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)

A new tumor cell line, designated SU-CCS-1, was established from the malignant pleural effusion of a 16-year-old Caucasian girl with clear cell sarcoma. Morphological studies at the light- and electron-microscopic levels revealed similar features between the SU-CCS-1 cells and the primary tumor. Ultrastructural and cytochemical techniques showed that both the SU-CCS-1 cell line and the original tumor were amelanotic in nature. The malignant derivation of the SU-CCS-1 cell line was demonstrated by intracranial and s.c. heterotransplantation in the nude, athymic mouse and by cytogenetic analysis which showed that the cell line had a hypodiploid chromosome number and several karyotypic abnormalities. Live-cell radioimmunoassay procedures using a large panel of monoclonal antibodies directed against tumor-associated antigens revealed that, phenotypically, SU-CCS-1 closely resembled melanoma tumor cell lines. Immunological assays for the detection of neuroendocrine-associated peptides, hormones, and enzymes revealed that, like melanoma, the SU-CCS-1 cell line was actively producing alpha-melanotropin, S-100 antigen, and nerve growth factor. A notable difference between these tumor types was the capacity of SU-CCS-1 to produce bombesin, an active neuropeptide whose synthesis has been found in cell lines from patients with small cell carcinoma of the lung. From these studies, we concluded that the SU-CCS-1 cell line is phenotypically similar to melanoma, yet displays unique characteristics which distinguishes it from other sarcomas. The availability of an established clear cell sarcoma cell line will greatly facilitate further studies aimed at uncovering the histogenesis of this rare cancer.
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PMID:Use of a newly established human cell line (SU-CCS-1) to demonstrate the relationship of clear cell sarcoma to malignant melanoma. 636 60

The antitumor activity of 7-N-(p-hydroxyphenyl)mitomycin C (M-83) against 7 kinds of ascitic tumors and 4 kinds of solid tumors was compared with that of mitomycin C (MMC). M-83 showed more potent activities than MMC against ascites sarcoma 180, fibrosarcoma Meth 1, sarcoma Meth A, melanoma B-16, leukemia P388 and lymphoma EL4, by a single intraperitoneal injection. Furthermore, M-83 gave markedly higher chemotherapeutic ratio than MMC in these tumor systems. M-83 was also markedly effective against solid tumors of sarcoma 180, Meth 1, Meth A and Lewis lung carcinoma, by a single intravenous injection. M-83 gave lower myelo-suppression than MMC at the doses which gave almost equal inhibition on the tumor growth of solid Meth 1. M-83 and MMC significantly inhibited the growth of HeLa S3 cells. Cell growth was observed at 24 hours after addition of 3 X 10(-3) mM of drugs, but no growth was shown thereafter. M-83 inhibited more strongly the incorporation of the radioactive precursor into DNA than that into RNA or protein at the concentration of 3 X 10(-3) mM.
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PMID:Comparative antitumor activities of 7-N-(p-hydroxyphenyl)mitomycin C (M-83) and mitomycin C. 640 71

(2R,5R)-6-Heptyne-2,5-diamine hydrochloride (MDL 72175) is a new, potent, and selective inhibitor of mammalian ornithine decarboxylase. MDL 72175 given p.o. in drinking fluid reduced by 80% the growth of EMT6 sarcoma in mice and of HTC hepatoma in rats. It prolonged the survival of mice bearing L1210 or P388 leukemias and inhibited the development of Lewis lung carcinoma in mice at doses 10- to 20-fold lower than those of alpha-difluoromethylornithine, the most widely used irreversible inhibitor of ornithine decarboxylase. MDL 72175 depleted putrescine and spermidine levels in the tumors to the same extent as did alpha-difluoromethylornithine. In the EMT6 sarcoma, MDL 72175 achieved at low doses a greater maximal antitumor effect than did alpha-difluoromethylornithine. In combination therapy, MDL 72175 plus Adriamycin gave at least additive antitumor effects on solid tumors and experimental leukemias in animals. The combination MDL 72175 plus methylglyoxal bis(guanylhydrazone) also gave additive antitumor effects on P388 leukemia, associated with an increased uptake of methylglyoxal bis(guanylhydrazone); in contrast, antagonistic effects were observed with this combination on EMT6 tumors in mice. Since MDL 72175 did not present toxicity at effective antitumor doses, this new ornithine decarboxylase inhibitor can be considered as a promising antitumor drug.
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PMID:Antitumor properties of (2R,5R)-6-heptyne-2,5-diamine, a new potent enzyme-activated irreversible inhibitor of ornithine decarboxylase, in rodents. 643 61

