Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PSK, a Coriolus preparation, inhibited the growth of not only the right but also the left, non-treated tumor in a double grafted tumor system. In order to examine the role of lymph nodes and the spleen in the antitumor activity of PSK, regional (axillary and inguinal) lymph nodes and spleen were resected. Since in resected mice the antitumor activity of PSK against the right and left tumors was weakened, the regional lymph nodes and the spleen probably have a very important role in the antimetastatic effect of intratumoral administration of PSK. TIL (tumor-infiltrating lymphocytes) obtained from left and right side tumors treated with PSK were examined by Winn assay for their antitumor activity against Meth-A sarcoma in BALB/c mice. TIL from both sides clearly inhibited the growth of admixed Meth-A cells, but control TIL did not. A primary growth of Meth-A sarcoma inoculated into the right flank resulted in the generation of concomitant immunity to the growth of a second graft of the same tumor cells in the left flank. A significant inhibitory effect on the proliferation of the tumor cells inoculated secondarily was shown in mice bearing a primary right tumor that had previously been inoculated with PSK 3 times. After surgical excision of the primary tumor on day 6, daily oral administration of PSK significantly inhibited the growth of the secondary tumor inoculated on day 21, that is, PSK treatment also enhanced sinecomitant immunity. These observations suggest that presurgical intratumoral injection and postoperative oral administration of PSK are highly effective in eradicating metastatic tumors.
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PMID:Antitumor effect of PSK: role of regional lymph nodes and enhancement of concomitant and sinecomitant immunity in the mouse. 249 50

To investigate the characteristics in antitumor effects of 2-trimethylsilylethylthioethylamine(KAS-010) and its conjugate with 5-FU (KAS-011), the antitumor and immunomodulating activities of these silicon compounds were examined with various systems. Both KAS-010 and KAS-011 administered orally was found to be effective to B 16 melanoma, Meth A sarcoma and MM 46 mammary carcinoma in vivo. On the other hand, KAS-011 administered orally exhibited a marked antitumor activity against L 1210 leukemia bearing mice. Furthermore, these silicon compounds inhibited significantly metastases to the lymph nodes and lung of Lewis lung carcinoma implanted id into the right ear of BDF1 mice. Especially, KAS-011 in combination with tumor amputation resulted in a remarkable prolongation of the survival time (% ILS: 93.8%) in this antimetastatic model. The cell killing effect was mainly dependent on the exposure time of these silicon compounds in cultured KB and human lung cancer (OAT) cells. Moreover, a significant increase of delayed type hypersensitivity reaction (DTHR) to sheep red blood cell (SRBC) induced by KAS-010 was seen in old aged mice. The DTHR in B 16 melanoma and Ehrlich carcinoma bearing mice treated with KAS-010 was significantly higher than those of non-treated tumor bearing mice, indicating an enhanced cellular immunity to KAS-010 possibly resulting in a remarked antitumor effect. We also found that tumor free mice treated these silicon compounds were acquired specific tumor immunity to Meth A sarcoma and MM 46 mammary carcinoma.
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PMID:[Characteristics in antitumor effects of organic silicon related compounds]. 254 47

The potential for a recombinant human interleukin-2 (rIL-2, TGP-3) alone, in combination with cyclophosphamide, and in combination with cyclophosphamide and normal immunocompetent cells to manifest biological activity in vivo was tested using allogeneic, semi-syngeneic, and syngeneic tumor-host systems in mice. The biological activity of rIL-2 was evaluated by the inhibition of the growth of tumors and the inhibition of metastases in short-term assays and, in long-term assays, the prolongation of the survival time of mice bearing subcutaneously (s.c.) or intradermally transplanted tumors. rIL-2 was injected s.c. daily continuously for up to 40 days or intermittently two to four times into mice bearing established tumors. In the short-term assays, the dose and schedule dependence of activity of rIL-2 alone was significantly manifested against sarcoma 180 in ICR mice (allogeneic) by the regression of the tumor, and was confirmed against Meth-A fibrosarcoma in BALB/c mice (syngeneic) by retarding the growth of the tumor. When assessed using these tumor, it was found that the antitumor activity of rIL-2 was schedule-dependent: the growth of tumors was more significantly suppressed when rIL-2 was injected every day for 10 days, starting on the 7th day after tumor transplantation, than when rIL-2 was injected five times every other day or twice every 5th day, even if the total amounts of rIL-2 injected were same. The continuous injection for 10 days was considered to be a standard regimen and the daily effective doses of rIL-2 were 5, 10, and 25 micrograms/mouse. Using the standard regimen and the effective doses, the activity of rIL-2 alone was also observed against two other syngeneic tumors: Colon carcinoma 26 in BALB/c mice, by retarding the growth of the tumor, and Lewis lung carcinoma in C57BL/6 mice by reducing the formation of lung metastases. When assessed using M5076 reticulum cell sarcoma, in a long-term assay, the activity of rIL-2 alone was not manifested in C57BL/6 mice (syngeneic) even when rIL-2 was injected for a long period (20 days) but it was observed in BDF1 (semi-syngeneic) mice. On the other hand, it was found that rIL-2 was effective in combination with cyclophosphamide in prolonging the survival time of C57BL/6 mice bearing the tumor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Therapeutic efficacy of human recombinant interleukin-2 (TGP-3) alone or in combination with cyclophosphamide and immunocompetent cells in allogeneic, semi-syngeneic, and syngeneic murine tumors. 259 80

