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)

Although 58 patients with peritonitis carcinomatosa underwent multidisciplinary therapy over the last 5 years in our department, about half of them died within 3 months after treatment. In addition, the prognosis was poor for gastric and colon cancer patients, who had macroscopic peritoneal dissemination. Therefore intraoperative intraperitoneal administration of either BRM or anticancer drugs was performed for the microscopic peritoneal dissemination of the cancer, and the immunological response in the peritoneal cavity was examined. In terms of subpopulation of peritoneal exudate cells, neutrophil leucocytes were predominant and thereafter lymphocytes increased. As for the cytokines in the exudate from peritoneal cavity, the concentration of interleukin-6 peaked within 24 hours after administration, followed by a gradual decrease, while the concentration of interferon-gamma was detectable at more than 24 hours after operation, followed by a gradual increase. Tumor necrosis factor-alpha was also detectable in the exudate. Its concentration decreased when both OK-432 and MMC were administered, but it increased when CDDP was administered. The above results indicated that preventive intraoperative intraperitoneal administration of BRM and anticancer drugs should bring about individual immunokinetic modulation in tumor bearing host and both cytokines and immunocytes could play an important role in locoregional tumor immunity.
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PMID:[Clinical studies on locoregional immunochemotherapy of peritonitis carcinomatosa]. 153 Mar 41

The antitumor effect of recombinant human interferon-beta (r IFN-beta) and recombinant interferon-gamma (r IFN-gamma) was studied in vivo using a pulmonary metastatic model involving nude mouse human colon cancer xenografts. The results indicated that both r IFN-beta and r IFN-gamma had an inhibitory effect on pulmonary metastases. Furthermore, a combination of r IFN-beta and r IFN-gamma acted synergistically in the inhibition of pulmonary metastases. These results suggested that a combination of r IFN-beta and -gamma could be a most effective form of interferon therapy for cancer.
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PMID:[Synergistic effect of recombinant human interferon-beta and -gamma on human colon cancer transplanted into nude mice]. 309 15

The development of useful therapy for the peritonitis carcinomatosa of gastrointestinal cancer is an important theme in cancer therapy. We developed an experimental model of peritonitis carcinomatosa in nude mice transplanted intraperitoneally human colon cancer cells. In this study, we investigated combined effect of human recombinant interferon-beta (rIFN-beta) and recombinant interferon-gamma (rIFN-gamma) in vivo using this model. The result indicate that each rIFN-beta and rIFN-gamma showed a significant prolonged survival compared with the control group (mean survival days: 41.8 +/- 5.0 days). Furthermore, combined administration of rIFN-beta and rIFN-gamma showed a marked prolonged survival (mean survival days: 114.0 +/- 7.4 days) compared with rIFN-beta or rIFN-gamma alone. These results suggest that a combined treatment of rIFN-beta and rIFN-gamma may be useful against peritonitis carcinomatosa of gastrointestinal cancer.
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PMID:[Combined effect of human recombinant interferon-beta and interferon-gamma against an experimental model of peritonitis carcinomatosa in nude mice]. 310 28

The antitumor effect of recombinant human interferon-gamma (rIFN-gamma) and adriamycin (ADM), alone or in combination, against a human colon cancer cell line (RPMI 4788) was examined in vitro and in nude mice. In the in vitro study, antiproliferative activities of ADM were augmented additively or synergistically by combination with rIFN-gamma in a dose-dependent manner. Growth of RPMI 4788 cells (2 X 10(6)/mouse) transplanted subcutaneously into CD-1 nu/nu nude mice (day 0) was not inhibited significantly by 28 daily injections from day 10 of rIFN-gamma alone, but the antitumor effect of ADM was augmented synergistically by the simultaneous injection of rIFN-gamma. In an experimental model of pulmonary metastasis, in which RPMI 4788 cells (2 X 10(6)/mouse) were inoculated intravenously into BALB/c nu/nu nude mice (day 0), 10 or 21 daily injections from day 2 of rIFN-gamma alone had significant inhibitory effects against pulmonary metastasis in a dose-dependent manner. Furthermore, the inhibitory effect of ADM was augmented synergistically by daily injections of rIFN-gamma.
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PMID:Antitumor effect of human recombinant interferon-gamma alone and in combination with adriamycin on a human colon cancer cell line (RPMI 4788) in vitro and in nude mice. 312 41