The antitumor activity of a new derivative of nitrosourea, 3-[3-(2-chloroethyl)-3-nitrosoureido]-3-deoxy-D-glucopyranose (CNUG), against murine tumors was studied. CNUG showed remarkable antitumor activity against leukemias L1210 and P388, Lewis lung carcinoma, and sarcoma-180 (solid form). In particular, the majority of mice with leukemia or sarcoma-180 tumor were cured when they were given a single injection of CNUG on day 1 after tumor inoculation, and this treatment was more effective than daily treatment. CNUG was also active against sarcoma-180 grown in the brain, lung, liver or under the capsule of the kidney, and even against autochthonous lung tumor induced by 1-ethyl-1-nitrosourea. The number of peripheral leucocytes was depressed by the treatment with CNUG but this depression was less than that with 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea.
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PMID:Antitumor effect of 3-[3-(2-chloroethyl)-3-nitrosoureido]-3-deoxy-D-glucopyranose on murine tumors. 645 68

It has been proposed that the elimination of excess scar tissue from the body is achieved by specialized killer cells, which are activated by vascular changes in the scar tissue. The malignant tumor is, according to this theory, considered to be a special type of excess scar tissue of fetal or near fetal age, the fetal blood supply of which prevents the activation of those specialized killer cells which were believed to eliminate excess scar tissue. Therefore, it is assumed that if the specialized killer cells of a malignant tumor patient are activated artificially, they would cause malignant tumor regression in vivo. This method of treatment is called autobiotherapy because it utilizes biological products from the patient to treat his own malignant tumor. Preliminary evidence is presented in support of autobiotherapy of malignant tumor disease.The peripheral leucocytes of 27 malignant tumor patients were activated separately by incubation in a serum-free medium containing the respective tumor cells or material. The effect of the injection of the activated leucocytes or their products, termed tumor leucocyte cultures (TLC), was studied in five patients with Kaposi sarcoma, five with carcinoma of the breast, four with carcinoma of the cervix, three with soft tissue sarcoma, two with carcinoma of the lung, two with carcinoma of the maxillary antrium, and a miscellaneous group of six patients. In 52 percent of cases, there was significant tumor regression. Tumor regression was most marked in patients with Kaposi sarcoma, carcinoma of the cervix, pharynx, and pancreas, one patient with a slow growing fibrosarcoma, one patient with a metastatic breast carcinoma, and also in one patient with myelogenous leukemia. However, not all the types of tumor studied responded satisfactorily to autobiotherapy. The reasons for the differences in response to autobiotherapy remain to be determined. Even so, the positive results obtained indicate that autobiotherapy is worthy of further research as an alternative in controlling malignant tumor disease.
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PMID:Clinical experience with autobiotherapy of malignant tumor disease: a preliminary report. 645 8

Incorporation of cholesterol hemisuccinate (CHS) into the membrane of tumor cell rigidifies the lipid layer, exposes cryptic antigens, and enhances immunogenicity. The local growth and metastatic spread of the 3LL Lewis lung carcinoma were studied in conjunction with immunizations by CHS-enriched 3LL cells. C57BL/6J mice received 2 consecutive immunizations with 10(7) CHS-treated, irradiated (10,000 rad) 3LL cells. Two control groups were immunized with MCA-102 sarcoma cells or CHS-enriched syngeneic spleen cells. All groups were challenged with viable 3LL cells after immunizations. Mice pre-immunized with CHS-enriched 3LL cells showed a delayed tumor growth after subsequent challenge with 3LL. Effect of immunization on the growth of established tumors was examined in 3LL-bearing mice which were treated with 10(7) CHS-enriched tumor cells on days 1-12 after initial tumor implantation. A second identical immunotherapy was given 6 days after the first immunization. Tumor growth was significantly inhibited in mice which received the first immunization 1 day after tumor implantation, while immunization on day 3 or after inhibited the growth rate to a lesser extent. Suppression of pulmonary metastases was assessed after excision of a primary 3LL tumor growing in the foot pad which had reached 8 mm in diameter. Immunization consisted of intraperitoneal injection of 10(7) irradiated CHS-enriched tumor cells following excision and repeated after 6 days. This immunization resulted in a significant decrease in pulmonary metastasis as scored by direct counts of metastatic nodules, by [125I]iododeoxyuridine (125IUdR) incorporation, and by lung weight. Metastatic 3LL cells from nodules which survived immune elimination were isolated and implanted into mice which were pre-immunized with primary 3LL cells enriched with CHS. For comparison, a group of mice was immunized and challenged with primary 3LL cells. Inhibition of tumor growth and pulmonary metastasis formation was observed only in the mice which were challenged with the primary tumor.
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PMID:Inhibition of growth and metastases in mice by immunization with cholesterol hemisuccinate-enriched tumor cells. 650 34