The antitumor mechanism of recombinant human interleukin-2 (rIL-2) was studied using two murine tumor systems. Meth 8 tumor cells were easily lysed in vitro by rIL-2-activated killer (AK) cells, which mainly consisted of Thy1.2+, Lyt2.2+, L3T4- T cells, and asialo GM1+ natural killer (NK) cells; on the other hand, X5563 tumor cells were only slightly lysed in vitro by AK cells under the same conditions. One of these two tumors was inoculated i.d. into C3H/HeN mice and then rIL-2 (5 X 10(4) J.U./mouse/day) was repeatedly injected s.c. For AK-sensitive Meth 8-bearing mice, rIL-2 therapy starting 1 day after tumor inoculation was more effective for the growth than the therapy starting 7 days later and the therapeutic effect was abrogated by in vivo treatment with anti-asialo-GM1 serum. In contrast, for mice bearing AK-resistant X5563 tumor cells, delayed administration starting on day 7 or later was more beneficial than earlier administration on day 1 or 4. This treatment schedule resulted in complete tumor regression in a dose-dependent manner including significant inhibition of metastases in the spleen and/or lymph nodes. These therapeutic effects of rIL-2 on X5563 were not seen in T-depleted mice with anti-mouse thymocyte serum but were found in NK-depleted mice upon treatment with anti-asialo-GM1 serum. The results of these studies showed that the growth of AK-sensitive Meth 8 tumor was inhibited by AK cells, while the growth and metastases of AK-resistant X5563 tumor was inhibited by tumor-specific T cells, which were generated after tumor development and activated by rIL-2 therapy, rather than AK cells.
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PMID:Distinct antitumor mechanisms of recombinant interleukin-2 on recombinant interleukin-2-activated killer-sensitive and -resistant murine tumors. 260 Jun 5

Antimetastatic effect of a stable prostacyclin analogue (PGI2-TEI8153) in combination use with adriamycin (ADM) was investigated. Meth A cell, which had membrane protein of 18,000 daltons specifically bound to platelets, induced platelet aggregation dose-dependently. This platelet aggregation was totally suppressed by PGI2-TEI8153. PGI2-TEI8153 also suppressed the pulmonary arrest as well as pulmonary metastasis of Meth A cells. Combined use of PGI2-TEI8153 and ADM exerted much less antimetastatic effect than that with PGI2-TEI8153 alone, indicating the counteracting effect of ADM against the PGI2-TEI8153. However, this combination use brought about additive antimetastatic effects with 2-fold reduction of pulmonary nodules compared to that of ADM alone. Consequently, even the anticancer drug itself has a negative influence on metastasis, the combined use of PGI2-TEI8153 with it is promising for the prevention of metastasis.
Invasion Metastasis 1988
PMID:Effect of combined administration of a prostacyclin analogue and adriamycin against the artificial metastasis of Meth A cell. 327 21

The effects of recombinant human interferon-alpha A/D (rIFN-alpha A/D, a subtype of recombinant human leukocyte interferon with biological activities against murine tumor cells) on the growth of murine tumors were studied. rIFN-alpha A/D significantly inhibited the growth of mouse M5076 reticulum cell sarcoma, MOPC-104E myeloma, colon carcinoma 26 and Meth A fibrosarcoma by dose-dependent fashion. rIFN-alpha A/D also inhibited the metastases and growth of Lewis lung carcinoma and showed a synergistic effect with combination of cyclophosphamide. The antitumor activity of rIFN-alpha A/D was observed by intra-muscular, intravenous, subcutaneous, intraperitoneal injections or by the injection at the site of the tumors.
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PMID:[Effects of recombinant human interferon-alpha A/D on the growth of experimental tumors in mice]. 330 69