Inflammatory bowel disease, in particular ulcerative colitis, is characterized by localization of leukocytes in close proximity to the colonic epithelium, which may be mediated by the expression of intercellular adhesion molecules (ICAM-1; CD 54). We previously reported the presence of an organ-specific M(r) 40K colonic protein that acts as an autoantigen in ulcerative colitis and is present on the surface of colonic epithelial cells and also in DLD-1 colon cancer cells. Using the colon tumor cell line DLD-1 and flow cytometry, ICAM-1 antibody binding by untreated cultured DLD-1 cells was similar to background antibody binding (mean channel number, MCN = 9.77 +/- 2.13). Interferon-gamma (100 U) induced a 1-2 log increase in anti-ICAM-1 antibody binding from as early as 12 hr after exposure up to 72 hr and a moderate increase (up to about 100%) in the binding of anti-M(r) 40K antibody. Additional studies showed that anti-ICAM-1 and anti-M(r) 40K antibodies bound to DLD-1 cells regardless of the presence of the other antibody. Taken together, the present observations suggest that the epitopes of ICAM-1 and M(r) 40K molecules are coexpressed by colonic epithelial cells, regardless of the presence of the other molecule. Furthermore, lymphocytes in the colonic mucosa that are activated to produce interferon-gamma may upregulate the expression of both of these molecules.
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PMID:Amplified expression of intercellular adhesion molecule-1 (ICAM-1) and M(r) 40K protein by DLD-1 colon tumor cells by interferon-gamma. 809 38

In vitro effects of cytokines and therapeutic drugs on antibody dependent cellular cytotoxicity (ADCC) mediated by anticolon antibody were investigated in serum samples from patients with ulcerative colitis. A 51Cr release assay was used to examine ADCC activity with the colon cancer cell line, colo 205, as the target and peripheral blood mononuclear cells as the effector. High ADCC activity was shown in 13 of 32 (41%) patients with ulcerative colitis. This ADCC activity was inhibited by protein A treatment of the serum samples. Interleukin 2 (IL2) activated effector cells could enhance ADCC activity, but interferon-gamma (IFN-gamma) or tumour necrosis factor-alpha (TNF-alpha) had no effect on the cytotoxic activity of effector cells. Treatment of target cells with IFN-gamma increased the vulnerability of these cells to ADCC with a large increase of intercellular adhesion molecule-1 (ICAM-1) expression on their surface. Monoclonal antibodies to ICAM-1 inhibited this IFN-gamma enhanced ADCC activity. Interestingly, prednisolone (PSL) reduced ADCC activity, but sulphasalazine (SASP) or 5-aminosalicylic acid (5-ASA) did not. These results suggest that IL2 and IFN-gamma could enhance colonic epithelial cell injury mediated by the ADCC mechanism in ulcerative colitis and that ADCC enhanced by cytokines is restored by PSL treatment.
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PMID:Interleukin 2 and interferon-gamma augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis. 810 Feb 5

Autolymphocyte therapy (ALT) is adoptive cellular therapy of cancer using ex vivo activation of autologous peripheral blood lymphocytes (PBL). Memory T cells are the principal effector population in ALT, with in vivo activity in patients with metastatic renal cell carcinoma (RCC) and melanoma, and ex vivo cytotoxicity against autologous tumor targets. However, the noncytolytic lymphocyte portion of ex vivo-activated memory T cells (ALT cells) may also contribute as antitumor effectors. Pretreatment of murine and human tumor cells ex vivo with chemotherapeutic agents can enhance their susceptibility to antitumor lymphocytes ex vivo and in vivo. To determine whether cis-diamminedichloroplatinum(II) (DDP) could enhance ex vivo antitumor effects of ALT cells by immunomodulation, human breast and colorectal carcinoma target cells were derived from both primary and metastatic surgical specimens and incubated in complete medium (CM) with DDP or in CM alone (control group). Viability of each group was confirmed by trypan blue-dye exclusion test. ALT cells were prepared from autologous PBL at surgery. Primary and metastatic tumor cells from each group were used as targets for ALT cells and levels of interferon-gamma (IFN-gamma) release were measured as a determination of antitumor effect and recognition. Primary tumor target cells incubated in DDP showed enhanced antitumor effects and recognition by autologous ALT cells, as measured by the IFN-gamma assay compared to non-DDP-treated controls. Metastatic autologous tumor target cells demonstrated less IFN-gamma release than did the primary targets, although this was enhanced by pre-treating metastatic tumor targets with DDP. ALT cells demonstrated minimal IFN-gamma release when incubated with allogeneic tumor targets. These data suggest that autotumor recognition of metastatic tumor targets is comparable to that of primary lesions following ex vivo pretreatment of metastatic cells with nonlethal doses of certain chemotherapeutic agents. DDP may somehow alter the physical properties of target cells, rendering them susceptible to immune-mediated attack and the combination of ALT and DDP may lead to increased therapeutic efficacy in patients with metastatic breast and colon cancer.
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PMID:Adoptive cellular therapy of human breast and colorectal tumor targets using ex vivo activated memory T lymphocytes with potentiation by cis-diamminedichloroplatinum(II). 815 4

