Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antitumor polyoxomolybdates have been recognized in the course of study on the medical utilization of polyoxometalates, inorganic polymers of metal oxide. [NH3Pri]6[Mo7O24].3H2O (PM-8) was found as a representative of antitumor polyoxomolybdates. The growth suppressions of PM-8 against Co-4 human colon cancer xenografted under the subrenal capsule in cd-1 mice were equal or superior to that of 5-FU, MMC, ACNU, ADM and CDDP. Potent antitumor activity of PM-8 is also established against MX-1 human breast and OAT human lung cancer xenografted in athymic nude mice. Polyoxomolybdate is a new type of antitumor substance.
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PMID:Antitumor activity of new antitumor substance, polyoxomolybdate, against several human cancers in athymic nude mice. 130 30

The purpose of this study is to assess effects of fibroblasts in the vitro chemosensitivity testing on human lung cancer cells and to remove them. Fourteen lung cancer cell lines and 14 fibroblasts derived from resected specimens of lung cancers were used, whose S.D (succinate dehydrogenase) activities were measured with MTT colorimetric assay. The chemosensitivity of a lung cancer cell alone was compared with that of mixed cancer cell and fibroblast. As results, S.D activities of fibroblasts were less 2-4 fold than those of lung cancer cells. Fibroblasts were as sensitive to CDDP, MMC and 5-FU as lung cancer cells, but more sensitive to ADM and VP-16 than them. When sensitivity testings were performed on mixed cancer cells and fibroblasts, or mixed cancer cells and conditioned media of fibroblasts to CDDP with 3 day's incubation times, the sensitivity was affected in 61%, or 10% of all the pairs, respectively. However, when these tests were done without any incubation times, the sensitivity was not affected. Therefore, it was suggested that anticancer drugs had to be simultaneously added when single cell suspensions were plated if resected specimens were used in a anticancer drug sensitivity test.
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PMID:[A study of fibroblasts in the chemosensitivity testing on human lung cancer cell lines]. 180 80

The antiproliferative and cytotoxic effects of purified IFN-alpha and recombinant IFN-gamma were investigated using both direct cell counting and a clonogenic assay on a panel of 5 established human lung cancer cell lines and for 2 of them also on their multidrug-resistant counterparts. There was considerable heterogeneity in the response of the cell lines to the IFNs in terms of growth inhibition. Clonogenic assay of IFN-treated cells indicated that, where a cell line had responded markedly to an IFN, only a small fraction of the cells remaining after IFN treatment were clonogenically viable. When cells were placed into the clonogenic assay in the presence of IFNs, the time course of colony formation was different from that seen in the control cultures for most of the cell lines. The measured "surviving fraction" was greatly dependent upon the time of colony counting. When the effects of IFNs in combination with ADM were studied, conclusions regarding the interaction of the effects of the agents also depended upon the time at which colonies were counted.
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PMID:The use of clonogenic assays in assessing the response of human lung cancer cell lines to alpha and gamma interferons alone or in combination with adriamycin. 211 86

A monoclonal antibody, MRK 16, specific to a human myelogenous leukemia cell line, K-562, and resistant to Adriamycin, was used to determine the localization of the antigen molecules (P-glycoprotein) recognized by the monoclonal antibody. P-glycoprotein was found to be expressed very strongly in the adrenal cortex and medulla of adults and strongly in the renal tubules of the kidney and the placenta. Interestingly, P-glycoprotein was not distributed in fetal and neonatal adrenals, and thus may be closely related to adrenal maturation. A high level of P-glycoprotein expression was also seen in one case each of untreated lung cancer (one of ten) and breast cancer (one of nine). Immunoelectron microscopically, the P-glycoprotein was distributed evenly on the membranes of K-562/ADM and 2780 cells. These results imply that the presence of the glycoprotein may be useful as a marker for in vitro studies of multidrug resistance in various malignancies and as an indicator of therapeutic efficacy of ex vivo eradication of multidrug-resistant cancer cells, although other mechanisms of drug resistance may exist, and there is a possibility that this MRK 16 monoclonal antibody may not recognize all P-glycoprotein.
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PMID:Tissue distribution of P-glycoprotein encoded by a multidrug-resistant gene as revealed by a monoclonal antibody, MRK 16. 289 94

An adriamycin-resistant cell line was established in culture by continuous exposure of SBC-3 cells, a cell line of human small-cell lung cancer, to increasing concentrations of adriamycin, followed by a cloning procedure. The resistant cells (SBC-3/ADM) were 30 times more resistant to the drug than the parent cells in terms of 70% lethal dose, determined by soft agar clonogenic assay. Uptake studies using [3H] daunomycin, which was completely cross-resistant to adriamycin, showed decreased influx and enhanced efflux of the agent. This resistance to adriamycin may be attributed to an alteration in membrane transport, resulting in reduced intracellular accumulation of the drug. Using the SBC-3/ADM cells, the activity of a variety of drugs was analyzed by soft agar clonogenic assay in order to search for a means of circumventing drug resistance. The SBC-3/ADM cells were markedly resistant to anthracycline antibiotics such as THP-adriamycin and 4'-epi-adriamycin. The cells were also resistant to structurally or pharmacodynamically unrelated compounds such as vincristine, mitomycin C, 40497S, an active compound of ifosfamide, and etoposide. However, the cells were as sensitive to mitoxantrone as the parent cells, and were considerably susceptible to cisplatin. These results suggest that mitoxantrone and cisplatin may exert a sufficient degree of activity for use against small-cell lung cancer resistant to adriamycin.
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PMID:[Establishment of adriamycin-resistant human small-cell lung cancer cells in culture: analysis of the mechanism of resistance and cross-resistance]. 303 7