The anti-tumor effect of immunization with heat-killed Mycobacterium tuberculosis (Tbc) and Tuberculin (PPD)-coupled syngeneic tumor cells was examined in vivo. Three tumor cell lines were employed. Immunization of Tbc-primed BALB/c mice with PPD-coupled syngeneic Meth-A tumor cells displayed a potent anti-tumor effect on viable Meth-A cells inoculated subcutaneously. Neither PPD-coupled LLC (Lewis Lung Carcinoma) cells nor sonicated PPD-coupled Meth-A cells were capable of immunizing these mice. PPD-coupled syngeneic whole tumor cells were indispensable for induction of this tumor-specific resistance. Immunization of Tbc-primed C3H/He mice with PPD-coupled syngeneic MH134 tumor cells did not elicit anti-tumor activity against MH134, but additional pretreatment of mice with cyclophosphamide brought on an anti-tumor effect. Antimetastatic reactivity was investigated in C57BL/6 mice bearing LLC, with a reduction in metastases noted. This antimetastatic effect was observed even when the mice were immunized with PPD-coupled LLC cells three days after removal of the initial tumor. Immunization with Tbc and PPD-coupled Meth-A cells together with intraperitoneal administration of murine or rat interleukin 2 (IL 2) further augmented anti-Meth-A resistance. Murine IL 2 further inhibited tumor growth during the early stage, while rat IL 2 showed an anti-tumor effect throughout the course of tumor growth.
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PMID:Augmentation of anti-tumor activity by immunization with Mycobacterium tuberculosis (Tbc) and tuberculin-coupled tumor cells. 392 81

DMG, a new polysaccharide with a well-characterized structure, isolated from the culture filtrate of an actinomycetes and then degraded by acid treatment, was tested for antitumor activity on allogeneic and syngeneic tumors in mice. In the allogeneic Ehrlich solid tumor system, DMG showed antitumor activity over a wide dose range, its optimal dose being 10-100 mg/kg. The optimal time of DMG administration was 1-2 weeks after tumor inoculation, but DMG was also effective when given before tumor inoculation. DMG was effective when given ip, sc, it (intratumorally) or iv. DMG also had antitumor effects on syngeneic tumors. It rapidly inhibited the growth of MM46 mammary carcinoma, MH134 hepatoma, and Meth A fibrosarcoma, and also inhibited spontaneous pulmonary metastases of B16-BL6 melanoma. However, it had no direct cytocidal action on tumor cells in vitro. Its antitumor activity was much less in athymic nude mice and in mice immunosuppressed by whole-body X-irradiation than in normal hosts.Thus, DMG was shown to exert antitumor activity via host-mediated mechanisms. Its antitumor activity is discussed in comparison with those of other antitumor polysaccharides.
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PMID:Host-mediated antitumor effect of DMG, a degraded D-manno-D-glucan from Microellobosporia grisea culture fluid. 623

Effects of lysozyme(LY) alone and combination with various antitumor agents were examined using syngeneic tumors mainly Meth-A and MH 134 transplanted into Balb/c and C3H/He mice, respectively. The effects of LY on pulmonary metastases were also examined in BDF1 mice bearing Lewis lung carcinoma (3LL). LY inhibited the growth of Meth-A tumor and enhanced antitumor effects of mitomycin C (MMC). bleomycin (BLM) and 5-fluorouracil (5-FU), LY activated antitumor effects of MMC, BLM and 5-FU on MH 134 tumor, however, LY alone did not show any significant antitumor effect on it. The combination treatments using LY with MMC or 5-FU showed a marked inhibition on pulmonary metastases of 3LL. The pre-treatment of LY inhibited the tumor growth of Sarcoma-180 in ICR mice.
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PMID:[Experimental studies on antitumor effects of lysozyme]. 718 34

Anti-intercellular adhesion molecule-1 (anti-ICAM-1) and anti-lymphocyte-function-associated antigen-1 (anti-LFA-1) monoclonal antibodies (mAbs) were injected into mice and their effects on tumor metastasis were investigated using two murine models. Depending on the dose, the anti-ICAM-1 mAb (KAT-1) expressed both inhibitory and promoting effects on liver metastases of ICAM-1 + LFA-1 + P815 mastocytoma cells, whereas it enhanced lung metastases of the ICAM-1-LFA-1-Meth-A fibrosarcoma cells at any doses. In contrast, anti-LFA-1 mAb (KBA) showed promoting effects only on the metastases of both tumor lines. Treatment of mice with either mAb enhanced metastases of P815 mastocytoma cells in the spleen.
Invasion Metastasis 1996
PMID:Effects of anti-intercellular adhesion molecule-1 and anti-lymphocyte-function-associated antigen-1 monoclonal antibodies on the metastasis of murine tumors. 883 Jul 64


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