Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The following evidence from our research has implicated the macrophage as an important effector cell in pyran and/or C. parvum induced host resistance to solid tumors: (1) Increased infiltration of tumors with histiocytes following systemic treatment with pyran;17 (2) activated peritoneal macrophages with tumoricidal activity have been recovered from the peritoneal cavity of normal or tumor bearing mice treated with pyran or C. parvum;17 (3) activated peritoneal macrophages mixed with tumor cells in vitro and transplanted into syngeneic recipients inhibited tumor growth; (4) trypan blue, an inhibitor of macrophage function, prevent C. parvum induced regression of methylcholanthrene tumors; and (5) direct intralesional injection of activated macrophages into the MCA 2182 tumor inhibited tumor growth and increased the MST.
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PMID:Macrophage mediated tumor cell cytotoxicity. 107 61

Eight patients with epithelial ovarian carcinoma persisting after chemotherapy, selected for having a residual tumor no larger than 1 cm in diameter, were treated intra-peritoneally (i.p.) with recombinant interferon-gamma twice weekly for 3 months. Toxicity consisted of fever and malaise in all patients and a transient rise in hepatic enzyme levels in 3 patients. The cytotoxic function of peripheral blood and peritoneal tumor-associated lymphocytes (TAL) and macrophages (TAM), was studied using cell lines as targets. I.p. IFN-gamma augmented the cytotoxic activity of lymphocytes and mononuclear phagocytes: stimulation was more marked and more frequently observed with TAL and occasionally TAM than with blood effectors, suggesting preferential modulation at the site of tumor growth and IFN administration. Surgical laparotomy revealed that 1 patient had a complete response, 2 a partial response and 2 had stable disease, while 3 patients had progressive disease. In this small series of patients there was no obvious, strict correlation between immunomodulation by IFN-gamma and clinical response. These results indicate that, in contrast to its lack of activity in advanced ovarian carcinoma, IFN-gamma has definite immunomodulatory and antitumor activity in the presence of limited tumor burden.
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PMID:Anti-tumor and immunomodulatory activity of intraperitoneal IFN-gamma in ovarian carcinoma patients with minimal residual tumor after chemotherapy. 156 43

The effects of three hormonal agents with a different mechanism of action (tamoxifen [TAM], medroxyprogesterone acetate [MPA] and estradiol [E2]) on tumor growth, differentiation and oncogene expression were evaluated using the estrogen-receptor positive human breast carcinoma cell line MCF-7 transplanted into nude mice. In MCF-7 tumors treated with E2, tumor incidence, mean weight of tumors, 3H-thymidine labelling index, differentiation antigen HMFGM (human milk-fat globule membrane) and ras p21, c-myc, neu oncogene products, the level was significantly increased. On the other hand MPA suppressed all of them. TAM increased the level of c-myc expression and HMFGM antigen, but suppressed the others. This evidence indicates that E2 induces both proliferation and differentiation of MCF-7 tumor cells. MPA suppresses both proliferation and differentiation, and TAM induces differentiation and suppresses proliferation.
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PMID:Effects of tamoxifen, medroxyprogesterone acetate and estradiol on tumor growth and oncogene expression in MCF-7 breast cancer cell line transplanted into nude mice. 183 73

Balb/c mice bearing a methylcholanthrene-induced fibrosarcoma were used to compare the activation levels of tumor-associated and peritoneal macrophages. Two stages of tumor growth were examined, namely "small" and "large" tumors, with average diameters of 10 and 30 mm, respectively. The activation state, determined by measurement of both phagocytic index and beta-glucuronidase content, was found to be markedly higher in tumor-associated macrophages than in their peritoneal counterparts and it was, in addition, independent of tumor progression. The percentage of tumor-associated macrophages, which were detected on the basis of Fc receptor expression, remained constant in the growing neoplasm, at approximately 23% of total cell population. None of these parameters were affected by inoculation with an immunopotentiating dose of heat-killed Candida albicans which, on the other hand, seemed not to alter the course of the tumor. These data suggest that within the tumor microenvironment macrophages would somehow be maintained at a constant proportion and at a highly activated state, while outside the tumor they would be at a lower activation level. Our results also suggest that TAM would not possess antitumor activity in vivo, although we have found this activity in vitro.
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PMID:Comparative activation states of tumor-associated and peritoneal macrophages from mice bearing an induced fibrosarcoma. 209 3

