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)

Treatment of C57B1 mice with the methanol extraction residue fraction of killed tubercle bacilli (MER) shortly before or after surgical removal of a syngeneic implant of lung carcinoma 3LL reduced the incidence of spontaneous, fatally progressing pulmonary metastases in a large number of instances. Under certain conditions, the protective action of MER was pronounced and statistically significant. Small quantities of MER (0.2 mg) were optimally effective, when administered i.p. two days before or one day after excision of the initial implant.
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PMID:Effect of treatment with the methanol extraction residue fraction of killed tubercle bacilli (MER) on the development of spontaneous pulmonary metastases from syngeneic implants of tumor 3LL in C57B1 mice. 82 Jun 72

In an attempt to characterize the antigens attached to cells of a line established from a human squamous cell carcinoma of the tongue (CAL 27), BALB/c mice were immunized with whole CAL 27 cells; hybridomas were then produced using spleen cells of the animals and cells of an NS1 syngeneic myeloma. A hybridoma secreting a monoclonal antibody was obtained (CALAM 27); CALAM 27 was directed against an epitope attached to the CAL 27 cells. CALAM 27, IgG2a, reacted with a membrane antigen specific to all epithelial cells. After immunoprecipitation, this antigen corresponded to two bands (Mr 22,000 and 54,000). Reactivity disappeared when the tissue was embedded in paraffin but was conserved after fixation with acetone or methanol. This antigen was conserved for both benign and malignant epithelial cell pathologies. The action of CALAM 27 was tested on 80 samples of pleural effusions, ascites, and cerebrospinal fluid samples; after conventional cytological examinations, CALAM 27 failed to recognize either reactive mesothelial cells or meningothelial cells. In addition, the cell structure recognized by CALAM 27 is not found on certain lymphoid tissue cells. CALAM 27 also failed to react with small cell carcinoma of the lung. Its strictly epithelial specificity therefore permits its use for the diagnosis of micrometastases of carcinoma in ascites and cerebrospinal fluid, in pleural effusions, and in bone marrow. CALAM 27 may also prove useful in confirming diagnosis of pathologies suspected to be of epithelial origin.
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PMID:Characterization of a new surface epitope specific for human epithelial cells defined by a monoclonal antibody and application to tumor diagnosis. 244 May 66

Patients with limited-stage small-cell carcinoma of the lung (SCCL) were randomly assigned to a four-drug chemotherapy program consisting of methotrexate, doxorubicin, cyclophosphamide, and CCNU (MACC) or to a regimen consisting of cyclophosphamide, CCNU, and vincristine alternated with Adriamycin (Adria Laboratories, Columbus, Ohio) and vincristine (CCV/AV). All patients received 4,500 cGy, in a split course, to the primary tumor, mediastinum, and supraclavicular lymph node drainage areas and 3,000 cGy to the whole brain. After four cycles of chemotherapy, patients were randomly assigned to chemotherapy plus methanol extractable residue of BCG (MER-BCG) or no MER-BCG. The complete response frequencies were similar for the two regimens (54% and 48%) as were the median survivals (12.0 and 11.5 months) and the two-year survival rates (15% and 17%). Immunotherapy with MER-BCG did not prolong the time to disease progression or improve survival. Women had a greater chance of achieving a complete remission independent of performance status. There was a complex interaction between sex and the chemotherapy regimens that may have important implications for the design and stratification of future trials in SCCL.
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PMID:Combined modality therapy with radiotherapy, chemotherapy, and immunotherapy in limited small-cell carcinoma of the lung: a Phase III cancer and Leukemia Group B Study. 299 78

6-Ethynyluracil (3) was prepared by two different synthetic procedures. In one approach, 6-formyluracil was reacted with (dibromomethylene)triphenylphosphorane to give 6-(2,2-dibromovinyl)uracil (2), which was silylated and treated with phenyllithium to yield 3. Alternatively, silylated 6-iodouracil was reacted with trimethylsilylacetylene in dry triethylamine in the presence of a palladium/copper catalyst to give 6-[(trimethylsilyl)ethynyl]uracil (5). Compound 5 was converted to 3 in refluxing methanol. At neutral pH, 3 reacted with thiols, such as glutathione, 2-mercaptoethanol, and L-cysteine, but did not react with glycine or L-lysine. This reaction was accompanied by a shift in the UV maximum of 3 from 286 nm to 321-325 nm. The reaction of 3 with 2-mercaptoethanol gave cis-6-[2[(2-hydroxyethyl)-thio]vinyl]uracil as the predominant product. Compounds 2 and 3 inhibited the growth of leukemia L1210, B-16 melanoma, and lewis lung carcinoma cells at concentrations ranging from 1 x 10(-6) to 2 x 10(-5) M. As determined with L1210 cells, the inhibition of growth caused by 2 and 3 was not prevented by the natural pyrimidines, indicating that the agents do not act as antimetabolites.
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PMID:Synthesis and biological evaluation of 6-ethynyluracil, a thiol-specific alkylating pyrimidine. 714 68

