Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using high voltage pulse (initial electric field strength 3kV/cm, duration 4 msec, applied energy 14.9 joule) as a local load, and concentration dependent anticancer drugs such as peplomycin (PEP) 20 mg/kg, cyclophosphamide (CPA) 100 mg/kg, mitomycin C (MMC) 3 mg/kg and cisplatin (CDDP) 5 mg/kg administrated intraperitoneally, the effects on the suppression of primary lesions and on formation of pulmonary metastasis in the spontaneous pulmonary metastatic system of Lewis lung carcinoma were investigated. Though only CPA among single administrated anticancer drugs showed a suppressive effect against tumor growth, remarkable reduction in the size of primary lesions was obtained with a combination of high voltage pulse and an anticancer drug, regardless of various kinds of drug. A maximal ratio of size before and after treatment was 0.05 in PEP, 0.2 in CPA, 0.38 in MMC and 0.14 in CDDP. A combination of PEP or CPA with high voltage pulse had a particularly good effect, reducing the volume of the primary tumor after treatment less than levels before treatment throughout 2 weeks. The use of high voltage pulse alone did not affect any growth kinetics of the primary lesion. The number of pulmonary metastatic nodules was significantly reduced only by CPA among various kinds of single administrated drugs, whereas it was reduced by all treatments with a combination of high voltage pulse and each anticancer drug. The use of high voltage pulse alone did not result in any increase of the number of pulmonary metastatic nodules.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anticancer effect of high voltage pulses combined with concentration dependent anticancer drugs on Lewis lung carcinoma, in vivo]. 227 15

Cytochalasin B (CB), at 100 or at 10 mg/kg single dose s.c. in carboxymethyl-cellulose (2%)/Tween-20 (1%) 24 h after s.c. challenge of B6D2F1 mice with trocar implants of B16F10 tumor s.c., delayed the appearance of measurable tumor nodules by 157 and 93%, respectively, and extended host survival by 65 and 26%. Tumor growth was also delayed when CB treatment was given 1 day after the appearance of palpable tumor nodules. By in vivo bioassay, in vitro cloning, and dye exclusion measurements, solid tumor nodules treated in vivo with CB at either 100 or 10 mg/kg showed the same viability and tumorigenicity as did vehicle-treated nodules 4 and 6 days after drug treatment, at which time growth inhibition was still apparent. This indicates that growth inhibition by CB is not dependent on a gross cytotoxic effect. CD2F1 mice challenged s.c. with Madison 109 lung carcinoma cells and treated with CB s.c. at 100 or 150 mg/kg 24 h later showed a 66% delay in the median day of tumor nodule appearance. When administered under these conditions or at the time of nodule appearance. CB markedly inhibited the rate of tumor growth, prevented tumor invasion at day 23, extended life span by 23%, and significantly inhibited spontaneous lung metastases measured 28 days after tumor challenge. Maximum tolerated doses of CB administered i.p., s.c., or i.v. in suspension or in solution are defined. These results delineate the conditions under which CB can be tested for in vivo biological activities and establish that this microfilament-active natural product in a single-agent protocol inhibits local tumor growth and extends survival in B16F10 melanoma and Madison 109 lung carcinoma, and, in the latter model, inhibits invasion and spontaneous lung metastases by mechanisms that do not appear to depend on cytotoxicity. This work on formulation, tolerated doses in vivo, and localized peritumoral effects of CB now permits evaluation of systemic antitumor effects of cytochalasin B as a single agent. It also permits chemotherapy studies using CB as a potential amplifier of the activity of other antitumor agents in vivo.
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PMID:Effects of cytochalasin B in culture and in vivo on murine Madison 109 lung carcinoma and on B16 melanoma. 230 8

The antitumor activity of the polar solvent N-methylformamide (NMF) was evaluated on three lines derived from the Lewis lung carcinoma (3LL), endowed with different metastatic potential. Two administration schedules were tested, these being repeated regimens of NMF (200 mg/kg per dose) for 12 consecutive days, starting 24 h or 6-10 days after tumor implantation (early or late treatment, respectively). The results of the present work can be summarized as follows: (1) NMF regimens did not greatly affect tumor growth behavior of 3LL lines; conversely, they markedly influenced their spontaneous colonizing ability in the lungs, either by delaying early metastatic spread or by reducing the number and size of pulmonary metastases already implanted. (2) A significant increase of NK cell activity during and after early treatment with NMF was observed in the more-metastasizing lines, thus suggesting the possibility of an immunomodulating effect of NMF.
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PMID:N-methylformamide affects spontaneous metastases of 3LL lines and increases natural killer activity of tumor-bearing mice. 231 55