Human intestinal intraepithelial lymphocytes (IEL) demonstrate target cell-restricted spontaneous cytotoxic (SC) activity that is due to CD2+CD3+CD8+CD16-CD56- effector cells; they kill epithelial cell (EC) tumours (such as DLD-1 colon cancer cells), but not natural killer (NK)-sensitive K-562 cells. The present study shows that the measured levels of SC activities by IEL correlated with those of autologous lamina propria lymphocytes (LPL), but not with those of peripheral blood lymphocytes (PBL). Also, the susceptibilities of DLD-1 cell clones to lysis by IEL and PBL effector cells did not correlate, suggesting different mechanisms of lysis. Antibody blocking experiments showed that the main surface molecules involved in lysis depended on the effector cell type: alpha E beta 7 (HML-1) on IEL and CD16 on PBL. No antibody-dependent cell-mediated cytotoxicity (ADCC) was demonstrated by IEL, even after stimulation with interferon-gamma (IFN-gamma). Few IEL expressed Fc receptors for IgG. This study describes further differences between the SC activities of IEL and PBL.
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PMID:Spontaneous cytotoxicity of intestinal intraepithelial lymphocytes: clues to the mechanism. 750 97

The homotypic cell aggregation of a carcinoembryonic antigen (CEA) positive colon cancer cell line (Colo 205) was induced in vitro by interferon-gamma (IFN-gamma) treatment. Divalent cations were required for this aggregation, as it was inhibited by EDTA. The partial inhibition by cytochalasin B and the complete inhibition by a mixture of sodium azide and 2-deoxyglucose suggests that the aggregation requires the integrity of cytoskeleton and active metabolism. The expression of CEA was increased in the cytoplasm and on the membrane of Colo 205 by IFN-gamma treatment. Furthermore, this aggregation was inhibited completely by anti-CEA monoclonal antibody (mAb) and partially by mAb against intercellular adhesion molecule-1. This in vitro study suggests that CEA molecule participates in the IFN-gamma induced homotypic adhesion of some CEA positive cancer cells and that IFN-gamma has an important role in the regulation of cell-cell interaction mediated by CEA molecule.
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PMID:Carcinoembryonic antigen mediates in vitro cell aggregation induced by interferon-gamma in a human colon cancer cell line: requirement for active metabolism and intact cytoskeleton. 836 86

Human intraepithelial lymphocytes (IEL), predominantly CD8+ T-lymphocytes located between intestinal epithelial cells (EC), may represent the first-line immune defense against colon cancer. The mechanism by which IEL bind to the colon cancer line, DLD-1, was evaluated. A larger fraction of IEL than peripheral blood mononuclear cells bound to DLD-1 monolayers (25 +/- 16 versus 8 +/- 4% binding, P < 0.05). Binding increased when DLD-1 monolayers were incubated with interferon-gamma but not with tumor necrosis factor-alpha. Similar numbers of IEL adhered to EC tumors, HT-29 and 5637, and the non-EC tumor, A375, but fewer bound to nonmalignant smooth muscle (HISM) and fibroblast (KD) lines (P < 0.01). Binding of IEL to DLD-1 was reduced by monoclonal antibodies to HML-1 and CD11a (47 +/- 9 and 26 +/- 13% inhibition, respectively) and was completely eliminated by both combined (93 +/- 4% inhibition). Anti-HML-1 also inhibited the binding of IEL to other EC tumors but did not affect binding to non-EC tumors or fibroblasts. To conclude, the binding of IEL to EC tumors is mediated by HML-1 and CD11a [A. I. Roberts, S. M. O'Connell, and E. C. Ebert. Binding of intraepithelial lymphocytes to colon cancer cells is mediated by HML-1 and LFA-1 (abstract). Gastroenterology, 102: A685, 1992].
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PMID:Intestinal intraepithelial lymphocytes bind to colon cancer cells by HML-1 and CD11a. 845 30


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