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)

The growth and metastasis of transplanted Lewis lung carcinoma in C57BL/6J mice were inhibited by an ip injection of whole serum from Carcharhinus plumbeus, the sandbar shark. Tumors failed to develop in 69% of the animals inoculated with shark serum on days 0, 3, and 6 after tumor transplantation. Histologic examination of the tumor site at days 3 and 6 showed that tumor cells were pyknotic, and evidence of lysis of tumor cells and minor leukocytic infiltration existed. Tumor cells were not in tissue sections from day 15, and these animals still had no symptoms at day 216. The mean tumor volume of the remaining 31% of the treated animals was less than that of controls; they had a prolonged mean survival time, but ultimately they died from metastases, as did the controls. Urea- and hemoglobin-treated animals and those pretreated or intralesionally treated with shark serum were similar to the controls in both tumor kinetics and survival times.
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PMID:Inhibitory effect of shark serum on the Lewis lung carcinoma. 99 8

The response of s.c. primary and metastatic Lewis lung carcinoma to five antitumour platinum complexes with or without tolerable whole-body hyperthermia (60 min to reach temperature then 60 min at 42 degrees C) was examined. The whole-body hyperthermia treatment produced about 2.8 days of tumour growth delay in the s.c. tumours. The addition of whole-body hyperthermia to treatment with each of the platinum complexes was well tolerated by the animals and increases of 1.6-2.0-fold in tumour growth delay resulted with the combined treatment compared with the platinum complexes alone. The combination of etanidazole (1 g/kg) and the platinum complexes followed by whole-body hyperthermia produced marked increases in tumour growth delay ranging from 2.5- to 3.6-fold over the growth delays obtained with the platinum complexes alone. FSaLLC tumour cell survival and bone marrow CFU-GM experiments indicated that local hyperthermia (43 degrees C, 30 min) produced greater potentiation of the cytotoxicity of three platinum complexes than did whole-body hyperthermia (42 degrees C, 60 min). Only the complete treatments including whole-body hyperthermia/etanidazole and the platinum complexes were effective in significantly reducing the numbers of lung metastases formed from s.c. primary tumours. Serum urea nitrogen and creatinine levels were monitored over a time-course post-treatment. Although some treatment combinations caused elevations in these normal tissue parameters by day 12 post-treatment both serum urea nitrogen and serum creatinine returned to the levels of the untreated control animals.
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PMID:Whole-body hyperthermia as an adjuvant to treatment with platinum complexes with or without etanidazole in mice bearing the Lewis lung carcinoma or the FSaLL fibrosarcoma. 147 4

(-)-(R)-2-Aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato++ +)platinum(II) monohydrate (DWA2114R), cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diamminedichloroplatinum(II) (CDDP) were compared for their antitumor effects and nephrotoxicity-inducing activities at the same dosage (1/8, 1/4, 1/3, 1/2, 2/3 or 3/4 of the LD10 or LD10) on the basis of their intravenous lethal doses in mice. DWA2114R was effective against murine tumor lines, Colon 26 and Colon 38 carcinomas, M5076 ovarian sarcoma and P388 L1210 leukemias, implanted subcutaneously (s.c.). Triple injection every other day of DWA2114R was more effective than a single injection at each sublethal dose. The antitumor effects of DWA2114R against these tumors were more effective than or were similar to those of CBDCA and CDDP. The antitumor effect against CDDP-resistant L1210 leukemia implanted s.c. was only observed in the treatment of DWA2114R, but not in CBDCA and CDDP. No excellent antitumor effects of three platinum complexes were observed against Lewis lung carcinoma and B16 melanoma implanted s.c. even at triple injection every other day, and no effect was obtained against Meth-A fibrosarcoma under similar conditions. While the treatment of CDDP showed marked increases in levels of blood urea nitrogen and of urinary protein and sugar at effective doses in the antitumor evaluations, the treatment of DWA2114R as well as CBDCA showed no increase in these parameters. These results indicate that DWA2114R represents a desirable second generation antitumor platinum complex.
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PMID:Antitumor effects of three platinum complexes, (-)-(R)-2-aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato)-platinum (II) monohydrate (DWA2114R), cis-diammine-(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diamminedichloroplatinum(II) (CDDP), in mice. 156 81

