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

Tumor spread may be favored by a reduced production and/or an enhanced degradation of extracellular matrix components (collagen, fibronectin, laminin). Most tumor cell behavior, from growth to spread, may be regulated by cytokines, the exact roles of which, however, are not yet fully understood. We here evaluate the effects of some cytokines (epidermal growth factor, transforming growth factor-beta 1, interleukin-1 alpha, and interleukin-1 beta) on both cell growth and the production of the aminoterminal peptide of type III procollagen, the urokinase plasminogen activator, and the plasminogen activator inhibitor-1 in neoplastic cell lines originating in the pancreas and colon. Cells were stimulated daily with the above cytokines and the aminoterminal peptide of type III procollagen, urokinase plasminogen activator, and plasminogen activator inhibitor-1 were measured in the conditioned media. Epidermal growth factor stimulated cell growth of both cell lines. Transforming growth factor-beta 1 counteracted cell proliferation and stimulated type III procollagen and plasminogen activator inhibitor-1 production only in the colon cancer cell line. Interleukin-1 alpha slightly stimulated cell growth, but inhibited plasminogen activator inhibitor-1 production in both cell lines; interleukin-1 beta did not affect cell growth, but stimulated plasminogen activator inhibitor-1 production by the colon cancer cell line. Our findings suggest that transforming growth factor-beta 1 and interleukin-1 beta may have an antidiffusive effect. These results confirm that cytokine-producing cells have a potential role in stimulating or counteracting tumor growth and spread and also confirm the pivotal role of host-tumor interactions in determining the outcome of a particular neoplasia.
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PMID:Cytokines may influence tumor growth and spread. An in vitro study in two human cancer cell lines. 900 14

In greater than 80% of colon tumors and established cell lines, the specific activities of the protein tyrosine kinases pp60(c-src) and pp62(c-yes) are increased with respect to normal colonic epithelial cells. However, no mutations in either gene have been identified in colon tumors. Therefore, the possible biological consequences of activations of these protein tyrosine kinases in colon tumors have been unclear. To determine if pp60(c-src) activation affects growth and tumorigenicity of established colon tumor cell lines, an antisense expression vector that specifically reduces pp60(c-src) expression was constructed. The vector was transfected into HT 29 cells, an established colon tumor cell line in which both pp60(c-src) and pp62(c-yes) are activated. Two stable subclones were isolated in which pp60(c-src) but not pp62(c-yes) expression and activity were reduced. These established cell lines proliferated more slowly than parental cells proportionately to reduction in pp60(c-src) expression. When injected into nude mice, antisense transfected cells formed slow-growing tumors; however, the rate of tumor growth was reduced far greater than would be predicted from decreased proliferation rates in tissue culture. In contrast, stable subclones transfected with a comparable "sense" expression vector were unaltered in growth rates in tissue culture and in nude mice with respect to parental HT 29 cells. These data demonstrate that the activation of pp60(c-src) alone contributes to the tumorigenicity of HT 29 cells, a cell line widely used as a model for biological properties of colon carcinoma. Furthermore, because pp60(c-src) and pp62(c-yes) appear redundant to the growth regulation of normal colonic epithelial cells, the data suggest that src-specific inhibitors might be of therapeutic value for colon cancer.
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PMID:Decreased tumorigenicity of a human colon adenocarcinoma cell line by an antisense expression vector specific for c-Src. 905 68

In a total of 1073 unradically resected patients (R1/R2) surprisingly we found a group of 31 with a more than 5-year-survival and seven patients living more than 10 years. The prognosis in patients presenting rectal carcinoma was significantly better compared to colon cancer, with a 5-year-survival of 5 +/- 2% compared to 1 +/- 1%. For a long local control of tumor growth in the residual tumor patients, the possibility of irradiation probably in combination with chemotherapy seems to explain these data; but half of our longterm survivors had no additional therapy. The influence of tumorbiological and immunological factors in such patients are of further interest.
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PMID:[Long-term survival after non-curative therapy of colorectal carcinomas]. 910 12

