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)

We treated a patient with undifferentiated carcinoma of the lung, with osteoclast-like giant cells resembling those of the giant cell tumor of bone. The clinical and morphologic characteristics of this case are documented, and the literature concerning this type of tumor is reviewed. The tumor differed histologically from the pleomorphic carcinoma, which occurs most commonly in the lung, and showed diverse pleomorphic manifestation with benign looking osteoclast-like multinucleated cells and bizarre giant cells. In addition, and undifferentiated carcinoma with a sarcoma-like appearance containing small areas of papillary adenocarcinoma was evident in the tumor.
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PMID:Undifferentiated carcinoma of the lung with osteoclast-like giant cells. 362 16

Over a 2-month period, 40 patients with untreated malignancy were studied for protein-C (PRC), antithrombin-III (AT-III), fibrinopeptide A (FPA), routine hemostatic screens, and presence of liver metastases to determine pretreatment changes of hemostasis and relate them to subsequent development of thrombotic or hemorrhagic complications. These patients were observed for a mean period of 18 months. There were 23 males and 17 females with a median age of 64 years. Nine patients had lung carcinoma, 8 colon carcinoma, 7 lymphoma, 5 breast carcinoma, 5 head and neck carcinoma, 2 acute leukemia, 2 prostate carcinoma, 1 adenocarcinoma of unknown primary, and 1 sarcoma. Eight patients had liver metastases. PRC was measured by ELISA, AT-III by radial immunodiffusion, and FPA by RIA. Four patients had decreased AT-III, 28 had decreased levels of PRC, and 39 had elevated levels of FPA. All patients with liver metastases had low PRC. Albumin levels were lower in patients with low PRC (mean 3.3 g/dL v 4.0 g/dL for others). Eight patients, five with liver metastases, developed thrombotic (4), hemorrhagic (3), or both (1) complications. Statistically significant associations were found between (1) presence of liver metastases and development of thrombotic and hemorrhagic complications (P less than .001), (2) presence of liver metastases and decreased PRC (P = .001), and (3) lower albumin levels and decreased PRC (P = .0001). Our study documents early changes of hemostasis in untreated malignancy. We extend previous observations that decreased PRC levels in malignancy may be due to poor synthetic functions of liver. Presence of liver metastases was the only factor associated with subsequent development of thrombotic and hemorrhagic complications. Biochemical markers of hemostatic abnormalities, even though encountered frequently at the time of presentation, are of little predictive value for development of thrombotic and hemorrhagic complications.
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PMID:Hemostatic abnormalities in untreated cancer: incidence and correlation with thrombotic and hemorrhagic complications. 368 81

PSK is a protein-bound polysaccharide prepared from cultured mycelium of the Basidiomycete Coriolus versicolor. Effects of PSK on the immunologic responsiveness in tumor-bearing animals were investigated using syngeneic or allogeneic tumors in mice (Lewis lung carcinoma, B16 melanoma, Meth A fibrosarcoma, adenocarcinoma 755, X5563 plasmacytoma, colon 26, MOPC 31C myeloma, sarcoma 180 and Ehrlich carcinoma), rats (BC47 bladder carcinoma, Walker 256 sarcoma and AH7974 hepatoma), hamsters (HA-1T tumor and RPMI 1846 melanoma), guinea pigs (line-10 hepatoma) and rabbit (VX2 and VX7 tumor). Oral or intraperitoneal administration of PSK restored the depressed delayed hypersensitivity against sheep erythrocytes to a normal level in these tumor-host systems. Also, oral administration of PSK lowered the activity of immunosuppressive substances in the serum of tumor-bearing animals. These results suggest that PSK exhibits antitumor effects by restoring the depressed immunologic responsiveness in tumor-bearing animals.
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PMID:[Restoration of immunologic responsiveness by PSK in tumor-bearing animals]. 378 58

Plasminogen activator (PA; urokinase) levels were studied in metastatic and nonmetastatic clones of the Lewis lung carcinoma (3LL) and of the T10 sarcoma. Tests of clones grown in vitro revealed that the cell content and secretion of PA correlated positively with the metastatic capacity of the clones of both tumors. When cell-associated activities were examined in cloned cell populations grown subcutaneously in vivo, the apparent activities in the solid tumors produced by low-metastatic clones were equal to or even higher than those in solid tumors produced by high-metastatic clones. This finding was attributed to the observation that solid tumors produced by low-metastatic clones, but not those produced by high-metastatic clones, were highly infiltrated with macrophages. Subsequent tests indicated that the ip inoculation of X-irradiated or mitomycin-treated tumor cells of low-metastatic clones elicited a significantly greater peritoneal infiltration of macrophages than did tumor cells of high-metastatic clones. Such "tumor-associated" macrophages manifested high levels of PA, whereas resident (nonactivated) peritoneal macrophages did not. These findings suggest that although PA may cause the initial detachment from the local tumor of both nonmetastatic (via the macrophage PA) and metastatic cells (via their own PA), the PA secreted by the metastatic cells may enable them to complete subsequent stages of the metastatic process that may be PA-dependent.
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PMID:Proteolytic enzymes in tumor metastasis. I. Plasminogen activator in clones of Lewis lung carcinoma and T10 sarcoma. 385 89

