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)

Tests were made to determine whether cell surface tumor antigens of metastases differed from the tumor antigens of the cell population of the local tumor growth. C57BL/6 mouse spleen lymphocytes sensitized against monolayers of the local growth of the 3LL Lewis lung carcinoma (L-3LL) in the presence of syngeneic serum generated lymphocytes that were cytotoxic to L-3LL but significantly less cytotoxic to target cells derived from lung metastases (M-3LL). Lymphocytes sensitized against M-3LL were significantly more cytotoxic against M-3LL than against L-3LL cells. Anti-M-3LL cytotoxic lymphocytes but not anti-L-3LL, admixed with either L-3LL cells or M-3LL tumor cells, when injected into syngeneic recipients reduced lung metastasis significantly. Results indicated that cells with high metastatic capacity and distinct antigenic properties exist within the tumor cell population and that immunoselection might be involved in the production of lung metastases.
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PMID:Differences in cell surface antigens of tumor metastases and those of the local tumor. 8 91

The effects of three different dosage schedules on both therapeutic effect and pulmonary toxicity of bleomycin were studied in mice. Therapy was assessed by both survival and decreased tumor size in mice bearing Lewis lung carcinoma. Lung toxicity was estimated in nontumored mice as increases in lung collagen content by measuring lung hydroxyproline concentrations. In the first set of experiments, bleomycin injections twice daily (low-dose, high-frequency) produced a significant (34%) increase in lifespan over controls, whereas the same total dose given twice weekly did not result in increased survival. Both schedules produced pulmonary toxicity. Continuous sc infusion of bleomycin via an osmotic minipump was compared to these two schedules of intermittent injection. Identical total doses of drug were administered in all three schedules. Continuous infusion for 7 days produced marked inhibition of tumor growth (T/C = 16%), which was significantly better than twice weekly or ten-times weekly injection of the same total dose. Furthermore, at a total dose of 40 mg/kg of bleomycin, continuous infusion did not result in measurable pulmonary toxicity, whereas both schedules of bolus injection produced significant increases in lung collagen content. Thus, continuous infusion of bleomycin improved its therapeutic effect against Lewis lung carcinoma and also reduced its pulmonary toxicity.
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PMID:Improved therapeutic index of bleomycin when administered by continuous infusion in mice. 8 69

Immunopotentiated rats, which were injected with Propionibacterium acnes or BCG, had the 50% survival twice as long as those in untreated controls after intravenous inoculation of Sato lung carcinoma (SLC) cells. The amount of labeled tumor cells in the lung of the adjuvant-treated rats decreased significantly in the first 20 hr after intravenous injection of 51Cr-labeled tumor cells compared to that of control animals. The elevated activities of ATPase and acid phosphatase in the whole nucleated spleen cells as well as spleen lymphocytes separated by Ficoll-Conray gradient were also demonstrated in adjuvant-treated groups. These data suggested that the elevation of ATPase and acid phosphatase activities in nucleated spleen cells as well as spleen lymphocytes has an important role for the suppression of tumor growth in adjuvant-treated rats.
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PMID:Effect of Propionibacterium acnes or BCG on enzyme activities in spleen lymphocytes of Donryu strain rats. 14 84

One hundred and eighteen patients with inoperable carcinoma of the lung were randomly selected for treatment with methotrexate, cyclophosphamide, procarbazine, and vincristine. These drugs were adminsitered simultaneously to one group of patients and sequentially to the second group. As the statistically sicame evident (51% vs. 21%), an additional 85 cases were treated in this manner without randomization. The objective clinical responses were associated with prolonged survival. A higher response rate with the simultaneous treatment was also evident in patients with anaplastic small cell carcinoma (65% vs. 36%) as well as those with epidermoid carcinoma (33% vs. 13%). These differences were not statistically significant. Toxicity remained within acceptable limits, with a 2% drug related mortality, and was similar in both treatment regimens. Initial performance status was definitely related to survival, but not to tumor response. Patients with epidermoid carcinomas showing stabilization of tumor growth under treatment had the longest survival. Maintenance therapy with continued four-drug polychemotherapy was not superior to single agent maintenance with cyclophosphamide.
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PMID:Treatment of bronchogenic carcinoma with simultaneous or sequential combination chemotherapy, including methotrexate, cyclophosphamide, procarbazine and vincristine. 18 13

Aprotinin, a wide range proteinase inhibitor, was given alone to tumor-bearing mice and life span and several tumor growth parameters were recordered. Aprotinin showed anti-tumor effects in Hepatoma 22 and Lewis lung carcinoma, remaining ineffective in Sarcoma 37, Leukemia L1210 and Ehrlich ascitic carcinoma.
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PMID:Effect of proteinase inhibitor in experimental tumors. 20 10

