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

Feeding an artificial, essentially polyamine-free diet which contained antibiotics for the decontamination of the gastrointestinal tract and 2-(difluoromethyl)ornithine (DFMO) and N,N'-bis-(2,3-butadienyl)putrescine for the inactivation of ornithine decarboxylase and polyamine oxidase, respectively, retarded the growth of several solid tumors by about 80%. In the present work the contribution of the major components of the treatment were analysed, using Lewis lung carcinoma growing in the hind leg of female C57BL mice. In addition to polyamine deprivation, malnutrition due to decreased food intake turned out to contribute significantly to tumor growth retardation. Ornithine decarboxylase was shown to be incompletely inhibited by administration of DFMO with the diet. A considerable improvement of polyamine deprivation can be expected from the continuous administration of this drug, or from analogous inhibitors with more favourable enzyme- and pharmaco-kinetic properties.
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PMID:Polyamine deprivation, malnutrition and tumor growth. 158 May 63

The effects of two new Ru(III) complexes, [mer-RuCl3(DMSO)2Im] degrees and Na[trans-RuCl4(DMSO)Im], were investigated on primary tumor growth and on the survival time using three solid metastasizing tumors of the mouse: Lewis lung carcinoma, B16 melanoma and MCa mammary carcinoma. Na[trans-RuCl4(DMSO)Im] appears to be the most promising compound, in that: (1) it is soluble in water and therefore easy to handle in comparison with the neutral species [mer-RuCl3(DMSO)2Im]degrees or to the already described BBR2382; (2) similarly to cisplatin, though at a lower level, it reduces tumor growth in its primary site in each tumor model employed; (3) unlike cisplatin, it increases the life span of tumor-bearing hosts in all tumors used, independently of the effects on primary tumor growth; and (4) it is also effective in reducing spontaneous metastasis formation when the effects on primary tumor growth are completely absent. Dimethylsulfoxide (DMSO), used for solubilizing poorly water-soluble compounds (i.e. [mer-RuCl3(DMSO)2Im]degrees) or for stabilizing the compound in the solution before injection (i.e. Na[trans-RuCl4(DMSO)Im]), reduces the anti-tumor potency. Conversely, the antitumor effects of Na[trans-RuCl4(DMSO)Im] are more pronounced in mice hydrated with isotonic saline. We conclude that Na[trans-RuCl4(DMSO)Im] is a good candidate for further investigations aimed at ascertaining the mechanism of the anti-metastatic activity and of the positive effects on survival time of mice bearing solid metastasizing tumors.
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PMID:Effects of the Ru(III) complexes [mer-RuCl3(DMSO)2Im]degrees and Na[trans-RuCl4(DMSO)Im] on solid mouse tumors. 162 12

A laminin-derived synthetic peptide, Cys-Asp-Pro-Gly-Tyr-Ile-Gly-Ser-Arg-NH2 (CDPGYIGSR-H2), containing an active site for cell binding inhibited both angiogenesis and solid tumor growth. It potently suppressed both embryonic angiogenesis of the chick chorioallantoic membrane and migration of vascular endothelial cells induced by a tumor-conditioned medium but neither the in vitro proliferation of endothelial cells nor that of tumor cells. Additionally, in in vivo tests, CDPGYIGSR-NH2 markedly inhibited both the growth of s.c. solid tumor of Sarcoma 180 and that of Lewis lung carcinoma (3LL) in the lungs. On the contrary, ascitic tumor growth of Sarcoma 180 was not affected by this peptide, even though the same cell source was used. It was concluded that solid tumor growth inhibition by CDPGYIGSR-NH2 was due not a direct effect on cell growth but to antiangiogenic effect mediated by the inhibition of endothelial cell migration.
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PMID:Inhibition of angiogenesis and tumor growth by a synthetic laminin peptide, CDPGYIGSR-NH2. 170 42

Angioarchitectures of ascites hepatoma AH109A and Sato lung carcinoma (SLC) were quantitatively compared by measuring the following morphometric parameters: vascular density, vascular length, distance between tissues and their nearest blood vessel, and total length of microvascular network per unit area. When the vascular networks in these two types of tumors were compared in the initial stage, the morphological parameters were almost identical. Correlations between tumor size and the number of starting vessels and between enlargement of the tumor and the ensuing increase in pressure of the starting vessel were also evaluated with a microcomputer and an apparatus for measuring microvascular pressure. The total length of tumor vascular network to which one starting vessel supplied blood increased exponentially as the tumor increased in size exponentially. There was a positive correlation between tumor size and the number of starting vessels. The range of the blood supply from one starting vessel was evidently limited. The pressure of the starting vessel increased with enlargement of the tumor size. As soon as the pressure of the starting vessel reached a plateau, however, there was a rapid increase in low-flow or no-flow areas in regions within the tumor. From the results obtained, we consider that low-flow or no-flow areas, resistant to delivery of anticancer drugs, inevitably appear with the progression of tumor growth.
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PMID:Characterization of heterogeneous distribution of tumor blood flow in the rat. 170 37