The efficacy of dietary selenium supplementation is currently being evaluated in intervention trials. However, the biological mechanisms underlying the cancer chemopreventive effects of selenium supplementation have yet to be elucidated. Selenium metabolism and polyamine biosynthesis are linked in their common requirement for S-adenosylmethionine. Selenomethionine was the predominant form of selenium in the dietary supplement, therefore we evaluated the anti-tumorigenic effects of selenomethionine. We found that selenomethionine inhibited tumor growth (both in A549 lung and HT29 colon cancer cells) in a dose-dependent manner. At 24 and 72 h, polyamine content of A549 and HT29 cancer cell lines was decreased at doses that inhibited 50% of normal growth. Selenomethionine treatment induced apoptosis in both cancer cell lines. Exogenous spermine administration, which replenishes intracellular polyamine levels, prevented selenomethionine induced apoptosis. Selenomethionine administration to the cancer cell lines increased the number of cells in metaphase. This cell cycle effect appeared to be reversed with the co-administration of selenomethionine and spermine. These data suggested that at least part of the anti-carcinogenic effects of selenium supplementation might be due to a depletion in polyamine levels. This depletion of polyamines leads to an induction in apoptosis and perturbations in the cell cycle.
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PMID:Involvement of polyamines in selenomethionine induced apoptosis and mitotic alterations in human tumor cells. 921 3

The effects of shock waves in combination with various anti-cancer agents i.e. Bleomycin(BLM), Cis-platinum (CDDP) and 5-fluorouracil(5-FU) on various human cancer cells were examined. It was only with BLM that enhancement was evident in all cell lines. The degree of chemotherapeutic enhancement was proportional to the amount of shock wave energy applied. Ladder formation of DNA in GCIY, a gastric cell line, was observed only when treated with both BLM and shock waves in combination. When SW 480, a colon cancer cell line, transplanted into the back of nude mice were treated with a combination of i.v. injected BLM and regional exposure to shock waves, a significant enhancement of chemotherapeutic effects was observed in terms of the tumor growth curve. When cancer cells exposed to shock waves and observed under scanning and transmission electron microscopes, microvilli on the cell surface disappeared and numerous dimples(diameters distributed from 0.05 to 0.5 microns) became apparent. These dimples were concluded to be pores penetrating through the cell membrane, because reagents such as propidium iodide or 5(6)-carboxyfluorescein could enter cells treated shock waves.
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PMID:Enhancement of chemotherapeutic effects with focused shock waves: extracorporeal shock wave chemotherapy (ESWC). 923 69

Cepharanthin (CE), a bisbenzylisoquinoline alkaloid drug, was tested in vitro and in vivo with chemotherapeutic agents, vincristine (VCR), vinblastine (VLB), and vindesine (VDS). The activity of these agents alone or in combination was tested against a human colon cancer cell line (RPMI 4788) or a human uterine cervical cancer cell line (HeLa), using a modified microcytotoxicity-viable cell staining assay. In the in vitro study, the antiproliferative activities of each vinca alkaloid were enhanced additively or synergistically by combination with CE in RPMI 4788 cells as well as HeLa cells. The sequential exposure of the RPMI 4788 cells or HeLa cells to both CE and each vinca alkaloid agent showed evidence of a more significant potentiation. The antiproliferative activity of the combination of each vinca alkaloid agent(VCR, VLB, or VDS) with CE was almost equivalent to the effect of each vinca alkaloid agent alone which was potentiated by CE tenfold through several hundredfold. In an experimental model of tumor growth and survival, in which RPMI 4788 cells were transplanted subcutaneously or intraperitoneally into BALB/c nu/nu mice respectively, CE (1 mg/kg) alone exerted not significant inhibitory activity against tumor growth or survival, and VCR (0.25 mg/kg) alone partially inhibited these antitumor activities. Furthermore, the antitumor effects of VCR were elevated synergistically by the simultaneous administration of CE. These studies indicate that due to their therapeutic potential, combinations of vinca alkaloid agent with CE might be a promising therapy for some human cancers.
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PMID:Positive interaction of bisbenzylisoquinoline alkaloid, cepharanthin, with vinca alkaloid agents against human tumors. 923 17