This work makes a brief summary of the scientific research carried out during the last fifteen years (1968-1982) in the Department of Biology and Biochemistry of Cancer (AISN, Department of Health and Consumption), identified with the Coordinated Center of Oncological Biochemistry of the CSIC (Department of Education and Science), with the valuable help of the Spanish Association Against Cancer (AECC) the first five years 1968-1972), and of the Scientific Foundation of the AECC the following ten years (1973-1982). A brief mention of the research work carried out between 1945 and 1967 is made before referring to the work done between 1968-1982. The researchers of the Department have done important studies in the fields of biochemistry, molecular biology, virology and immunology of cancer. They described for the first time the existence of immunological processes in ontogenic evolution and cell differentiation; the transfection with DNA from several kinds of tumors, including a mouse sarcoma induced by 20-methylcholanthrene (now 3-methylcholanthrene) and a human lung carcinoma; the evolution of the humoral immunological response in SWR and AKR mice along the whole life; the isolation of a polytumoral DNA virus; the carcinogenic activity of viral DNA; the establishment of a virus-transformed cell line "in vitro", the incorporation of the viral genome to the cell genome; the reverse transcription; the antiblastogram, an "in vitro" predictive assay of anti-cancer chemotherapy agents; and the isolation of tumor-specific and tumor-associated antigens.
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PMID:[15 years' cancer research at the Department of Cancer Biology and Biochemistry]. 654 81

The effect of RA233 alone or in combination with radiation was investigated in vivo on the S180 sarcoma, the B16 melanoma and the Lewis lung carcinoma. The combined treatment was a significant improvement over radiation alone for the B16 and S180 tumours. RA233 alone did not influence the growth of these tumours. When the primary 3LL was irradiated, tumour size was unaffected but the number of pulmonary metastases was reduced. They were further reduced by the combination of RA233 and radiation. The number, volume and cytokinetics of the B16 cells and the 3LL cells were affected to varying degrees by RA233. The significance of these changes relative to the effects of RA233 are discussed.
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PMID:Antitumor effect of RA233 alone and combined with radiotherapy. 654 97

Three distinct transforming genes present in human tumor cell lines are all related to the viral oncogenes of Harvey and Kirsten murine sarcoma viruses, designated v-H-ras and v-K-ras, respectively. The transforming gene of a bladder carcinoma cell line has been shown to be a human homolog to v-H-ras [Parada, L. F., Tabin, C. J., Shih, C. & Weinberg, R. A. (1982) Nature (London) 297, 474-478; Santos, E., Tronick, S. R., Aaronson, S. A., Pulciani, S. & Barbacid, M. (1982) Nature (London) 298, 343-347]. The transforming gene common to one colon (SK-CO-1) and two lung carcinoma (SK-LU-1 and Calu-1) cell lines is the same human homolog of v-K-ras as is the transforming gene previously identified in a lung carcinoma cell line Lx-1 [Der, C. J., Krontiris, T. G. & Cooper, G. M. (1982) Proc. Natl. Acad. Sci. USA 79, 3637-3640]. The transforming gene of SK-N-SH neuroblastoma cells is weakly homologous to both v-H-ras and v-K-ras. NIH 3T3 cells transformed with the SK-N-SH transforming gene contain increased levels of a protein serologically and structurally related to the protein products of the v-H-ras and v-K-ras genes. Therefore, it represents a third member of the ras gene family, which we have called N-ras. Based on the homology with the v-ras genes, we have established the orientation of transcription and approximate coding regions of the cloned human K-ras and N-ras genes.
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PMID:Three human transforming genes are related to the viral ras oncogenes. 657 64

This paper demonstrates that lectin-activated lymphocytes of selected mouse strains can lyse fresh autologous or allogeneic tumor cells but not the fresh normal cells tested in short-term 51Cr release assays. Murine splenocytes, incubated with concanavalin A for 3 days, lysed tumor cells from fresh syngeneic P815 mastocytoma, 102 methylcholanthrene sarcoma, and FBL3 lymphoma; fresh allogeneic 3LL lung carcinoma and MethA sarcoma; and tissue-cultured YAK cells in 18-hr51Cr release assays. Natural killer cells in fresh splenocyte preparations only lysed tissue-cultured YAK cells and not the other targets. Syngeneic and allogeneic lymphoblasts, lung, or liver cells were not lysed by the concanavalin A-activated killer (CAK) cells. The induction of cytotoxicity by concanavalin A incubation was abrogated by alpha-methylmannoside in the 3-day incubation, but not in cytotoxicity assay. Radiosensitive cells and adherent cells were necessary for the generation of CAK cells. The CAK effectors themselves were radioresistant, nonadherent, and mostly Thy 1+ and Ly 2+. The CAK phenomenon may be mediated by lymphokine production by an Ly 1+ cell, since depletion of Ly 1+ cells prior to activation abrogates CAK induction, and the ability of numerous mouse strains (and nude mice) to generate CAK cells correlated with their ability to produce Interleukin 2. The biological and therapeutic role of these cells is currently being investigated in murine syngeneic primary and metastatic tumor models.
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PMID:Lysis of fresh natural killer-resistant tumor cells by lectin-activated syngeneic and allogeneic murine splenocytes. 664 May 24


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