Modulation of the immune response by the use of biological response modifiers (BRM) is aimed at amplifying the host resistance against cancer. Studies on inhibition of tumor growth on an in vitro model, in which human breast carcinoma (HBL-100) and human lung carcinoma (H125) cells were used as target tumor cells, confirmed that interferons (IFNs) alpha and beta can amplify the antineoplastic effects of immunochemotherapy by enhancing the cytotoxic activity of effector cells and by antagonizing the immunodepressive effects of radiation or anticancer drugs. Moreover, data obtained from a pilot clinical trial, designed to test the effect of low concentrations of beta-IFN on natural cell-mediated cytotoxicity, pointed out a good correlation between the in vitro and in vivo responsiveness to beta-IFN in cancer patients. The immunomodulating and antiproliferative effects of BRM were also evaluated in a model of viral leukemogenesis in vitro, after infection of cord blood derived mononuclear cells (CB-MNC) with the human leukemic retrovirus HTLV-I. Alpha-and beta-IFN were previously shown to regulate differentially the antiviral competence of recipient CB-MNC, by interfering with viral replication and delaying the emergence of the transformed clone(s). One of the mechanisms of IFN action that contributes to control HTLV-I infection in vitro can be ascribed to their property of partially counteracting the depression of cell-mediated cytotoxicity that follows exposure to HTLV-I. In the light of data previously and herein described, it seems that alpha- and beta-IFN can be considered potential candidates to define combined therapy with antiviral drugs, to control the early stages of retrovirus-associated disease in human pathology.
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PMID:Role of biological response modifiers in immunochemotherapy of solid tumors and retroviral-induced leukemia. 170 53

In this study we have investigated the effects of thymosin alpha 1 (T alpha 1) and interleukin-2 (IL-2), singly or in combination with cyclophosphamide (CY), on tumor growth, survival and cytotoxicity in C57Bl/6NCrlBR mice with Lewis lung carcinoma (3LL). Combined administration of T alpha 1 plus IL-2, after CY treatment, was much more effective than use of each biological response modifier (BRM) alone, and induced complete tumor regression in all of the mice studied. Combination immunotherapy alone without CY only slightly reduced the rate of tumor growth, and these results are in accordance with previous studied which showed that the 3LL carcinoma is resistant to cytokines. Combined chemo-immunotherapy also increased the cytotoxicity of spleen cells and markedly enhanced long-term survival in all treated animals. Depletion of immune cells, using either total-body sub-lethal irradiation (400 rads) or antibodies directed against T-cell (anti-CD4 and CD8) or NK-cell (anti-asialo GM1) populations, abolished the positive response to combination therapy. Histological analysis of the tumors obtained from mice treated with combination chemo-immunotherapy revealed a high number of infiltrating lymphoid cells surrounding a well-circumscribed area of necrosis consisting solely of dead cells. Our studies show that T alpha 1 potentiates IL-2-induced cytotoxic activities in vitro as well in vivo, and that these compounds have a powerful anti-tumor action when associated with chemotherapy.
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PMID:Combination therapy with thymosin alpha 1 potentiates the anti-tumor activity of interleukin-2 with cyclophosphamide in the treatment of the Lewis lung carcinoma in mice. 173 18

