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 antitumour activity of the alkaloid thaliblastine was studied on 7 ascitic and solid transplantable tumours in mice. It was found that the compound has a pronounced antitumour effect on ascitic tumour of Ehrlich, NK/Ly lymphoma (i.p.), sarcoma 37 (s.c. and i.p.), sarcoma 180 (s.c.) and Lewis lung carcinoma (i.m.). With a number of tumours, it was found that the single and intermittent drug administration exerts a better therapeutic effect than the chronic treatment.
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PMID:Effect of thaliblastine on transplantable tumours in mice. 13 2

A phase I clinical study was done with quelamycin, a recently synthesized triferric derivative of adriamycin. Twenty-one good-risk patients were studied: 19 patients with non-small cell carcinoma of the lung and two patients with metastatic sarcoma. Acute toxicity occurred in all patients and consisted of high fever, flushing, hypertension, generalized body aches, tremors, and confusion, which lasted 3-6 hours. Potentially dangerous cardiotoxicity occurred in eight patients who had previous minor rhythm disturbances, and was characterized by tachycardia, atrial extrasystoles, atrial fibrillation, and branch block which lasted 6-14 hours. The dose-limiting hematologic toxicity was found to occur at 125 mg/m2 iv single-dose. Objective responses were observed in three of 19 patients with lung cancer and in one patient with metastatic osteogenic sarcoma resistant to adriamycin therapy. In conclusion, quelamycin is a new derivative of adriamycin with potential interest. However, the acute generalized toxicity and the immediate cardiotoxicity found in the presently used schedule are excessive. Further studies directed to suppress these side effects are in progress.
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PMID:Phase I clinical study of quelamycin. 36 Dec 26

A novel nitrosourea derivative, methyl-6-[[[(2-chloroethyl)nitrosoamino]carbonyl]-amino]-6-deoxy-alpha-D-glucopyranoside (MCNU), is a water-soluble compound in which a methoxyl group is attached to the C-1 position and an N-(2-chloroethyl)-N-nitrosoureido group is attached to the C-6 position of the glucose moiety. MCNU exhibited a marked life-prolongation or growth-inhibitory effect against mouse L1210 leukemia, adenocarcinoma 755, Nakahara-Fukuoka sarcoma, Lewis lung carcinoma, and B16 melanoma. Ip, oral, or iv administration of MCNU was markedly effective against L1210 leukemia, and the therapeutic ratio by ip administration was larger than that of chlorozotocin or CCNU. The life-prolongation effect of MCNU against established Lewis lung carcinoma was similar to that of methyl-CCNU. The bone marrow toxicity of MCNU was less than that of CCNU but considerably more than that of chlorozotocin.
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PMID:Biologic activity of MCNU: a new antitumor agent. 46 55

The character of metastasis of 9 strains of transplantable mouse tumours in conventional subcutaneous inoculation was studied. There were differences in the frequency, intensity, and types of metastasis of different tumours. Periods of onset of metastases of Lewis lung carcinoma and RL-67, and also of sarcoma-37 were established. Sarcoma, Lewis and RL-67 lung carcinomas, adenocarcinoma of the colon AKATOL, Cloudman's melanoma and B-16 metastasized most intensively. Sarcoma-37 metastasizing into the regional and remote lymph nodes, Lewis lung carcinoma and melanomas metastasizing into the lungs, RL-67 lung carcinoma metastasizing into the lungs, kidneys, adrenal glands, ovaries, the heart, and also adenocarcinoma of the colon AKATOL metastasizing into the lymph nodes and the liver can be used as models for the research in the field of drug action upon metastases and the metastasis process.
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PMID:[Frequency, time and type of metastasis of different transplantable tumors in mice]. 56 18

The procoagulant activity of cells from some experimental tumours isolated in culture or in single-cell suspensions from ascitic fluid was investigated. Cells from Lewis lung carcinoma (primary and metastasis), Ehrlich carcinoma ascites and JW sarcoma ascites were able to shorten markedly the recalcification time of normal, Factor VIII- and Factor VII-deficient but not of Factor X-deficient human plasma. The same cells generated thrombin when mixed with a source of prothrombin and Factor X, absorbed bovine serum (as a source of Factor V), phospholipid and calcium chloride. Thrombin formation was not influenced by the presence of Factor VII. Cells from Sarcoma 180 ascites were completely inactive in both test systems. It is concluded that cells from some experimental tumours have the capacity to activate Coagulation Factor X directly. These findings suggest the existence of an alternative "cellular" pathway in the initiation of blood clotting distinct from both the intrinsic and extrinsic mechanisms.
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PMID:Evidence that cells from experimental tumours can activate coagulation factor X. 57 31

The effector arm of antibody-dependent cellular cytotoxicity (ADCC) was evaluated using 51Cr-labelled chicken erythrocytes as targets in BALB/c mice transplanted with the Moloney sarcoma virus-induced tumours T-MSV and MS2, and in C57BL/6 mice transplanted with the chemically induced FS6 sarcoma, Lewis lung carcinoma and B16 melanoma. Tumour-bearing animals showed higher levels of ADCC than normal mice, a stimulation confirmed in MS2-bearing mice, using SL2 lymphoma cells as targets in a cytostasis assay. ADCC effector-cell capacity was higher in animals transplanted with the immunogenic, spontaneously regressing T-MSV than in mice bearing the poorly immunogenic metastasizing MS2 sarcoma. The increased ADCC activity detectable in the spleen of tumour-bearing hosts was not abolished by removal of phagocytic-adherent cells.
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PMID:Activation of K cells in mice with transplanted tumours differing in immunogenicity and metastasizing capacity. 58 12