Red blood cell deformability is a major determinant of capillary blood flow. In mice with L1210 leukemia and with Lewis lung carcinoma, red blood cell deformability was significantly decreased during tumor growth. In mice with L1210 leukemia, deformability was significantly decreased by day 5 after transplantation and progressively decreased through day 9. Terminally, red blood cell deformability returned to normal or above normal values. In mice with Lewis lung carcinoma, significant decreases in deformability were noted 21--28 days after transplantation and persisted throughout the remainder of the tumor course. Impaired capillary blood flow, secondary to abnormal red blood cell deformability, is therefore associated with advanced cancer.
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PMID:Impairment of red blood cell deformability by tumor growth. 28 42

Host resistance to tumor growth was studied in athymic nude mice of C57BL background. Animals were pretreated in the left hind leg by local hyperthermia, local X-irradiation, or combined local hyperthermia and X-irradiation. Twenty-four hr posttreatment, the animals were inoculated with the metastatic Lewis lung carcinoma tumor. Half of the animals in each group were inoculated in the pretreated leg and animals of the other half of the group were inoculated in the contralateral untreated leg. An increase of 30 to 45% in life span was achieved in normal and nude mice pretreated by combined local hyperthermia and irradiation. The increase in life span was similar in animals inoculated in the pretreated leg or in the untreated contralateral leg. These results indicate that T-lymphocytes are not involved in the protection against tumor growth.
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PMID:Stimulation of resistance to tumor growth of athymic nude mice pretreated by combined local hyperthermia and X-irradiation. 31 80

The antimetabolite antibiotic L-(alphaS,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (AT-125) showed significant antitumor activity against L1210 and P388 mouse leukemias and the M5076 mouse ovarian tumor. Depending on the schedule of administration, increases in lifespan of greater than 100% were observed. Activity was observed after ip, oral, or sc inoculation of AT-125 in mice inoculated with L1210 by the ip route. Lewis lung carcinoma and B16 melanoma were not affected by AT-125. The compound was used to treat human tumor xenografts in athymic (nude) mice. The MX-1 mammary tumor regressed when treated with either 8 or 16 mg/kg/day for 10 days, while a dose of 32 mg/kg was toxic. On an every-4-days x 3 schedule there was a marked slowing of MX-1 tumor growth at 50, 100, and 200 mg/kg. The LX-1 lung tumor xenograft growth was slowed significantly by a dose of 32 mg/kg. Growth of colon tumors, CX-1, CX-2, and CX-3, was not affected by AT-125.
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PMID:Therapy for mouse tumors and human tumor xenografts with the antitumor antibiotic AT-125. 42 27

The sensitivity to local tumor hyperthermia (43 degrees, 60 min) of a spectrum of eight different solid mouse tumors (Lewis lung carcinoma, M5076 ovarian carcinoma, colon carcinoma 38, colon carcinoma 26, mammary adenocarcinoma C3HBA, mammary adenocarcinoma 16C, glioma 26, and B16 melanoma) was investigated. A microwave (2.45-GHz) apparatus produced localized heating of the tumors without generation of whole-body hyperthermia. The temperature at the center of the heated tumors was regulated to within +/- 0.1 degrees while the temperature uniformity within the tumor was +/- 0.5 degrees. The local hyperthermia treatments reduced the size and retarded the growth of the treated tumors compared with control values for each of the tumors tested. The faster-growing Lewis lung carcinoma and B16 melanoma were the least responsive to treatment, while the slower-growing colon 38 and M5076 ovarian carcinomas were the most responsive. Multiple treatments resulted in longer grwoth delays and greater tumor growth inhibition than did single treatments. No consistent difference in life span between the control and treated groups was measured, and only five of 188 treated animals were cured.
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PMID:Effects of local tumor hyperthermia on the growth of solid mouse tumors. 49 85

Because zinc is an essential nutrient for tissue growth, cellular division, protein synthesis, and DNA and RNA replication, it also ought to play a critical role in the growth of tumors. To test this thesis, a series of experiments were performed to test the effect of zinc deficiency on the lethality of a variety of solid and ascites tumors in mice and rats. Specifically, the following models were tested: Walker 256 carcinosarcomas, solid and ascites forms in rats; three mouse leukemias (L5178yf, L1210, and P388) in CDF, male mice; and Lewis lung carcinoma in C57BI/6 male mice. Rats receiving a zinc-deficient diet showed marked reduction of tumor growth, both of solid or ascites models, and this was accompanied by striking increase in survival. Survival of mice with transplanted leukemia was also significantly prolonged by zinc deficiency. In addition, growth of the Lewis lung carcinoma was inhibited, but the survival through increased, was probably limited by the adverse effects of zinc deficiency. The results suggest that tumor inhibition is a general effect of zinc deficiency, irrespective of cell type, cell growth rate, species, or site of growth. There are numerous potential applications of zinc metabolism to the diagnosis, therapy, and understanding of cancer.
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PMID:Implications of the inhibition of animal tumors by dietary zinc deficiency. 60 51


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