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)

Pirarubicin (THP) is a derivative of adriamycin (ADM) which has been reported to have a lower cardiotoxicity than ADM. The authors investigated the in vivo antitumor effect of THP against human colon cancer cells (RPMI 4788) xenografted into nude mice. In the model of intra-abdominal carcinomatosis, intraperitoneal administration of THP (6 mg/kg) resulted in a significant prolongation of the survival compared with the saline control group (p less than 0.01). Intravenous administration of THP (8 mg/kg) significantly inhibited tumor growth compared with the saline control group. Labeling index with bromodeoxyuridine (BrdU) of RPMI 4788 tumors treated with THP was smaller than that in the control group. Mitotic index was also smaller in the group treated with THP. Labeling index with BrdU indicates the proportion of cells in the S phase. Thus, the tumor cells in both S and M phases have decreased after treatment with THP. This change in the cell cycle progression may be due to the accumulation of G2 phase similar to in vitro study. From these results, it was suggested that the change in cell cycle progression revealed in vitro might be caused by THP in vivo.
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PMID:[Antitumor effect of pirarubicin (THP) against human colon cancer transplanted into nude mice and the mechanism of cell cycle progression]. 154 63

The therapy of colorectal cancer may be improved by biologic response modifiers that enhance natural killer (NK) cell and antibody-dependent tumoricidal mechanisms. This study examined the effect of a recently discovered cytokine purified from the supernatant of an Ebstein-Barr virus-transformed B-lymphoblastoid cell line (RPMI-8866), natural killer cell stimulatory factor (NKSF), on NK and antibody-dependent cellular cytotoxicity (ADCC) of human colon adenocarcinoma cell lines. Human peripheral blood lymphocytes were cultured for 24 hr in the presence or absence of NKSF (3.6 pM) or interleukin-2 (1 nM). The cultured lymphocytes were analyzed for lytic potential toward chromium-51-labeled colon carcinoma targets SW 1116, 498 LI, and WC 1. ADCC was measured by incubating chromium-51-labeled SW 1116 or WC 1 targets with the monoclonal antibody CO17-1A, an IgG2a antibody reactive with gastrointestinal cancer-associated cell antigen, or control mouse IgG prior to testing NKSF-treated or control PBL effectors in a 6-hr cytotoxicity assay. NKSF significantly enhanced NK cytolysis of colon carcinoma and NK-resistant lymphoma cell lines, and on a molar basis was approximately 300 times more potent than interleukin-2 in generating NK cytotoxicity. Furthermore, NKSF significantly augmented lymphocyte-mediated ADCC against colon carcinoma targets, and the combination of NKSF with the antibody CO17-1A had an additive effect on lymphocyte tumoricidial capacity. Thus, NKSF may have a potential role in the treatment of colon cancer.
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PMID:Natural killer cell stimulatory factor (NKSF) augments natural killer cell and antibody-dependent tumoricidal response against colon carcinoma cell lines. 167 86

We have studied the mechanism of the synergistic effect of the combination of tumor necrosis factor-alpha (TNF-alpha) and interferon-alpha (IFN-alpha) on cell cycle progression using two-parameter flow cytometry in vitro and an immunohistochemical staining method in vivo. The cells used were human colon cancer cell line RPMI 4788 in vitro and in vivo, and human breast cancer cell line MX-1 and human renal cancer cell line NAMKO-1 in vivo. In the in vitro experiment, the cell cycle progressed normally as time elapsed in the control group. However, in the group treated with TNF-alpha and IFN-alpha in combination (combination group), it appeared that the transition from the S phase to the G2/M phase was blocked, and the cells that accumulated in the S phase died. In the in vivo experiment with male nude mice of a CD-1 genetic background, the antitumor effect on all three kinds of cancer cells was significantly greater in the combination group than in the control group. The cell labeling index on staining with bromodeoxyuridine in the combination group became markedly larger and the mitotic index smaller than in the other groups. From these results, it was concluded that in the combination group, both in vitro and in vivo, tumor cells markedly accumulated in the S phase and their progression from the S phase to the G2/M phase in the cell cycle was inhibited.
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PMID:Mechanism of the combined antitumor effect of natural human tumor necrosis factor-alpha and natural human interferon-alpha on cell cycle progression. 182 50