A novel antitumor compound, N-[4-(5-bromo-2-pyrimidinyloxy)-3-chlorophenyl]-N'-(2-nitrobenzoyl ) urea (HO-221) was evaluated for its antitumor activity in experimental tumor models. HO-221 preparation was given orally to tumor-bearing animals. The compound exhibited significant effects against various tumors such as P388 and L1210 leukemias; M5076 reticulum-cell sarcoma; colon 38 carcinoma; human xenografts MX-1, LX-1, GA-1, and Co-1; Lewis lung carcinoma; sarcoma 180; and Walker 256 carcinosarcoma and was especially effective against solid tumors. However, its effect on murine B16 melanoma was moderate. Intermittent administration of HO-221 produced better results. The effects of HO-221 on human tumor xenografts were compared with those of other antitumor agents. HO-221 showed activity against LX-1 lung and Co-1 gastrointestinal tumor and was also effective against advanced-stage L1210 leukemia and Lewis lung carcinoma. Furthermore, the effect of HO-221 on drug-resistant tumors was examined using murine leukemias L1210 and P388. It showed no cross-resistance with the known antitumor agents Adriamycin (ADM), daunomycin (DM), vincristine (VCR), mitomycin C (MMC), cisplatin (CDDP), 5-fluorouracil (5-FU), cytosine arabinoside (Ara-C), methotrexate (MTX), cyclophosphamide (CPA), or carboquone (CQ), and collateral sensitivity to HO-221 was found in MMC-, CDDP-, and CPA-resistant sublines. HO-221 exhibits significant reproducible, broad-spectrum antitumor activity against experimental tumors as well as human neoplasms.
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PMID:Antitumor activity on murine tumors of a novel antitumor benzoylphenylurea derivative, HO-221. 191 78

Protective effect of sodium selenite (Se) on the nephrotoxicity of cis-diamminedichloroplatinum (CDDP) was studied in mice. The administration of CDDP alone at doses of 50 mumols/kg caused the increase of blood urea nitrogen (BUN) and urinary N-acetylglucosaminidase (NAG) and the degeneration of proximal tubule cells pathologically. The co-administration of Se, especially at doses of 20 mumols/kg/day, inhibited the increase of BUN and urinary NAG and depressed the degeneration of proximal tubule cells. The administration of CDDP at doses of 20 mumols/kg caused a mild reduction of transplanted Lewis lung carcinoma and a decrease of metastasis to lung. The co-administration of Se at doses of 8 mumols/kg didn't inhibit the antitumor effect of CDDP against Lewis lung carcinoma. Co-administration of Se didn't influence concentration of CDDP in plasma, blood cells, kidney and liver. In mice fed Se deficient diet, the nephrotoxicity of CDDP increased and activities of glutathione peroxidase (G-Px) in blood and kidney decreased. In mice co-administered with Se, G-Px activities didn't increase. These results suggest that co-administration of Se may allow use of CDDP at higher doses in cancer chemotherapy. Interaction between CDDP and Se differs from that between mercury and Se, and cadmium and Se(formation of compound). Intake of Se is related to appearance of the nephrotoxicity of CDDP. G-Px may be related to a part of the protective effect of Se on the nephrotoxicity of CDDP.
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PMID:[Studies on protective effect of selenium on the nephrotoxicity of cis-diamminedichloroplatinum (CDDP) in mice]. 216 95

HO-221, N-[4-(5-Bromo-2-pyrimidinyloxy)-3-chlorophenyl]-N'-(2-nitrobenzoyl ) urea is a novel benzoylphenylurea derivative. We had interested in various pharmacological actions of benzoylphenylurea compounds. Therefore, many compounds were synthetized and tested in various screening systems. In the process with these tests, we found HO-221 which showed an excellent antitumor activity. The antitumor activity of HO-221 was judged from the survival time and the tumor weight of experimented tumor-bearing animals. HO-221 preparation was orally administered. The compound exhibited significant effects against various animal tumors (P388, L1210, M5076, LLC, C38, S180, W256), and especially effective against the solid tumors. HO-221 was also markedly effective to MX-1 and LX-1 implanted into nude mice. However, the effect against mouse B16 melanoma was moderate. In addition, HO-221 showed a schedule dependency and once every 4 or 7 days treatments were most effective. The antitumor activities of the compound against advanced L1210 and Lewis lung tumors were examined. Tegafur and ara-C were used as reference drug for the study. Three agents showed the antitumor activities against L1210. Against Lewis lung carcinoma, HO-221 showed both the increase of life span and the tumor growth inhibition. On the other hand, tegafur and ara-C were ineffective for the increase of life span.
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PMID:[Antitumor effect of a benzoylphenylurea derivative HO-221]. 226 Aug 71