KRN 5500 is a new semi-synthetic antitumor compound derived from spicamycin and has a unique structure. The compound showed a broad spectrum of antitumor activity against human colon, stomach, esophageal, breast and lung cancer xenografts in nude mice. Therapeutic efficacy of KRN 5500 against liver metastasis of COL-1 human colon cancer scid mice was examined. The treatment with KRN 5500 inhibited tumor growth in the liver and reduced the serum TPA concentration to a normal level. KRN 5500 inhibits protein synthesis in rabbit reticulocyte lysates. Among several metabolites of KRN 5500, only SAN-Gly showed a potent inhibitory activity against protein synthesis in reticulocyte lysates. TLC analysis of KRN 5500 metabolites using 7 human colon cancer cell lines and 3 normal cell lines demonstrated a correlation between the cytotoxicity of KRN 5500 and converting activity from KRN 5500 to SAN-Gly. These results indicate that SAN-Gly is the intracellular active metabolite and that converting activity from KRN 5500 to SAN-Gly is the major determinant of KRN 5500 cytotoxicity.
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PMID:[Protein synthesis inhibitor--antitumor activity and mode of action of KRN 5500]. 930 56

Zymosan, a non-specific macrophage-stimulating agent, modifies favourably tumour growth in the liver but has minor effect on renal tumours. The mechanism accounting for variation is still to be clarified. The effect of zymosan on liver cancer may be mediated by the macrophage-monocyte system. Kupffer cells are in vitro cytotoxic against colon cancer cell lines. The kidney is sparse in macrophage elements. The prostaglandin synthesis inhibitor, indomethacin, inhibits tumor growth. In Wistar-FU rats inoculated in the liver and the kidney with an adenocarcinoma cell suspension, pretreatment with zymosan (3 mg x 100 g[-1]) significantly reduced both tumour take and liver volume. This effect was attenuated by concomitant administration of indomethacin (0.2 mg x 100 g[-1]). After 2 weeks there was still reduced liver tumour volume. No significant effects on tumour take or growth were observed when the cells were inoculated into the kidney. There was no significant effect of zymosan on an hepatoma in Lister-Hooded rats. Pretreatment with indomethacin had no effect on tumor take or initial growth.
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PMID:The influence of zymosan and indomethacin on liver and kidney tumor growth. An experimental study in rats. 938 96

Herpes simplex virus-thymidine kinase (HS-tk) gene therapy with ganciclovir (GCV) treatment has been reported to inhibit the tumor growth, which is applied to the gene therapy targeted to the malignant brain tumor. To suppress the tumor growth completely, the authors designed the HS-tk gene therapy in combination with granulocyte macrophage-colony stimulating factor (GMCSF) gene using the hepatic metastatic model of murine colon cancer. The transduction of the HS-tk gene in combination with the GMCSF gene, followed by GCV, showed a complete inhibition of hepatic metastases of murine colon cancer, which was significantly superior to that of HS-tk gene alone. The growth of cancer cells transduced with both HS-tk and GMCSF genes was inhibited in vitro, and long-lasting antitumor immunity after hepatic metastasis of cancer cells transduced with both HS-tk and GMCSF genes was acquired. It is suggested that HS-tk gene therapy in combination with the GMCSF gene is effective for the complete inhibition of hepatic metastasis of murine colon cancer.
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PMID:Inhibition of establishment of hepatic metastasis in mice by combination gene therapy using both herpes simplex virus-thymidine kinase and granulocyte macrophage-colony stimulating factor genes in murine colon cancer. 940 3

Metastatic rat colon cancer cells but not normal rat hepatocytes showed activity of cathepsin B on their plasma membranes. Activity was visualized in living cells with a new fluorogenic substrate, [Z-Arg]2-cresyl violet, and confocal microscopy. When these cancer cells were injected into the portal vein of rats, the animals developed tumors in the liver in a heterogeneous fashion. Three- to four-fold more tumors were found in the small caudate lobe than in the other three large lobes of the liver. Oral treatment with a selective water-soluble inhibitor of extracellular cathepsin B, Mu-Phe-homoPhe-fluoromethylketone, resulted in 60% reduction of the number of tumors and 80% reduction of the volume of tumors in the three large lobes whereas tumor development was not affected in the small caudate lobe. This study supports the conclusions that (a) extracellular cathepsin B plays a crucial but complex role in liver colonisation by rat colon carcinoma cells in vivo, (b) its selective inhibition suppresses tumor growth heterogeneously in the liver and (c) the caudate lobe of the liver is a relatively large risk factor for tumor development.
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PMID:Heterogeneous suppression of experimentally induced colon cancer metastasis in rat liver lobes by inhibition of extracellular cathepsin B. 951 97


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