumor-producing phorbol esters [e.g., 12-O-tetradecanoylphorbol-13-acetate (TPA)] induce changes in a human colon cancer cell line, VACO 10MS, that mimic terminal differentiation: a rapid blockade of DNA replication and cell division, a marked increase in cell adhesion properties with striking changes in morphology, and the acquisition of ion-transporting activities. The present report shows that the triggering of this terminal differentiation sequence by TPA is associated with a rapid release of heparan sulfate proteoglycans from the cell surface that is soon followed by an acceleration of proteoglycan synthesis. The activation of the release mechanism is independent of ongoing protein synthesis, whereas the resynthesis of the proteoglycans requires the production of new proteins. A persistent high rate of proteoglycan synthesis and release appears correlated with the progression of the colon cell into the terminal differentiation state. Bryostatin 1, an agent which has been shown previously to block the TPA-induced terminal differentiation of this cell line, also largely prevents the TPA effects on proteoglycan metabolism. Since both TPA and bryostatin 1 produce their effects through the activation of members of the protein kinase C class of enzymes, it is proposed that the differentiation state of these colon cancer cells may be regulated by a differential activation of isozymes or a ligand-directed phosphorylation of proteins that are involved in proteoglycan metabolism.
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PMID:Phorbol esters activate proteoglycan metabolism in human colon cancer cells en route to terminal differentiation. 227 82

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

Alterations in cell surface proteins and glycoproteins may play a key role in determining the metastatic behavior of tumor cells. The cell surface proteins of a series of related murine colon cancer cells selected in an animal model for colon cancer metastasis (R. S. Bresalier et al., Cancer Res., 47: 1398-1406, 1987) were therefore compared by a variety of biochemical methods. Lactoperoxidase-catalyzed iodination of cell surface proteins followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated quantitative and qualitative differences in the cell surface protein profiles of parental cell line 51B (low metastatic potential) and its metastatic derivatives 51B LiM 5 and 51B LiM 6. Labeling of sialic acid-containing proteins suggested that, in the case of at least four of these proteins (Mr 170,000, 120,000, 95,000, and 55,000), this represented an increase in radioactive labeling of sialoglycoproteins from the metastatic lines. Affinity chromatography of solubilized 125I-labeled cell membrane proteins revealed a 2- to 3-fold increase in wheat germ agglutinin and Sambucus nigra lectin binding associated with the metastatic lines, compared to the poorly metastatic parent. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of material eluted from these columns demonstrated enhancement of proteins from the metastatic cells corresponding in molecular weight to the previously identified major sialoglycoproteins. Neuraminidase-releasable membrane-associated sialic acid and sialyltransferase activities were 2- to 3-fold higher in the metastatic cell lines compared to the parental line. Liver colonization after intrasplenic injection of the various lines into syngeneic mice was dramatically reduced by prior removal of cell surface sialic acid. Immunohistochemical staining of primary and metastatic tumors formed after cecal injection of parental 51B suggested selective metastasis by wheat germ agglutinin-binding tumor cells. These results further support the concept that cell membrane sialylation is important in determining the metastatic potential of cancer cells.
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PMID:Cell surface sialoprotein alterations in metastatic murine colon cancer cell lines selected in an animal model for colon cancer metastasis. 229 75


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