The availability of lectin-resistant cell lines with altered carbohydrate moieties in cell surface glycoproteins and glycolipids has greatly facilitated study of the involvement of cellular glycoconjugates in tumor growth and metastasis. We present here a new animal model for metastasis study based on mouse Lewis lung carcinoma LL2 in vitro cell line. From this line, five lectin-resistant variant sublines were selected with the following lectins: wheat germ agglutinin (WGAR), Ricinus communis agglutinin II (RCA IIR) and Aleuria aurantia agglutinin (AAAR). The correlation of the lectin resistance with their in vitro and in vivo growth properties, and especially lung colonizing ability, were investigated. Three WGAR variants with well-preserved tumorigenicity revealed reduced metastatic ability, both spontaneous, after subcutaneous (s.c.) administration and experimental, after intravenous (i.v.) administration. The RCA IIR variant also possessed reduced spontaneous and experimental metastatic ability, but exhibited higher growth rate of local s.c. tumors. The AAAR variant possessed reduced spontaneous metastatic ability but its ability to colonize the lungs after i.v. administration was five-fold higher than that of the parent LL2 line, whereas its tumorigenicity remained unchanged. The relative differences among WGAR variants and parent LL2 line, concerning their experimental metastatic ability, remained similar in cyclophosphamide-modified mice to those in normal recipients.
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PMID:Lectin-resistant variants of mouse Lewis lung carcinoma cells. I. Selection and in vivo properties. 232 48

The role of prostaglandins and their synthesis inhibitors in malignant disease is undefined. The following studies were done to determine the effects of continuous intravenous prostaglandin E1 (PGE1) or a prostaglandin synthesis inhibitor, indomethacin, on tumor growth and metastasis in mice bearing Lewis lung carcinoma. Male B6D2F1 mice underwent tumor implantation in the right axilla on day 0. After 10 days of tumor growth, mice underwent intravenous (IV) catheterization and were infused with either PGE1 at 3 micrograms/kg/minute (PG-LOW), PGE1 at 6 micrograms/kg/minute (PG-HIGH), indomethacin (INDO) at 1 microgram/kg/minute, or normal saline (NS). After 10 days of infusion, tumor volume, tumor weight, and the number of metastases greater than 2 mm in diameter were significantly decreased, and tumor doubling time was significantly prolonged in the PG-HIGH group compared to NS controls. None of the other experimental groups showed differences in these parameters. A second experiment with a similar experimental design was done infusing PGE1 at 6 micrograms/kg/minute and at 12 micrograms/kg/minute to determine the maximum dose response of IV PGE1. Again a decrease in tumor volume, tumor weight, and metastatic rates were identified when compared to saline control, but there were no significant difference between the two doses of PGE1.
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PMID:Inhibition of tumor growth and metastasis by chronic intravenous infusion of prostaglandin E1. 236 3

BMY-25067, N-7[2-(4-nitrophenyldithio)-ethyl] mitomycin C was selected from a number of disulfide derivatives of the highly active compound RR150, N-7(thioethyl) mitomycin C for further study. BMY-25067 had tumor inhibitory effects equivalent to mitomycin C (MMC) against ascitic P388 and L1210 leukemias and M109 lung carcinoma in mice with i.p. treatment. However, it demonstrated superior activity against B16 melanoma with a high percentage of cures when both tumors and drug were given i.p. Additionally, in separate tests against B16 melanoma implanted s.c. with treatment i.v., BMY-25067 was also consistently superior to MMC. This activity was observed when therapy was initiated either one day post-tumor implant or delayed until the ninth day post-tumor implant. Slight activity was seen against a line of L1210 partially resistant to MMC and none against a line of P388 completely resistant to MMC. Against s.c. M109, BMY-25067 inhibited tumor growth but did not prolong survival with the treatment schedule used. At their respective maximum non-lethal doses in mice, BMY-25067 was less neutropenic than MMC. This was confirmed in ferrets which were also examined for the compound's effects on platelets. BMY-25067 appeared to have much less effect on platelets than MMC; the nadir for BMY-25067 was 3.8 x 10(5) platelets/cmm compared to 7 x 10(4) platelets/cmm for MMC when the drugs were compared at a dose ratio of 2:1, BMY-25067:MMC (determined to represent their relative potencies). This initial evidence of superior antitumor effectiveness particularly to a solid tumor separated from site of treatment and reduced hematologic toxicity suggest that BMY-25067 may be a worthwhile candidate for clinical trial.
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PMID:Antitumor activity and toxicity in animals of N-7[2-(4-nitrophenyldithio) ethyl] mitomycin C (BMY-25067). 238 13