The localization of proteasome epitopes in the lung cancer cell lines NCI-H82, derived from a small cell lung cancer, and MR65, derived from a squamous cell lung carcinoma, was studied in relation to cell growth conditions. For this purpose the proteasome monoclonal antibodies MCP34 and MCP20 were applied to the cells growing under different nutritional conditions, resulting in different proliferative states. Using indirect immunofluorescence microscopy with brief fixation in methanol (5 sec, -20 degrees C) followed by three dips in acetone (5 sec at room temperature), it became obvious that the intracellular detectability of the proteasomes changes depending on the nutritional and proliferative status of the tumor cells. Two types of experiments were carried out: (1) cells were grown for two days at different cell densities, with an excess of culture medium, and (2) cells were seeded in a low cell density and monitored for 6 days without change of medium. In cells grown at low density, the proteasomes can be detected mainly in the nuclei, while the nucleoli are almost devoid of staining, and the cytoplasm is only slightly stained. In cells grown at high density, the staining pattern changes with a much less pronounced nuclear staining than in the cells at low density, while the cytoplasm remains slightly stained. In the nutrient depletion experiment similar changes were seen. In cells growing under favorable conditions (1 or 2 days in fresh medium) proteasomes are detected mainly in the nuclei, whereas when the medium becomes depleted of nutrients (4 or 5-day-old medium) the staining pattern changes to one with a much less pronounced nuclear staining. However, in immunofluorescence studies on cells grown under similar conditions but fixed in ethanol (-20 degrees C) for 15 min, the changes in proteasome localization pattern were not detected during medium depletion. Using this fixation protocol the proteasomes are detected mainly in the nuclei at all stages of the medium exhaustion experiment. These apparently contrasting results suggest that upon nutrient depletion the proteasome epitopes become less accessible to the antibodies used. Apparently, the epitopes can regain accessibility if an extended ethanol fixation is used. This hypothesis was confirmed by flow cytometry and immunoblotting experiments. In flow cytometry of ethanol-fixed cells the fluorescence intensity of only a minor part of the cell population decreases to some extent with medium depletion, but in the majority of the cells fluorescence remains at its initial level. The immunoblotting experiments show no quantitative changes in proteasome content of the tumor cells at the different growth conditions.
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PMID:Changes in immunocytochemical detectability of proteasome epitopes depending on cell growth and fixation conditions of lung cancer cell lines. 753 47

Gnidimacrin, a diterpene compound, isolated from the methanol extract of Stellera chamaejasme L, showed significant antitumor activities against mouse leukemia P-388 and L-1210 in vivo. At the dosages of 0.02-0.03mg/kg ip, the in increase in life span (ILS) was 70% and 80%, respectively. Gnidimacrin was also active against murine solid tumors in vivo, such as Lewis lung carcinoma, B-16 melanoma and colon cancer 26. It showed ILSs of 40%, 49% and 41% at the dosages of 0.01-0.02mg/kg ip, respectively. Gnidimacrin strongly inhibited cell proliferation of human cancer cell lines such as leukemia K562, stomach cancers Kato-III, MKN-28, MKN-45, and mouse L-1210 by the MTT assay and colony forming assay in vitro. The IC50 of gnidimacrin was 0.007-0.00012microgram/ml. It is concluded that gnidimacrin is the principal antitumor element in Stellera chamaejasme L. with strong antitumor activities.
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PMID:[The antitumor activities of gnidimacrin isolated from Stellera chamaejasme L]. 765 81

A methanol extract (500 mg/kg x 2/day) of the heartwood of Cassia garrettiana inhibited the tumor growth and metastasis to the lung in Lewis lung carcinoma (LLC)-bearing mice. We isolated the two active substances from the methanol extract of C. garrettiana: compound 1 was identified as Cassigarol A and the determination of the structure of compound 2 is now in progress. We examined the effect of the active substance (compound 1, Cassigarol A) on tumor growth and lung metastasis in LLC-bearing and primary tumor-removed mice and found that Cassigarol A (50 mg and 100 mg/kg x 2/day) inhibited the tumor growth and metastasis to the lung. In addition, Cassigarol A inhibited the plasmin activity and the formation of capillary-like networks of human umbilical vein endothelial cells (HUVECs) at concentrations of 10 to 100 microM. Therefore, it is suggested that the antitumor and antimetastatic activities of Cassigarol A might be due to the inhibition of plasmin activity and formation of tubes (angiogenesis) from HUVECs.
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PMID:Inhibitory effects of active substances isolated from Cassia garrettiana heartwood on tumor growth and lung metastasis in Lewis lung carcinoma-bearing mice (Part 1). 1106 99