The effects of sodium thiosulfate (STS) were studied in patients who received a combination therapy of cis-dichlorodiammineplatinum (CDDP) and vindesine. In this study, 61 patients with non-small-cell lung carcinoma were randomized to receive either CDDP and vindesine (both given i.v.) with i.v. STS [30 patients, STS(+) group] or CDDP and vindesine without STS [31 patients, STS(-) group]. In the STS(+) group, 16 patients who showed an improvement (reduction in tumor size or relief of symptoms) after the first course received the second STS(+) treatment, and 15 patients in the STS(-) group who showed an improvement after the first course received the second STS(-) treatment. Urinary levels of beta 2-microglobulin (BMG) and N-acetyl-beta-D-glucosaminidase (NAG) were measured as an index of proximal tubular function. Analysis of both levels indicated that STS suppressed CDDP nephrotoxicity to a minimal level. Serum BMG, blood urea nitrogen (BUN), and total as well as 24-h creatinine clearance levels were measured as an index of glomerular function. There were no significant differences in these levels between the STS(+) and STS(-) groups. The urinary recoveries of total platinum 24 h after CDDP administration were 29% and 21% in the STS(+) and STS(-) groups, respectively. The mean plasma concentrations of total platinum at 24 h after CDDP administration were 2.24 and 2.70 micrograms/ml in the STS(+) and STS(-) groups, respectively. There were no significant differences in the response rates of the STS(+) and STS(-) groups at a fixed dose of 100 mg/m2 CDDP. Therefore, the present study clearly demonstrates that systemic administration of STS reduces the side effects of CDDP to a minimal level without impairing its antitumor activity and that STS treatment is applicable in a repeated chemotherapy using CDDP alone or in combination with other antitumor agents.
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PMID:Effects of sodium thiosulfate in combination therapy of cis-dichlorodiammineplatinum and vindesine. 253 52

A study was conducted to determine the incidence and extent to which anorexia, a decrease in spontaneous food intake, contributes to the occurrence of cancer cachexia. Data for ten male subjects with small cell carcinoma of the lung are reported for a five-month period following diagnosis. Although body weights of the subjects at the time of diagnosis averaged less than 95% of the usual weight (weight 6 months prior to diagnosis), they were greater than 109% of the mean ideal weight. At five months, the mean weight (N = 8) was 88% of the preillness weight. From the time of diagnosis, there was a mean loss of 7.2 kg (15.8 lb). The urinary creatinine excretion was below the normal range, whereas the urinary urea nitrogen values were within the normal range. At the time of diagnosis, the mean triceps skin-fold measurements were approximately 80% of the standard reference for males. During the five-month period, the mean midarm muscle circumference determinations remained greater than 90% of the reference standard. The mean serum transferrin values were 10% or more below the reported lower range of normal, whereas the great majority of the serum albumin values were 3.0 g/dl or above during the five-month period. The mean caloric intake of 2,204 kcal at the time of diagnosis was only 86% of the estimated basal energy expenditure (BEE) times a factor of 1.5 used to account for moderate activity. Four months following diagnosis, the mean caloric intake had fallen to 1,702 kcal, only 67% of the BEE X 1.5 (calculated from the weight at diagnosis). The findings provide evidence of a decline in spontaneous food intake, a small decrease in body fat, and a greater than 13% weight loss. The oral intake was less than adequate for any activity beyond the basal state. Decreased intake could account for most of the weight loss observed in the subjects.
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PMID:Anorexia and weight loss: indicators of cachexia in small cell lung cancer. 299 21

Human lung carcinoma cells (A549) were oxidatively stressed with mildly-toxic or non-toxic amounts of hydrogen peroxide (H2O2, 0.1 mM to 120 mM) for 5 min. Hydrogen peroxide exposure resulted in a dose dependent inhibition of binding (pH 7) of the thiol reagent iodoacetic acid (IAA) to a 38 kDa cell protein. Incubation of cells in saline for 60 min following H2O2 removal restored the ability of IAA to bind to the protein. Treatment with 20 mM dithiothreitol or 2 M urea also restored IAA binding, but 10% Triton X102 or 1 mM Brij 58 had no effect. Increasing to pH 11 during the IAA binding also increased thiol availability. Glyceraldehyde 3-phosphate dehydrogenase (EC 1.2.1.12) has been identified as the protein undergoing thiol/disulfide redox status and enzymic activity changes.
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PMID:Reversible oxidation of glyceraldehyde 3-phosphate dehydrogenase thiols in human lung carcinoma cells by hydrogen peroxide. 367 70

The novel antitumor antibiotic, trioxacarcin C, was studied for antitumor activities against murine tumor systems. When mice with i.p.-inoculated B16 melanoma were given intraperitoneal injections of trioxacarcin C, the maximal T/C% was 164 by successive administration of 0.125 mg/kg/day (day 1 approximately 10). It also gave the prolongation of life span of mice bearing i.p. P388 leukemia (T/C 141%) by i.p. injection for 10 days, and inhibited the growth of sarcoma 180 (T/C 42%) and Lewis lung carcinoma implanted s.c. (T/C 23%) by i.v. administration for 6 or 7 days. It inhibited the growth of P388 leukemia cells in vitro and showed significant inhibition on the colony formation of HeLa S3 cells. DNA and RNA synthesis were more strongly inhibited than protein synthesis by trioxacarcin C. Also, it induced strand scission of PM-2 DNA without reducing agents or metals. It did not effect the number of white blood cells and blood urea nitrogen value of the peripheral blood.
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PMID:Antitumor activity of trioxacarcin C. 619 42


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