We investigated the synergistic anti-tumor effects of K-18 (conjugate of human gamma-globulin and melphalan) and concomitantly administered hyperthermia on Lewis lung carcinoma in mice. The antitumor effect of a subeffective dose of K-18 or an equivalent dose of melphalan alone was enhanced by local hyperthermia. K-18 administration demonstrated a greater potentiation for inhibition of tumor growth than that of melphalan alone. Local hyperthermia plus K-18 reduced the dose of melphalan required for tumor growth inhibition by melphalan alone. The combined application of K-18 and hyperthermia for treating cancer warrants further study.
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PMID:Synergistic effect of K-18 and concomitant hyperthermia for treatment of Lewis lung carcinoma in mice. 240 15

Cadeguomycin retarded growth of sc solid IMC carcinoma in CDF1 mice, and pulmonary metastasis of Lewis lung carcinoma in C57BL/6 mice. The antibiotic enhanced phagocytic activity of murine peritoneal macrophages and IL-1 production by P388D1 cells. Delayed type hypersensitivity was stimulated and interferon was induced by the drug. The results suggest that cadeguomycin inhibits tumor growth and metastasis in association with modification of the immune system. The cytotoxicity of arabinosylcytosine to K562 and YAC-1 cells was markedly enhanced by cadeguomycin in culture. The combined administration of arabinosylcytosine and cadeguomycin displayed potentiation in the inhibition of growth of ip-implanted P388 leukemia and metastasis of sc-implanted P388 leukemia to the regional lymph nodes. Cadeguomycin showed low toxicity for mice.
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PMID:Biological activity of cadeguomycin. Inhibition of tumor growth and metastasis, immunostimulation, and potentiation of 1-beta-D-arabinofuranosylcytosine. 241 Mar 97

The antitumor effect of combination immunochemotherapy with Ge-132 and antitumor agent was studied using C57BL/6 mice bearing Lewis lung carcinoma (3LL). Ge-132 was administered orally at a daily dose of 100 mg/kg. Antitumor agents were administered intraperitoneally once a week. Initially, the effect of combination immunochemotherapy with Ge-132 and 5-fluorouracil (5-FU) was studied on 3LL local tumor growth, pulmonary metastases, survival, delayed type hypersensitivity (DTH) and body weight in tumor-bearing mice, and the following results were obtained: Inhibition of tumor growth in the combined group; Enhanced anti-metastatic effect; Prolonged survival time, and; Recovery of loss of both DTH and body weight as a result of combination therapy. These antitumor effects were also obtained by adoptive transfer of Ge-132-stimulated splenocytes in 5-FU-treated mice bearing 3LL. These results therefore suggest that the effects of Ge-132 were expressed through modification of immunocytes. Furthermore, Ge-132 enhanced the antitumor activity of bleomycin as well as that of 5-FU. These facts suggested that Ge-132 is useful for antitumor combination immunochemotherapy.
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PMID:[Effect of combination immunochemotherapy with an organogermanium compound, Ge-132, and antitumor agents on C57BL/6 mice bearing Lewis lung carcinoma (3LL)]. 242 32

A combination of heparin and cortisone acetate significantly inhibited both embryonic angiogenesis and the tumor growth of Lewis lung carcinoma (3LL) transplanted into C57BL/6 mice, although each of these agents used alone affected neither angiogenesis nor tumor growth. On the other hand, this combination neither decreased the number of metastatic foci in the lung nor prolonged the survival time of mice with 3LL. All tumor-bearing mice died of hemothorax due to pulmonary metastases. Cortisone acetate by itself increased metastasis, and addition of heparin did not affect accelerated metastasis. Because an antiangiogenic activity appears independent of metastasis acceleration by cortisone acetate, the use of steroids other than cortisone acetate having no metastasis-promotion effect should be required for an antiangiogenic tumor therapy in the presence of heparin. Heparin plus cortisone acetate prevented the DNA synthesis of cultured vascular endothelial cells but not that of cultured 3LL cells. Additionally, oral administration of this combination decreased the [3H]thymidine labeling of endothelial cells of tumor blood vessels prior to the suppression of tumor growth. The specific inhibition of the growth of endothelial cells by heparin plus cortisone acetate was revealed in both the in vitro and the in vivo tests.
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PMID:Inhibitory effects of heparin plus cortisone acetate on endothelial cell growth both in cultures and in tumor masses. 243 5


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