The current report presents the data of the Division of Cancer Treatment of the National Cancer Institute (NCI) on the antitumor activity of the anthracycline antibiotic 4'-epidoxorubicin in experimental tumor systems. Direct comparisons are made with doxorubicin in individual experiments, and the data are related to those of earlier studies in the form of a review of experimental activity, in order to assess the relative activity of 4'-epidoxorubicin and doxorubicin. The experimental test models utilized by the NCI for these studies included the leukemias P388 and L1210, B-16 melanoma, Lewis lung carcinoma, the colon tumors 26 and 38, and the mammary tumors CD8F1 and C3H16/C. The human tumors growing in xenograft in athymic mice included the models LX-1 lung tumor, CX-1 colon tumor, and MX-1 mammary tumor. Additional comparisons were made with the tumor models Gross leukemia, sarcoma 180, MSV-induced sarcoma, MS-2 tumor, and a variety of human tumors growing in athymic mice, as well as with in vivo toxicologic and in vitro cytotoxicity models. Although for 4'-epidoxorubicin there is only a minimal alteration of the configuration of the doxorubicin molecule, quantitative comparison of 4'-epidoxorubicin and doxorubicin revealed not only similarities but also differences in biological activity. Both drugs showed activity against a broad spectrum of experimental tumors, with 4'-epidoxorubicin more effective against some tumors and equally effective against others. 4'-Epidoxorubicin evidenced less toxicity than doxorubicin in both acute and chronic toxicity studies with retention of therapeutic effectiveness and showed reduced cardiotoxicity. With 4'-epidoxorubicin there resulted a higher therapeutic index and therapeutic ratio, permitting the use of higher dosage and a greater margin of safety. The preclinical differences in therapeutic and toxicologic manifestations of 4'-epidoxorubicin, reflecting apparent alterations in pharmacologic properties and mode of action in comparison with doxorubicin, support the broad spectrum clinical trials of this already-demonstrated clinically active drug.
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PMID:The effectiveness of the anthracycline analog 4'-epidoxorubicin in the treatment of experimental tumors: a review. 388 88

Although weight loss has an adverse impact on cancer patient survival, the ability of caloric provision via total parenteral nutrition (TPN) to favorably influence outcome in chemotherapy-treated populations is not established. In randomized trials, no significant improvement in either response or survival was associated with TPN addition to chemotherapeutic treatment of adult patients with lymphoma, sarcoma, colon cancer, adenocarcinoma and small cell carcinoma of the lung, or testicular carcinoma. In two instances, TPN addition was associated with decreased survival, again raising the concern that caloric support in the absence of effective antitumor therapy might stimulate cancer growth. In any event, the hypothesis that nutritional repletion of a malnourished cancer patient receiving chemotherapy will improve clinical outcome remains to be critically tested, as studies demonstrating sequential improvement in lean body mass have not been reported. Most recently, consideration of potential mechanisms underlying the development of cancer cachexia has led to new strategies for nutritional intervention. For example, hypogonadism or low testosterone levels have been described in male patient populations with advanced cancer and correlated with weight loss and adverse outcome, leading to trial of replacement therapy with nandrolone decanoate. Similarly, the frequent identification of abnormal glucose metabolism in the patients with cancer cachexia has stimulated clinical trials with agents such as hydrazine sulfate and insulin designed to reverse the metabolic abnormality. Whether such efforts designed to alter metabolic abnormalities associated with cancer cachexia will improve clinical outcome will be determined in ongoing clinical trials.
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PMID:Critical evaluation of the role of nutritional support with chemotherapy. 391 60