Mitoxantrone is similar to Adriblastin in its mechanism of action and antitumor activity. Objective remissions were obtained in 20-30% pretreated patients and in 23-44% of untreated patients by single-drug treatment of patients suffering from metastatic breast cancer. The objective response rates to Mitoxantrone in combination with CTX, 5-FU, MTX, VCR, MMC. Prednimustine or Vindesine were 16-46% in treatment and 38-89% in primary treatment. Randomized studies comparing Mitoxantrone with Adriblastin in single-drug and combination treatment did not show any significant differences in efficacy. However, Mitoxantrone was significantly less toxic. Remission rates of between 24 and 54% were achieved by single-drug treatment in pretreated patients suffering from non-Hodgkin lymphoma. Mitoxantrone appears to be active in ovarian cancer, lung cancer and hepatocellular carcinoma.
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PMID:Mitoxantrone: mechanism of action, antitumor activity, pharmacokinetics, efficacy in the treatment of solid tumors and lymphomas, and toxicity. 332 53

Circulating immune complexes (CIC) levels were evaluated in two groups of cancerous patients to try to correlate CIC levels, tumor stage and chemotherapy received. There were 40 patients with Lung Cancer (LC) clinical stages III and IV; 60 patients with Breast Cancer (BC) stages II, III and IV and 38 normal controls. LC patients showed significant increase in CIC values before, during and after treatment as compared to controls, without any difference among groups under different treatment combinations and tumor stage. Stage II BC patients showed decreased CIC levels during treatment (p less than 0.01 vs initial value). This decrease was maintained after treatment (p less than 0.02). Stage III BC patients showed different behaviour according to treatment: those who only received chemotherapy (ADM + CTX) showed no significant differences during treatment, and those treated with ADM + CTX and megestol acetate (MA) displayed decreased CIC levels after treatment (p less than 0.05) reaching similar control values. Stage IV patients treated with ADM + CTX + MA returned to normal CIC values during treatment. These results proved that combined treatment of chemotherapy and hormone therapy diminished CIC levels in BC patients, while therapy given to LC patients did not present any modifications.
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PMID:Circulating immune complexes in breast and lung cancer, before and after chemotherapy. 360 38

In order to evaluate the effect of an immunomodulator (thymostimulin-TS) added to a traditional combination chemotherapy (ADM, VCR, CTX, CCNU) in advanced lung cancer (oat cell excluded), we began a trial in immuno-depressed patients showing at least 2 out of three appropriate test criteria (see text). Of the 22 fully evaluable patients (all male), 12 in Arm A were given chemotherapy (CH) alone, and 10 in Arm B received chemotherapy (CH) plus TS (1.5 mg/kg/day, beginning the day after the end of the chemotherapeutic cycle). The mean age was 57 +/- 11 for Arm A and 58 +/- 8 for Arm B. The histological type was squamous for all 12 in Arm A and 9 of the 10 in Arm B. No significant differences were found between the mean survival of the two groups (8.1 +/- 3.6 Arm A and 12.1 +/- 84 Arm B); all the patients in Arm A died (maximum survival 12 months for 3 patients), and 2 patients of Arm B are still alive after 23 and 16 months respectively (one patient died after 23 months). Infections occurred on 2 occasions in 2 patients in Arm B, and 13 times in 5 patients in Arm A of which 2 died during a bronchopneumonia. Bone-marrow toxicity was lower in Arm B than in Arm A. Immunological tests failed to improve in the Arm-B patients receiving TS + CH although their resistance to infections seemed to be better than in patients treated by CH only. The quality of life remaining has been better in the patients of Arm B than in those of Arm A.
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PMID:Secondary immunodeficiency in advanced lung cancer: effects of chemotherapy plus thymostimulin in immunodepressed patients: updating results. 653 Mar 54

100 lung cancer operated fresh specimens were collected for in vitro drug sensitivity testing, most of them were NSCLC. Those drugs were MMC(M), ADM(A), PDD(P) and VCR(O). 42% of them were sensitive to 2-4 drugs, but 39% were not sensitive to any of the 4 drugs, the sensitive rate of ADM was higher, 41%, MMC, VCR, and PDD were 37% and 32% respectively, but with no statistical meaning. There were 9 sensitive chemotherapy combination, MAPO combination was the highest, 73.8% of the specimens was sensitive to ADM and PDD, 73.8% of the combination included MMC. The in vitro sensitive drugs and sensitive rate were corresponded to the response rate on NSCLC clinically. As above-mentioned, it convinces us that in vitro drugs sensitivity may be meaningful for the design of combination chemotherapy regimen and developing new drugs for lung cancer.
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PMID:[In vitro drug sensitivity testing and chemotherapy of lung cancer]. 803 31

In an attempt to predict the antitumor activity of a new podophyllotoxin analogue, NK 611, in the treatment of lung cancer, we compared the drug with etoposide and teniposide using four human small cell lung cancer (SCLC) cell lines, SBC-2, -3, -4, -7, and two non-small cell lung cancer cell lines, ABC-1, EBC-1. In terms of the fifty percent tumor growth inhibitory concentration (IC 50) determined by MTT assay, teniposide was most potent among the drugs. The degree of cross-resistance of each drug was investigated using an etoposide-resistant SCLC subline (SBC-3/ETP), an adriamycin-resistant subline (SBC-3/ADM 100), and a cisplatin-resistant subline (SBC-3/CDDP). As for relative resistant (the ratio of IC 50 for resistant subline to that for the parent subline), NK 611 was least cross-resistant to etoposide, adriamycin, and cisplatin among drugs tested. These results indicate that NK 611 may play a role in a salvage chemotherapy for patients with resistant SCLC.
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PMID:[In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines]. 838 49


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