A total of 72 human leukemia-lymphoma cell lines were studied for reactivity with the monoclonal antibody (MAb) A7, an anti-human colon-cancer-cell-associated antigen reagent, by indirect membrane immunofluorescence. Nine of the 72 cell lines expressed the antigen recognized by A7 MAb. Five of the 34 T-cell lines, 2 of the 21 B-cell lines, and 2 of the 3 non-lymphoid-non-myeloid cell lines were reactive with A7 MAb. By means of SDS-PAGE and immunoblotting, the antigens isolated from both colon cancer cell lines (WiDr, SW1116 and LoVo) and leukemia cell lines (A3/KAWAKAMI, H9, RPMI 8226 and SPI-801) showed an identical MW of 42-43 kDa. The non-glycosylated antigen recognized by A7 MAb, which was expressed on both the colon cancer line (SW1116) and the leukemia line (H9) in the presence of tunicamycin, also showed an identical MW of 36 kDa. However, the quantity of the antigen in the leukemia cells was significantly lower than in the colon cancer cells. Although expression of this colon-cancer-associated antigen in the non-colon cancer cells is real, the significant expression of this antigen in colon-cancer cells makes it useful for clinical monitoring of colon cancer patients.
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PMID:Identification and characterization of a colon-cancer-associated antigen expressed on leukemia-lymphoma cell lines. 199 51

Interferon (IFN) increases cytoplasmic free calcium ([Ca2+]i) in RPMI 4788 cells, a human colon cancer cell line. Addition of IFN to the cells loaded with Fura-2, a fluorescent Ca2+ indicator, causes an immediate increase in [Ca2+]i, which is the earliest event after IFN stimulation. A cyanine dye, dis-C3- (5) was used to determine the effects of IFN on the membrane potential in cancer cells. The depolarization was seen with IFN-gamma, but not with IFN-beta. These results taken together, suggest that the IFN-gamma and -beta induced [Ca2+]i mobilization are clearly different in their dependence on Ca2+ entry through voltage-gated Ca2+ channels.
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PMID:Interferon-gamma activates the voltage-gated calcium channel in RPMI 4788 cells. 245 15

A study on the antitumor effect and distribution to tumor tissue of 1-(2-tetrahydrofuryl)-5-fluorouracil (FT-207) when administered with cepharanthine was performed using RPMI 4788 human colon cancer cell line or murine Sarcoma-180 tumor cells in vitro and in vivo. Combined treatment with FT-207 or 5-fluorouracil (5-FU) and cepharanthine showed a marked anti-proliferative effect on DNA synthesis of RPMI 4788 cells when measured by 3H-thymidine incorporation in vitro. Combination of FT-207 (1 microgram/ml) and cepharanthine (1 microgram/ml or 5 micrograms/ml) exhibited a similar antitumor effect to FT-207 (25 micrograms/ml). Also the DNA synthesis of RPMI 4788 cells was inhibited by low dose of 5-FU with cepharanthine similarly by high dose of 5-FU alone. On the other hand, Sarcoma-180 tumor was transplanted to the back of mice, and FT-207 (50 mumole/kg; 10 mg/kg) and cepharanthine were orally coadministered once at day 7 after tumor transplantation. This combined therapy significantly inhibited the growth of Sarcoma-180 tumor. Furthermore, antitumor activity of FT-207 was enhanced significantly by coadministration of cepharanthine daily for 10 days. The concentration of FT-207 or 5-FU in the tumor tissue, normal tissues and serum were measured in mice with Sarcoma-180 tumor. The mice were given FT-207 and cepharanthine orally once at day 7 (I) or daily for 10 days (II) after transplantation of Sarcoma-180 tumor cells. No remarkable difference was found in the concentration of FT-207 between tumor tissue and serum. The concentration of 5-FU in the tumor tissue was significantly higher than that in the serum. The ratio of 5-FU concentration in the tumor tissue to that in the serum (T/S) was 15.9 (I) or 13.0 (II) in the two administration systems. Maximum concentration of 5-FU was found when cepharanthine and FT-207 were given simultaneously at the molar ratio of 0.5:1, and this combination ratio seemed to be optimal. These results suggest that 5-FU is delivered and selectively accumulated into the tumor tissue by the presence of cepharanthine, but not in serum, and this mechanism should be correlated with antitumor activity shown by combination of FT-207 and cepharanthine. This mechanism is one of the reasons why the 5-FU concentration in the tumor tissue increases much more than that in normal tissues after administration of FT-207 by cepharanthine. Accordingly clinical application of cepharanthine is considered to be a useful adjuvant chemotherapy for cancer.
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PMID:[Effect of cepharanthine on antitumor activity of 1-(2-tetrahydrofuryl)-5-fluorouracil (FT-207)--5-fluorouracil delivery into tumor tissue]. 250 3