TSP-180 is a Mr 180,000 cell surface protein found on several murine lung carcinomas but not on fibroblast or sarcoma cell lines. Monoclonal antibody 135-13C binds to TSP-180 with high affinity but could not be used to quantitate the protein in tumors and normal tissue (Cancer Res., 41: 3465-3470, 1981). TSP-180 was purified from a transplantable BALB/c carcinoma (line 1 cells) by immunoaffinity chromatography and used as an immunogen to produce another monoclonal antibody (346-11A) to a different epitope on the molecule. A two-site solid-phase radioimmunoassay for TSP-180 was developed to quantitate TSP-180 in tissue extracts. The assay can detect as little as 3 ng of TSP-180 in samples up to 10 mg of protein. Analyses of several lung carcinoma cell lines confirmed that TSP-180 is present in all (five of five) cell lines ranging from 40 to 800 ng per mg of cell protein extract. Mouse tissues from normal and tumor-bearing mice were analyzed for TSP-180. Values for line 1 tumors growing i.m. were about 70 ng of TSP-180 per mg of protein. Normal tissue from normal and tumor-bearing mice contained low levels of TSP-180 from less than 0.3 ng/mg of protein for liver to a high of about 11 ng/mg of protein for leg muscle. Finally, small benign urethane-induced adenomas (1 to 2 mm) from BALB/c mice had moderate amounts of TSP-180 (11 ng/mg of protein), while two primary lung adenocarcinomas in the same animals had 20 and 47 ng/mg of protein, respectively, suggesting that TSP-180 expression may increase with increasing cancer of these tumors. Analyses of individual urethane-induced lung tumors from A/J mice showed that 11 of 13 carcinomas had high levels of TSP-180, while only 1 of 6 adenomas had a detectable amount of TSP-180, and that was at a moderate level. Specific quantitation of tumor markers in normal, benign, and malignant lung tissue may be helpful in identifying different levels of gene expression as tumors progress to more malignant states.
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PMID:Tumor antigen on benign adenomas and on murine lung carcinomas quantitated by a two-site monoclonal antibody assay. 394 Jun 37

The antitumoral activity and metabolism of 1-(4-acetylphenyl)-3,3-dimethyltriazene [pAc-(CH3)2] and 1-(4-acetylphenyl)-3,3-diethyltriazene [pAc-(C2H5)2] were studied in mice. pAc-(CH3)2 showed significant antitumoral activity against M5076 ovarian reticular cell sarcoma, L1210 leukemia, EL 4 lymphoma in mice, but not against Lewis lung carcinoma. pAc-(C2H5)2 was inactive in all these murine tumors and was much more toxic than pAc-(CH3)2. pAc-(CH3)2 and pAc-(C2H5)2 were rapidly metabolized in vitro and in vivo to their respective monoalkyltriazenes and to 4-aminoacetophenone (pAc-NH2). In vitro, 79% of the dimethyltriazene was metabolized to its monomethyl analogue, but only 27% of the diethyltriazene was metabolized to the monoethyltriazene. The monoalkytriazenes were almost completely biotransformed to pAc-NH2 by a 9000 g liver fraction. The metabolic pattern in the in vitro study was comparable to that found in vivo.
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PMID:Comparison of metabolism and activity of an aryldimethyltriazene and an aryldiethyltriazene. 394 96

Histological description of human cancer strains (lung carcinoma, laryngeal cancer, Jewing's sarcoma, fibrosarcoma, Wilms' tumor, renal carcinoma) transplanted into 6- to 8-week-old nude mice and 4- to 6-week old nude rats is presented. Human origin of these strains is proved by an analysis of lactate dehydrogenase isoenzymes. The growth rate of human cancer strains in rats is considerably higher than in mice.
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PMID:[Human tumor lines transplantable to athymic mice and rats]. 397 Oct 37

8-Carbamoyl-3-(2-chloroethyl)imidazo[5,1-d]-1,2,3,5-tetrazin-4(3H) -one (mitozolomide) demonstrates curative action against a range of murine tumor model systems. At single doses of between 20 and 40 mg/kg, the latter of which approximates the 10% lethal dose value in mice, the compound elicited cures against the L1210 and P388 leukemias irrespective of the route of tumor and/or drug administration; in these tests, animals receiving 10(5) cells i.p. survived greater than 60 days after treatment. Potent effects were also observed against the TLX5 lymphoma (s.c.) and B16 melanoma (i.p.). In other experiments, 7 of 10 animals implanted with 2 X 10(5) Lewis lung carcinoma cells survived greater than 60 days while 10 of 10 animals survived greater than 60 days after implantation of the Colon 26 tumor. Potent inhibition of the solid tumor models was also observed with complete cures of the Colon 38, M5076 sarcoma, and ADJ/PC6A plasmacytoma. In cross-resistance studies, the compound was ineffective against an L1210 leukemia made resistant to 1,3-bis(2-chloroethyl)-1-nitrosourea and against a TLX5 lymphoma resistant to dimethyltriazenes but cured animals bearing the L1210 leukemia with derived resistance to cyclophosphamide.
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PMID:Experimental antitumor activity against murine tumor model systems of 8-carbamoyl-3-(2-chloroethyl)imidazo[5,1-d]-1,2,3,5-tetrazin-4(3 H)-one (mitozolomide), a novel broad-spectrum agent. 400 40


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