Thirteen experimental mouse neoplasms were tested by cytidine (CR)-deaminase and deoxycytidine (dCR)-kinase levels. Four neoplasms, Sarcoma T241, Adenocarcinoma E0771, Lewis lung carcinoma (LL), and Sarcoma 180 Japan (S180J), considered to have high deaminase and sufficient dCR-kinase activities, were tested in vivo for combination chemotherapy with cytosine arabinoside (ara-C) and the CR-deaminase inhibitor, tetrahydrouridine (THU). THU did not significantly improve the growth inhibition of ara-C in a wide range of combinations in T241, E0771, LL, and the solid form of S180J, but more than doubled the survival time of the S180J ascites-bearing animals. Toxicity in the form of weight loss and toxic deaths was observed in some but not all groups, especially at high dosages of ara-C and THU. Tissue distribution of [3H]-ara-C and [14C]-THU in T241-bearing mice revealed an accelerated clearance of ara-C-derived radioactivity under the influence of THU in the tumor and five host tissues, but not in the small intestines. With the exception of the small intestines, clearance of THU-derived radioactivity was faster in all tissues studied compared to the clearance of [3H]-ara-C-derived radioactivity. Intracellular CR-deaminase levels were inhibited significantly, ie, dose dependent, in tumor and host kidney after a single ip injection of THU to E0771--bearing mice. In the solid S180J, with or without simultaneous ip administration of THU, [3H]-ara-C was not converted to 5'-di- and tri-phosphates at all. In mice bearing the ascites form of S180J, [3H]-ara-C was extensively converted to ara-C 5'-di- and tri-phosphates. THU increased both overall ara-C-derived radioactivity and the relative amounts of ara-C 5'-di- and tri-phosphates.
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PMID:Combinations of tetrahydrouridine and cytosine arabinoside in mouse tumors. 58 1

RNA biosynthesis catalyzed with DNA-dependent RNA polymerase was demonstrated in the reconstructed system containing isolated lymphocyte nuclei, Mg2+ or Mn2+ salts, ammonium sulphate, in the presence of four nucleosidetriphosphates. Both the Mg2+ and Mn2+-dependent forms of this enzyme were revealed in the nuclei of normal lymphocytes and those of patients suffering from melanoma, carcinoma of the lung and sarcoma. The activities of both forms of RNA-polymerase were greater in the nuclei of the lymphocytes from sick individuals than in the normal analogues. DNA-dependent RNA-polymerase sensitivity to dexamethasone and PHA of the nuclei of lymphocytes obtained from patients with carcinoma of the lung, melanoma, and sarcoma was decreased in comparison with the normal.
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PMID:[Sensitivity of the lymphocyte RNA-synthesizing system of patients with different malignant neoplasms to phytohemagglutinin and dexamethasone]. 85 72

Growth of tumors was inhibited or enhanced in mice by a synthetic (pyran) or a biologic (corynebacterium parvum) immunopotentiator. Marked inhibition of leukemogenesis induced by Friend leukemia virus was produced by prophylactic intraperitoneal treatment with pyran, while intravenous treatment with pyran (in the same dose and regimen) significantly enhanced growth of tumor virus. Paradoxical effects were also seen with the biologic immunopotentiator C. parvum in solid tumor systems. Treatment with C. parvum either potentiated disease or had no effect on the life span of most mice bearing the Lewis lung carcinoma. In contrast, the same treatment could produce a high percentage of tumor regressions in mice bearing the MCA 2182 sarcoma, although the effect was somewhat variable. These data, which show that a change in route of drug administration or in the type of tumor treated may reverse the effect of treatment, emphasize that the mechanism of action of immunopotentiators must be elucidated before consistent beneficial treatment of tumor viruses or tumors can be achieved.
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PMID:Paradoxical effects of immunopotentiators on tumors and tumor viruses. 93 3

Changes in in vitro lymphocyte-stimulation protein synthesis (SPS) of 40 melanoma patients following incubation with 3M KCl extracts of allogenic melanoma, lung carcinoma, and sarcoma antigens and phytohemagglutinin (PHA) were quantitated by measuring H-3-leucine uptake. One of eleven "untreated" melanoma patients stimulated significantly to the melanoma antigen. However, this lymphocyte response was not significantly different from that of the normal subjects. Patients who received systemic bacillus Calmette-Guerin (BCG) by the tine technique for 3 months and for 6 months had significant increase in lymphocyte protein synthesis following incubation with melanoma antigen. There were no significant differences in PHA responses between the "untreated" melanoma patients and the BCG-treated group. Testing of serial lymphocyte samples from nine melanoma patients before treatment and at monthly intervals thereafter confirmed these observations. Furthermore, no change in serial complement-fixing antibody titers to melanoma antigen was noted in the BCG-treated patients. These results demonstrated that in vitro lymphocyte responses to melanoma antigen may be augmented by BCG therapy.
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PMID:Effect of bacillus Calmette-Guerin immunotherapy on tumor antigen-induced lymphocyte-stimulated protein synthesis in melanoma patients. 113 1


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