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

Human recombinant interferon-alpha A/D (IFN-alpha A/D) is known to be as active on murine cells as on human cells. We studied the antitumor effect of pure IFN-alpha A/D on Meth-A sarcoma cells in vivo. When administered systemically (intraperitoneally), IFN-alpha A/D (total dosage: 7 X 10(5) units/mouse) was only marginally but significantly (p less than 0.05) effective in reducing the growth of Meth-A sarcoma cells transplanted subcutaneously into syngeneic BALB/c mice. By lesional (intra-tumor) administration (total dosage: 5 X 10(4) to 5 X 10(5) units/mouse), however, IFN-alpha A/D strongly inhibited the growth of Meth-A sarcoma cells and even led to a complete regression of tumor growth and subsequent immunity to Meth-A sarcoma cells in the host animals when treatment was started early after transplantation and at a high dose. Indomethacin or cyclophosphamide administered intraperitoneally at a dose at which, although not directly effective against tumor growth, both were expected to stimulate the host immune system by inhibiting suppressor macrophage function or suppressor T cells, respectively, showed neither enhancing nor suppressing effect on the above mentioned strong antitumor effect of locally administered IFN-alpha A/D.
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PMID:[Antitumor effect of human recombinant interferon-alpha A/D in mice(I): Comparison between systemic and lesional treatment of meth-A sarcoma in BALB/c mice]. 400 83

Partially purified mouse interferon type I (Mu IFN-beta), crude mouse interferon type II (Mu IFN-gamma) serum, and the interferon inducer polyinosinic acid-polycytidylic acid (poly I:C) were evaluated for their effects on the growth of spontaneously occurring mammary carcinomas in BALB/c mice. As soon as their tumors had reached a palpable size (diameter: 3-5 mm), the mice received three ip injections of Mu IFN-beta, Mu IFN-gamma, or poly I:C per week for 6 weeks. A significant (fourfold to fivefold) reduction in tumor size was achieved with Mu IFN-beta (at 10(6) U/mouse), Mu IFN-gamma (at 10(3) U/mouse), and poly I:C (at 1 mg/mouse). A similar reduction in tumor size was noted when the mice were treated with cyclophosphamide (2.5 mg/mouse, three ip injections per wk for 6 wk). Treatment with Mu IFN-beta combined with Mu IFN-gamma resulted in a greater tumor growth-inhibitory effect than treatment with either Mu IFN-beta or Mu IFN-gamma alone. In addition to inhibiting the growth of primary tumors, interferon also reduced the incidence of lung metastases. However, complete tumor regression was not observed in any mouse while under interferon therapy.
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PMID:Inhibitory effect of interferon on the growth of spontaneous mammary tumors in mice. 618 Feb 10

The presence of 4 human malignant tumors (1 breast, 1 lung, and 2 colon carcinomas) growing subcutaneously as heterotransplants in nude mice did not significantly affect the body weights of adult animals until the tumors reached very large dimensions (tumor wt greater than 15% of the body wt). However, a colon carcinoma (HT 29) induced a cessation of the natural rate of body weight increase when it grew in young adults (animals weighing approximately equal to 25 g which will gain 6 g or approximately equal to 25% body wt in 1 mo). Calorie restriction at all the levels tested (8, 6, 4, and 2 g/day/mouse) with standard pelletized mouse food produced both weight loss in the animals (with and without tumor) and a lowering of the growth rate of all the 4 tumors tested growing at a subcutaneous site and/or under the kidney capsule. Each tumor responded differently to the calorie restriction. The 4 tumors tested grew equally in both male and female nude mice. Young animals weighing 20 g inoculated with a fifth tumor (MeWo melanoma) exhibited tumor growth inhibition proportional to restriction of calorie intake. Their survival, however, did not improve.
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PMID:Calorie restriction: effect on growth of human tumors heterotransplanted in nude mice. 627 89

In order to avoid the complex dual effects of estrogen and antiestrogen, the attempt was made to establish the tumor lines in which estrogens show either stimulatory or inhibitory property in terms of the tumor growth. The administration of estrogen to host mice bearing one of the mouse Leydig cell tumor lines, called T 124958-R, resulted in marked enhancement of the tumor growth even at pharmacological levels of estrogen. On the other hand, estrogenization of host mice almost completely inhibited the growth of the other tumor line (T 22137) without detectable stimulatory effects. The physiocochemical properties of the cytosol estrogen receptor in both sublines were found to be similar in relation to the affinity toward ligands, steroid specificity, sedimentation profile, and the dissociation rate kinetics. Using these tumor lines, the action mechanism of tamoxifen on the tumor growth was examined. Daily administration of this compound (30 micrograms/mouse) led to enhanced tumor growth in T 124958-R, while the growth of T 22137 was inhibited by the same procedure. In the combination experiments, tamoxifen was found to be unable to antagonize estrogen-induced enhancement or inhibition of the growth in these tumors. In addition, both tumors contained similar levels of the antiestrogen binding sites. These results suggest that tamoxifen modulated the tumor growth through its estrogenic potency.
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PMID:Effects of tamoxifen on estrogen-induced enhancement or inhibition of tumor growth in mouse Leydig cell tumor lines. 646 99

We studied the effect of human leukocyte interferon (HuIFN-alpha) on a human osteosarcoma (OS-OH) transplanted and passed serially in athymic mice. The growth of OS-OH was strikingly inhibited by HuIFN-alpha (50,000 IU/mouse), regardless of whether the interferon treatment was initiated 24 hr after tumor inoculation or 2 weeks later, when tumors had grown to an appreciable size (4-6 mm). The antitumor effect of HuIFN-alpha was found to be dose-dependent and a daily administration of HuIFN-alpha (50,000 IU/mouse) all but completely arrested the tumor growth.
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PMID:Antitumor effect of human leukocyte interferon on human osteosarcoma transplanted into nude mice. 658 Jan 70