The phenotypes of the affector and effector cell populations involved during the induction of permanent tumor regression by combined therapy using cyclophosphamide (CY) and immune spleen cells were identified. Permanent tumor regression was dependent on the presence of Thyl+ Lyt-2+ lymphocytes in the immune spleen cell population that was injected i.v. 2-4 h after an intraperitoneal injection of CY (240 mg/kg) into C57BL/6J mice bearing 1.0-1.5 g. MCA/76-9 or MCA/76-64 sarcomas. Histological evaluation after the combined treatment indicated an intense influx of putative lymphocytes 6-10 days after the combined treatment, over and above the inflammatory response involving macrophages and neutrophils induced by CY treatment alone. These infiltrating cells were shown to be T lymphocytes, most of them having the Lyt-1 and Lyt-2 antigens on their cell membrane. Isolated MCA/76-9 or 76-64 tumor-associated cells (TAC), lymphocytes (TAL) and macrophages (TAM) inhibited MCA/76-9 or 76-64 tumor growth respectively in a Winn test in an immunologically specific manner, having no effect on the growth of the B6 sarcoma cells, MCA/76-45 and 77-23. The tumor-free mice from the Winn test were not resistant to a subsequent challenge inoculum of either MCA/76-9 or 76-64 cells. Isolated TAC were usually non-specifically cytotoxic in vitro, while TAL and TAM showed some degree of specificity. The overall data indicated that the ultimate rejection of those tumor cells remaining after the direct anti-tumor action of CY had been dissipated was probably mediated by the combined action of TAL and TAM.
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PMID:Phenotypes associated with tumor rejection mediated by cyclophosphamide and syngeneic tumor-sensitized T lymphocytes: potential mechanisms of action. 660 93

Tamoxifen is the endocrine treatment of choice for breast cancer. However, resistance to therapy and patient relapse inevitably occurs. In future treatment schedules, interferons could be administered with tamoxifen, in an attempt to prevent disease recurrence. Human recombinant interferon-beta SER (rIFN-beta SER) inhibited the growth in vitro of the estrogen receptor (ER) positive breast cancer cell line MCF-7 and the ER negative breast cancer cell line MDA-MB-231. This inhibitory effect was achieved at doses of 50 U/ml and above. The growth of MCF-7 tumors in estradiol-stimulated athymic mice was greatly inhibited by high dose rIFN-beta SER treatment (10(6)U/day). In spite of the impressive antitumor effects upon MCF-7 tumors, rIFN-beta SER had no effect upon ER levels within the tumors at either the RNA or protein level, as measured by Northern blotting and ER-EIA respectively. High dose rIFN-beta SER (10(6)U/day) did result in some inhibition in the growth in vivo of the tamoxifen-stimulated MCF-7 variant MCF-7 TAM, although not to the same extent as was observed with the estradiol-stimulated MCF-7 tumors. rIFN-beta SER was also administered to animals bearing MCF-7 tumors and treated with estradiol and tamoxifen. In the animals undergoing high dose therapy (10(6)U/day), tumor growth was completely suppressed. Furthermore, tumor growth continued to be suppressed in those animals in which the rIFN-beta SER therapy was halted and the tamoxifen capsule removed. No tumors were observed in spite of the environment of estradiol stimulation. Thus, the combination of interferon and tamoxifen was totally growth suppressive for MCF-7 xenografts in nude mice.
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PMID:Human recombinant interferon-beta SER and tamoxifen: growth suppressive effects for the human breast carcinoma MCF-7 grown in the athymic mouse. 834 46

The influence of estrogens and tamoxifen on estrogen receptor (ER)-positive human breast cancer (MCF-7) cells transplanted into athymic nude mice was investigated. The mice were divided into the following three groups: (1) an E2 group with mice receiving 17 beta-estradiol dipropionate; (2) a TAM group with mice receiving tamoxifen; (3) a control group with mice given no hormone. (1) Tumor growth was significantly increased in the E2 group, but significantly decreased in the TAM group compared to control; (2) the tumor contents of insulin-like growth factor-I (IGF-I) and the rate of IGF-I-positive cells were significantly lower in the E2 group, but significantly higher in the TAM groups compared to control; (3) the IGF-I-positive cell rates were in significant inverse correlation with the [3H]thymidine-labeled cell rates in the E2, TAM and control groups. Thus, the tumor contents of IGF-I and the rate of IGF-I-positive cells were inversely correlated to the tumor growth and the [3H]thymidine-labeled cell rate in this in vivo study, although IGF-I is known to be a mitogen for breast cancer cells in vitro. Further studies are necessary to answer the questions as to the in vivo roles of immunoreactive IGF-I in ER-positive breast cancer.
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PMID:Influence of hormones on tumor growth, cell kinetics, estrogen receptor and insulin-like growth factor-I-related protein of human breast cancer (MCF-7) cells transplanted in nude mice. 847 69