Previously, we reported that a methanol extract (500 mg/kg x 2/day) of the heartwood of Cassia garrettiana inhibited the tumor growth and metastasis to the lung in Lewis lung carcinoma (LLC)-bearing mice. Furthermore, we isolated the two active substances from the methanol extract of C. garrettiana and identified compound 1 as cassigarol A. In the present study, compound 2 was identified as 3, 3', 4, 5'-tetrahydroxy stilbene (piceatannol) based on the 1H-NMR spectral data and products formed by oxidation with potassium permanganate. We examined the active substance (compound 2, piceatannol) and its acetylated derivative on the tumor growth and lung metastasis in LLC-bearing and carcinectomized mice. Piceatannol (50 mg and 100 mg/kg x 2/day) did not affect the tumor growth, while piceatannol acetate (50 mg and 100 mg/kg x 2/day) significantly inhibited the tumor growth. Piceatannol and its derivative piceatannol acetate inhibited the metastasis to the lung dose-dependently in carcinectomized mice. Moreover, piceatannol and piceatannol acetate prolonged the survival time and increased the survival rate in carcinectomized mice. In addition, piceatannol inhibited the formation of capillary-like networks of human umbilical vein endothelial cells (HUVECs) at the concentrations of 10 to 100 microM, but its acetylated derivative did not. Therefore, it is suggested that the antimetastatic activities of piceatannol might be due to the inhibition of tube formation (angiogenesis) of HUVECs.
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PMID:Inhibitory effects of active substances isolated from Cassia garrettiana heartwood on tumor growth and lung metastasis in Lewis lung carcinoma-bearing mice (Part 2). 1106 2

The Basidiomycete fungus Agaricus blazei Murill has traditionally been used as a health food for the prevention of cancer, diabetes, hyperlipidemia, arteriosclerosis and chronic hepatitis. In the present study, we examined the antitumor activities of various substances isolated from the lipid fraction of A. blazei. Tumor growth was retarded by the oral administration of the lipid fraction extracted from A. blazei with a chloroform/methanol mixture in sarcoma 180-bearing mice. The substance with the antitumor activity in the lipid fraction was isolated via silica gel column chromatography, eluted with an acetonitrile/methanol (3:2) mixture and identified as ergosterol by direct comparison of the (1)H NMR and mass spectrometry spectral data of an authentic sample. The oral administration of ergosterol to sarcoma 180-bearing mice significantly reduced tumor growth at doses of 400 and 800 mg/kg administered for 20 d without side effects, such as the decreases in body, epididymal adipose tissue, thymus, and spleen weights and leukocyte numbers induced by cancer chemotherapy drugs. Ergosterol had no cytotoxicity against tumor cells. To clarify the antitumor activity of ergosterol, we examined the effects of ergosterol on tumor-induced angiogenesis using two in vivo models. Intraperitoneal administration of ergosterol at doses of 5, 10 and 20 mg/kg for 5 consecutive d inhibited the neovascularization induced by Lewis lung carcinoma cell-packed chambers, suggesting that either ergosterol or its metabolites may be involved in the inhibition of tumor-induced neovascularization. Therefore, we further examined the inhibitory effects of ergosterol on Matrigel-induced neovascularization. Female C57BL/6 mice were subcutaneously inoculated with Matrigel containing acidic fibroblast growth factor and heparin with or without ergosterol. Ergosterol inhibited the Matrigel-induced neovascularization, suggesting that ergosterol directly inhibits Matrigel-induced neovascularization. From these results, it seems likely that the antitumor activity of ergosterol might be due to direct inhibition of angiogenesis induced by solid tumors. This is the first report of ergosterol as an antiangiogenic substance.
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PMID:Isolation of an antitumor compound from Agaricus blazei Murill and its mechanism of action. 1134 91

The lipophilic partition of a methanol extract of the Red Sea sponge Hyrtios erecta yielded a novel pentacyclic sesterterpene ester salmahyrtisol A (1), three new scalarane-type sesterterpenes, 3-acetyl sesterstatin 1 (3), 19-acetyl sesterstatin 3 (4), and salmahyrtisol B (5), together with the previously reported sesterterpenes hyrtiosal (2), scalarolide (6), and salmahyrtisol C (7). The structure determination was based on extensive NMR studies and high-resolution mass spectral measurements. In addition, salmahyrtisol A has a previously unknown pentacyclic carbon skeleton. The new compounds show significant cytotoxicity to murine leukemia (P-388), human lung carcinoma (A-549), and human colon carcinoma (HT-29). A biosynthetic relationship between 1 and 2 is briefly discussed.
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PMID:Salmahyrtisol A, a novel cytotoxic sesterterpene from the Red Sea sponge Hyrtios erecta. 1180 54


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