5-Chlorodeoxycytidine (CldC), coadministered with modulators of pyrimidine metabolism, is an effective radiosensitizer of murine tumors. Past studies that utilized RIF-1 tumors in C3H mice and Lewis lung carcinoma (LLC) in BDF1 mice have been extended with an emphasis on using multiple cycles of drug administration followed by irradiation of LLC and the use of two additional tumor models. Four of seven cures of BDF1 mice bearing LLC were obtained with three doses of 20 Gy irradiation, in which the first and third dose were preceded by a "Standard Protocol" that includes N-(phosphonacetyl)-L-aspartic acid (PALA), 5-fluorodeoxycytidine (FdC), tetrahydrouridine, and the radiosensitizer, 5-chlorodeoxycytidine. No cures were obtained in groups of mice receiving radiation alone or drugs alone, and there were no "no takes" in untreated control groups (six mice/group). Extensive tumor inhibition, exceeding that obtained with drugs or radiation alone, was obtained with two cycles of drugs and radiation combined when a dimethybenzanthracene-induced mammary adenocarcinoma was used in BALB/c mice. With the EMT-6 tumor in BALB/c mice, doses of 10 and 20 Gy were administered 9 and 16 days after tumor implantation, each preceded with the Standard Protocol; this resulted in a tumor growth delay of 24 days. No tumor growth delay occurred with drugs or radiation alone. The omission of PALA, FdC or CldC from the Standard Protocol resulted in loss of tumor control, which was obtained with the complete protocol. The fact that 5-chlorodeoxycytidine is an effective radiosensitizer in four rodent tumor systems is compelling evidence that it has potential as a radiosensitizer of human tumors, especially in view of its tumor selectivity and its resistance to catabolism when used with modulators of its metabolism, and in view of the high levels of the key enzymes in human tumors, which can convert 5-chlorodeoxycytidine to 5-chlorodeoxyuridine triphosphate, the proximate radiosensitizer.
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PMID:5-chlorodeoxycytidine, a radiosensitizer effective against RIF-1 and Lewis lung carcinoma, is also effective against a DMBA-induced mammary adenocarcinoma and the EMT-6 tumor in BALB/c mice. 173 88

Previously we found that the reconstituted basement membrane matrix Matrigel, when premixed with human small-cell lung carcinoma cells and injected subcutaneously into athymic mice, permitted tumor growth, whereas cells injected in the absence of Matrigel did not form tumors. In the present study, we examined additional cell types and determined some of the underlying mechanisms involved in the promotion of tumor formation by Matrigel. The tumor cell lines that we studied included transformed mouse Englebreth-Holm-Swarm tumor cells (T-EHS), human submandibular carcinoma A253 cells, mouse melanoma B16F10 cells, human epidermoid carcinoma KB cells, and human primary renal cell carcinoma cells. When coinjected subcutaneously with Matrigel, these cell lines formed rapidly proliferating tumors. Primary biopsy specimens of human colon carcinoma, when dispersed and coinjected with Matrigel, also formed tumors. Only A253, KB, and B16F10 cells formed small tumors in the absence of Martrigel, but a fivefold to tenfold increase in tumor size was observed in the presence of Matrigel. These data demonstrate a useful method for improving the growth of human tumors in athymic mice.
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PMID:Enhanced tumor growth of both primary and established human and murine tumor cells in athymic mice after coinjection with Matrigel. 192 May

Ilmofosine (1-hexadecylthio-2-methoxymethyl-1,3-propanediol-phosphocholine, BM 41.440) is a thioether phospholipid with cytostatic/cytotoxic properties. The antineoplastic activity of this compound was investigated in vivo in the 3Lewis-lung carcinoma system. 3Lewis lung tumor-bearing C57Bl/6 mice were treated with 0.625 to 40 mg Ilmofosine/kg per day p.o. either from days 1 to 9 or from days 11 to 28 after intrafoot-pad tumor cell inoculation. Ilmofosine caused a significant dose-related response on tumor growth and metastases, expressed in terms of tumor diameter, tumor weight, survival time and number of metastases-free animals as compared to sham-treated and positive (cyclophosphamide) controls. The results suggest that direct cytostatic/cytotoxic effects, rather than immune-modulatory mechanisms, preferentially contribute to the antitumor activity of Ilmofosine in vivo.
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PMID:Antitumor activity of Ilmofosine (BM 41.440) in the 3Lewis-lung carcinoma model. 181 46

Zinc sulfonated phthalocyanine (ZnSPc) 10 mg.kg-1 was injected iv into mice bearing S-180 and RA795 lung carcinoma, after 24 h tumor site were irradiated with red light. In mice bearing S-180, tumor regression rate was 31.8-43.5%, tumor growth inhibition rate was 57.4%. The highest concentration was in tumor tissue 24 h after injection of this dye, on d 5 it still retained relatively highest concentration. However, in most other tissues the dye was not detected at this time, disappearance of ZnSPc from plasma was rapid, it showed an open two compartment model, t1/2 alpha 135.8 min, t1/2 beta 70.1 h, Vd 1.92 x 10(-3) L. In blood, most ZnSPc was bound with plasma protein, the peak light absorption showed blue shift. ZnSPc 2.5 micrograms.ml-1 plus light, percent of DNA double strands greatly decreased, this indicated that DNA was one of target sites for ZnSPc photodynamic action.
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PMID:[Photodynamic therapy of zinc sulfonated phthalocyanine on murine transplanted tumors, its tissue distribution, and damaging effect on DNA of cancer cell]. 181 3


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