A colon tissue-bound disease specific IgG (CCA-IgG) antibody can be eluted from the colonic tissue of patients with ulcerative colitis (UC). CCA-IgG recognizes an Mr 40,000 protein present in both normal and diseased colon. Using an anti-Mr 40,000 murine monoclonal antibody this protein has been localized exclusively in colonic epithelial cells mainly along the baso-lateral domains of plasma membrane. Non-colonic epithelial tissues from 12 different organs including small intestine did not react with the anti-Mr 40,000 monoclonal antibody. The Mr 40,000 protein is present in the RPMI-4788 colon cancer cells but not in HeLa. The antibody dependent cell-mediated cytolysis by UC sera against RPMI-4788 cells was inhibited by anti-Mr 40,000 polyclonal antibody. These findings suggest that CCA-IgG and the Mr 40,000 colonic epithelial protein are involved in an autoimmune reaction and may be important in the pathogenesis of UC.
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PMID:Ulcerative colitis: specific antibodies against a colonic epithelial Mr 40,000 protein. 273 74

The antiproliferative activity of recombinant human interferon (rIFN)-beta and rIFN-gamma, alone or in combination, against a human colon cancer cell line (RPMI 4788) was examined in vitro and in nude mice. rIFN-beta and rIFN-gamma interacted synergistically in vitro. In experimental pulmonary metastasis and intraabdominal carcinomatosis in nude mice, rIFN-beta and rIFN-gamma were administered iv and ip, respectively, alone or in combination, for 10 consecutive days beginning 2 days after RPMI 4788 cells were inoculated. In both models, rIFN-beta and rIFN-gamma alone had significant antitumor effects compared with the saline-control group. Combined administration of rIFN-beta and rIFN-gamma resulted in marked antitumor effects. In the pulmonary metastasis model, there were no pulmonary metastatic nodules in the group treated with the combination of rIFN-beta and rIFN-gamma (P less than 0.001), while there were 324.6 +/- 83.1 (mean +/- SD) nodules in the control group. In the intraabdominal carcinomatosis model, the mean survival time was 114.0 +/- 8.2 days (P less than 0.01) for the combination therapy group, but only 41.8 +/- 5.6 days for the control group. These results suggest that combined treatment with rIFN-beta and rIFN-gamma might be a promising therapy for pulmonary metastasis and intraabdominal carcinomatosis of human cancers.
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PMID:Antitumor effect of recombinant human interferon-beta and interferon-gamma in combination against human colon cancer cell line in vitro and in nude mice. 312 61

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

The development of useful therapy for intraabdominal carcinomatosis originating from gastrointestinal cancer is an important theme in cancer therapy. We developed recently an experimental model of intraabdominal carcinomatosis in nude mice by intraperitoneal transplantation of human colon cancer cells (RPMI 4788). Using this model, we investigated the antitumor effects of recombinant human interferon (rIFN)-beta and rIFN-gamma administered singly or in combination. Treatment was initiated 2 days after CD-1 nude mice were inoculated intraperitoneally with 5 X 10(6) RPMI 4788 cells. Intraperitoneal administration for 10 consecutive days of either rIFN-beta (2.5 X 10(5) IU/mouse/day) or rIFN-gamma (2.5 X 10(5) JRU/mouse/day) resulted in a significant prolongation of survival compared with the saline control group [survival in the control: 41.8 +/- 5.6 days (mean +/- SD)]. Combined administration of rIFN-beta and rIFN-gamma for 10 days yielded a marked synergistic effect on the prolongation of survival (114.0 +/- 8.2 days). However, combined administration of rIFN-beta and rIFN-gamma in a single dose equal to the total dose given fractionally over 10 days did not yield a synergistic effect. These results suggest that daily administration of rIFN-beta and rIFN-gamma combined may provide a highly potent antitumor effect against human peritoneal carcinomatosis.
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PMID:Antitumor effect of combined intraperitoneal administration of human recombinant interferon-beta and interferon-gamma against intraabdominal carcinomatosis in nude mice. 313 27


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