The therapeutic results of liver transplantation for primary liver cancer have not been satisfactory. The high rate of recurrence appears to be due to the inadequate care taken in selecting the most appropriate candidates for orthotopic liver transplantation (OLT), the presence of circulating hepatocellular carcinoma (HCC) cells and micrometastases at the time of liver transplantation, and the tumor growth-promoting effects of immunosuppressive agents. We believe that HCC patients must be carefully staged in order to identify those most suitable for OLT. We therefore induced HCC in pure-strain rats by the oral administration of diethylnitrosamine (DEN) and studied the outcomes of liver transplantation at various time points (70, 120, and 134 days) after the initiation of carcinogenesis. The mean survival time (MST +/- SD) of the non-OLT control group (N = 14) was 18.2 +/- 5 days after Day 120. The survival time of the four rats in the OLT Day 120 group was 81.3 +/- 20.6 days after transplantation. One rat showing full weight recovery soon after transplantation survived for 97 days after transplantation and then succumbed to recurrence. The survival time of the four rats in the OLT Day 134 group was 7.3 +/- 5.0 days after transplantation. The survival time of the three rats in the OLT Day 70 group was 145.3 +/- 70.0 days after transplantation, with a maximum survival of 221 days until death. Significantly prolonged survival, as compared with that in the non-OLT group, was observed in the OLT Day 70 and OLT Day 120 groups (p < 0.01), while there was no significant prolongation in the OLT Day 134 group (NS). The timing of liver transplantation is a very important factor. Preoperative assessment of factors potentially affecting recurrence in HCC patients is imperative for selecting the most appropriate candidates for OLT. Careful selection of candidates for OLT should always be considered the key to successful liver transplantation (i.e., long-term survival) for patients with liver cancer.
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PMID:The outcome of liver transplantation at various times (70, 120, and 134 days) after the initiation of carcinogenesis in rats. 961 50

MST-16, a derivative of bis(2,6-dioxopiperazine), is a newly developed anticancer agent that is potentially effective in combination with anthracyclines. It has a structural similarity to ICRF-187. The effects of MST-16 and its active form, ICRF-154, on the cytotoxic activities of six anthracyclines were investigated both in vitro and in vivo. Adriamycin (ADM), therarubicin (THP) and ME2303 (ME) showed synergistic cytotoxicity against colon 26 cells, when combined with MST-16. Epirubicin (EPI) and menogaril (TUT-7) and daunomycin (DM) all had a combination index of less than 1.0 only in the lower fraction affected range and, so there were probably no synergistic interactions between these drugs and MST-16. In colon 26 tumor-bearing mice, a significant delay in tumor growth was noted in the mice treated with ADM (7.5 mg/kg) and MST-16 (750 mg/kg) compared with mice given either drug alone. Similarly, tumor growth in mice treated with THP (10 mg/kg) or ME (10 mg/kg) with MST-16 (750 mg/kg) was significantly delayed. To elucidate the mechanism of synergy between these anthracyclines and MST-16, the concentration of anthracyclines in the treated cells was measured by flow cytometry. No increased intracellular accumulation of ADM. THP or ME was evident even when combined with MST-16. Cell cycle analysis revealed that MST-16 enhanced the accumulation of cells in G2M induced by ADM, THP and ME 1.6, 1.4, and 1.5 times, respectively. We thus conclude that the administration of ADM, THP and ME combined with MST-16 is synergistic and that the mechanism may not include an increase in the intracellular drug uptake but rather an increase in G2M accumulation.
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PMID:MST-16, a novel derivative of bis(2,6-dioxopiperazine), synergistically enhances the antitumor effects of anthracyclines. 968 54

MST-16 [4,4-1,2-(ethanediyl)bis(1-isobutoxycarbonyl-oxy-methyl-2,6-pipera zinedione)], recently approved as an oral anticancer drug for clinical use in Japan, was evaluated as a chemotherapeutic agent in combination with doxorubicin (DOX) in vitro and in vivo. Cytotoxicity was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and murine Colon 26 and human KATO III adenocarcinoma cells were used. The combination index derived from these cytotoxic values indicated a synergistic interaction between DOX and MST-16 or its active metabolite, ICRF-154 (1,1'-ethylenedi-3,5-dioxopiperazine). A maximal tolerated dose of DOX administered to female BALB/c mice bearing a solid Colon 26 tumor resulted in severe body weight loss and diarrhea, but a limited tumor growth delay (1.8 days). However, when combined with an oral dose of MST-16, DOX-induced body weight loss and diarrhea were significantly ameliorated, and an additive tumor growth delay (8.7 days) was obtained. The LD50 of DOX administered i.p. to control female BALB/c mice increased more than 1.5-fold when combined with MST-16. Thus, MST-16 ameliorates DOX-induced acute toxicity while maintaining antitumor efficacy. These results indicate that MST-16 may be effective chemotherapy for cancer patients when combined with DOX.
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PMID:MST-16, a novel bis-dioxopiperazine anticancer agent, ameliorates doxorubicin-induced acute toxicity while maintaining antitumor efficacy. 1063 73


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