Recent findings that OK-432 induces IFN gamma both in vivo and in vitro prompted us to examine the host-mediated antitumor effects of OK-432 previously observed, such as activation of cytotoxic macrophages and augmentation of NK cell activity, through the action of induced IFN. By using partially purified IFN gamma produced in vitro with mouse spleen cells in the presence of OK-432, antitumor effects were examined against Meth-A cells both in vivo and in vitro. Repeated intratumoral injections of IFN gamma (300 U/mouse) resulted in 75% inhibition of tumor growth. In vitro studies also showed that 50 U/ml was enough to inhibit the growth of Meth-A cells. Augmentation of NK cell activity was found both in vivo by a single i.p. injection of 200 U/mouse, and in vitro, with as low a concentration as 5 U/ml. When macrophages obtained from mice after i.p. injection of thioglycolate medium were treated in vitro with OK-432 induced IFN gamma, 20 U/ml was shown to activate the cytotoxic effect of M phi on Meth-A cells. All of the experiments were conducted with a positive control of purified mouse IFN-alpha/beta. With antitumor and cell activating effects compared in units, OK-432 induced IFN gamma was almost 10 times or more as active as IFN alpha/beta.
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PMID:[Antitumor effect of OK-432 (1)--antitumor effect of OK-432 induced interferon-gamma (IFN gamma)]. 682 Aug 88

C3H/He mice bearing a mammary carcinoma, MM2, were treated by systemic hyperthermia with microwave irradiation (2450 MHz). An output of 30 watts of microwaves for 5 min at a distance of 20 cm from the animal raised and maintained the rectal temperature of mice to higher than 42 degrees C for 2.2 min and higher than 40 degrees C for 10.2 min. The mice were inoculated i. p. with MM2 tumor cells (2 X 10(6) cells/mouse), and then they were exposed to hyperthermia every day; 10 watts for 2, 4, or 6 min, or 20 watts for 2, 4, 6 min. The control mice receiving no irradiation and the mice treated with irradiation of 10 watts for 2 min or 20 watts for 2 min died within 21-23 days. Whereas, 40 percent of the mice treated with microwave irradiation of 10 watts for 4 or 6 min, or 20 watts for 4 or 6 min survived longer than 30 days. The 6 mice, which survived longer than 120 days, were challenged by reinoculation with MM2 tumor cells (2 X 10(6)cells/mouse). All the mice but one survived longer than 30 days with no accumulation of ascites. These experimental data suggest that the systemic hyperthermia with microwave irradiation (24 50 MHz) might suppress the tumor growth in vivo.
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PMID:[Experimental study on the anti-tumor effect of microwaves]. 687 Mar 4

Preinjection of a low dose of cyclophosphamide (Cy) (500 microgram/mouse) either delayed or inhibited tumor appearance following the inoculation of transplantable 3-methylcholanthrene-induced fibrosarcomas in inbred male C3H/HeJ mice. This dose of Cy decreased the spleen weight by 13% and the total spleen cell count by 23%. However, the same dose could potentiate the footpad swelling reaction (FPSR) measured against Staphylococcus aureus antigen. Splenic lymphocytes from Cy-treated animals showed increased blastogenic response against phytohemagglutinin-M and bacterial lipopolysaccharide. Thus 500 micrograms Cy/animal may have depleted suppressor cell populations leading to: a) an increase in FPSR, b) increased blastogenic transformation of lymphocytes, and c) tumor growth inhibition.
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PMID:Low-dose cyclophosphamide inhibition of transplantable fibrosarcoma growth by augmentation of the host immune response. 694 15

Experiments on mice with Ehrlich's ascites carcinoma were made to explore absorption, intertissue distribution and excretion of 3H-pyridoxine upon enteral and parenteral administration of labeled vitamin in a dose of 0.5 microgram per mouse. The rate of 3H-pyridoxine penetration to the blood flow of the tumor-bearing animals was not different from that in the controls. This may be viewed as the absence of abnormalities in vitamin absorption in the gastrointestinal tract. As the tumorous process develops, there takes place a progressive binding of the labeled vitamin in the tissues: in the muscle, by 17%, in the liver, by 32%, in the brain, by 42%, and in the heart, by 54%. Excretion of radioactive metabolites with the urine decreases. In the tumorous cells, the concentration of the labeled vitamin by the 10th day of the tumor growth increases 1,5-fold as compared to that seen within the initial observation period. Additional administration of pyridoxine (100 microgram/mouse) for 8 days did not stimulate the tumor growth, while the injections of vitamin B6 in a dose of 1 mg/mouse suppressed the growth of Ehrlich's ascites carcinoma in mice by 17%.
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PMID:[Vitamin B6 metabolism in mice with Ehrlich ascites tumor]. 707 78

The antitumor effect of dicyclohexylammonium sulfate (DCHA), a potent inhibitor of spermidine synthase, was tested on BDF1 mice inoculated i.p. with P388 leukemia (1 X 10(6) cells/mouse). DCHA prolonged the survival time of mice bearing P388 leukemia at the doses of 10-100 mg/kg administered daily for 6 days. The spleen weight increased by 30% at 7 days after tumor inoculation. DCHA treatment had no effect on the tumor-induced increase in splenic weight. The spermidine concentration of the ascites tumor cells and spleens of mice bearing the tumor was lowered by the treatment, while spermine concentration hardly changed. The depletion of spermidine in the ascites tumor cells and spleens might be a cause of the suppression of tumor growth.
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PMID:Antitumor effect of dicyclohexylammonium sulfate, a potent inhibitor of spermidine synthase against P388 leukemia. 711 28


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