Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on the clinico-morphological estimation of scannograms, performed by means of sodium selenite--selenium-75, chloromercury-197 and gallium citrate-67 in 231 patients with tumor (185) and nontumor (46) lung diseases, it was found that the best results were obtained in scannographic visualization of primary tumors of the lung (87%). Positive scintigraphy was found to be of high diagnostic value in recognition of lung cancer proceeding against the background of atelectasis, inflammatory processes and other "disguises" hampering the clinico-roentgenological diagnosis. Positive scintigraphy may be employed in establishing the differential diagnosis between malignant and benign lung tumors.
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PMID:[Positive scintigraphy in the diagnosis of lung cancer]. 88 14

Mechanisms contributing to reduced cytotoxic drug accumulation were studied in two multidrug-resistant (MDR) human lung cancer cell lines without P-glycoprotein expression. In these (non-small cell) SW-1573/2R120 and (small cell) GLC4/ADR MDR cells, the steady-state accumulation of [14C]daunorubicin was 30 and 12%, respectively, of that in the parent cells. When cells, at steady state, were permeabilized with digitonin, the amount of daunorubicin binding increased only in the resistant cells. The reduced accumulation of daunorubicin in the SW-1573/2R120 and GLC4/ADR cells was accompanied by a lower initial (2 min) uptake rate of this drug. No difference in initial efflux rate of daunorubicin from preloaded cells could be detected between sensitive and resistant SW-1573 cells. However, daunorubicin was extruded 5-fold faster from GLC4/ADR cells than from the parental cells. In the presence of the energy metabolism inhibitors sodium azide and deoxyglucose, the reduced daunorubicin accumulations in the SW-1573/2R120 and GLC4/ADR MDR cells were (almost) completely reversed. The effects of these inhibitors on drug uptake were already apparent during the earliest measured time points (less than 15 s). Also, the enhanced efflux of daunorubicin from GLC4/ADR cells was inhibited. In ATP-depleted cells, the intracellular pH was lowered by approximately 0.3 units in resistant as well as in sensitive cells. The lower intracellular pH, however, could not account for the increase in daunorubicin accumulation in the resistant cells. Also, for vincristine and etoposide, the increases in drug accumulation under energy-deprived conditions were more pronounced in the resistant SW-1573/2R120 cells than in the parent SW-1573 cells. These results suggest that accumulation of drugs in the non-P-glycoprotein MDR human lung carcinoma cell lines SW-1573/2R120 and GLC4/ADR is reduced by an energy-dependent drug export mechanism which prevents efficient transport of drug to the target. Since P-glycoprotein expression in lung tumors is generally low, these MDR lung cancer cell lines can be used as a model to study alternative mechanisms leading to multidrug resistance in this tumor type.
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PMID:Energy-dependent processes involved in reduced drug accumulation in multidrug-resistant human lung cancer cell lines without P-glycoprotein expression. 130 22

We examined a serum-free medium (designated as TYI 101) for the generation of lymphokine-activated killer (LAK) cells from human lymphocytes, regional lymph node lymphocytes (RLNL) and peripheral blood lymphocytes (PBL). TYI 101 medium consisted of, in addition to nutrient mixture, transferrin, insulin, fetuin, sodium selenite, 2-mercaptoethanol, o-phosphorylethanolamine, chick egg yolk and porcine kidney extract. These hormones were effective for supporting RLNL proliferation as assessed by (3H)-thymidine uptake. When human lymphocytes from two different sources were cultivated with recombinant interleukin 2 (rIL-2) in TYI 101 medium, LAK activity was generated. In cultures of PBL from a healthy donor, LAK cells were generated in TYI 101 medium as efficiently as in RPMI 1640 medium supplemented with 10% human AB-type serum (RPMI-AB). In cultures of RLNL from lung cancer patients, LAK activity obtained in TYI 101 medium was about sixty-five percent of that in RPMI-AB. However, the addition of a small amount of AB-type serum improved the generation of LAK activity, LAK cell expansion, and cell viability in TYI 101 medium. We conclude that TYI 101 medium can be used for the generation of LAK cells from human lymph node lymphocytes with supplementation of none or only a reduced amount of human serum.
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PMID:Studies of serum-free medium for the generation of lymphokine-activated killer cells. 136 99

Plasma and IgG obtained from 10 Lambert-Eaton myasthenic syndrome (LES) patients (5 with carcinoma, 5 without associated cancer), 6 healthy subjects, and 1 patient with small-cell lung cancer (SCLC) were examined in their ability to recognize chromaffin cell antigens on Western blots. The pattern of antigen recognition was compared with the magnitude of inhibition of voltage-dependent calcium and sodium currents recorded with the patch-clamp technique from chromaffin cells. Eight of the 11 patients with LES and/or SCLC recognized plasma membrane proteins and 9 of the patients' IgG interacted with cytoplasmic antigens with no apparent pattern of antigen recognition between patients. Also, there was no obvious band pattern distinguishing patients with LES from those with LES and concurrent SCLC. Eighty percent of the LES patients' antibodies were capable of reducing the calcium current (ICa) in chromaffin cells. One of the novel findings of this study is that 30% of the patients had produced antibodies which were able to inhibit both calcium and sodium currents (INa). The heterogeneous response of the IgG on the Western blots does not appear to correlate with the efficacy of reducing the inward currents.
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PMID:Lambert-Eaton syndrome: antigen-antibody interaction and calcium current inhibition in chromaffin cells. 147 Jan 96

McAb LC-1 was derived from fusion of myeloma cells and murine spleen cells immunized with human lung adenocarcinoma SPC-A-1 cells. The immunoglobulin isotype of LC-1 belonged to IgM. LC-1 was direct against the common epitope of lung cancer. It not only reacted with small cell lung cancer but also with non small cell lung cancer. LC-1 was purified from ascitic fluid by euglobulin precipitation and Sephadex G-200 filtration chromatography, and was iodinated with Iodogen, the specific reactivity of 125I-labeled LC-1 was determined by comparing standard curve with self-displacement curve. The immunoreactive fraction of 125I-LC-1 was determined by its binding to excess of antigen. The RIA data were plotted in Scatchard-form as binding of SPC-A-1 cells to LC-1. The binding constant of LC-1 binding to SPC-A-1 was 4.8 x 10(8) M-1. The LC-1 binding sites on SPC-A-1 were 7.2 x 10(4) per cell. The RIA inhibition test showed that LC-1 and LAC-122 (another IgM isotype McAb reacted only with non small cell lung cancer) had no cross-reactivity. The treatment of SPC-A-1 cells by proteinase and sodium periodate inhibited LC-1 binding to these treated target cells by 39% and 66% respectively. These results suggested that the biochemical nature of antigen recognized by LC-1 was glycoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on binding characteristics of 125I-labeled McAb LC-1 to lung adenocarcinoma cells in vitro and in vivo]. 159 1

A sequential combination chemotherapy regimen was evaluated in 23 patients with small-cell lung cancer (16, limited disease; 7, extensive disease). All patients had an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, normal serum sodium and albumin levels and alkaline phosphatase values of less than 1.5 times the upper limit of normal. Treatment comprised ifosfamide and either vindesine or vincristine given on weeks 0, 2 and 4; cisplatin and etoposide given on weeks 6, 9 and 12; and doxorubicin and methotrexate given on weeks 15 and 17. The overall response rate at the end of chemotherapy was 91% and the complete response rate was 43%. Treatment was generally well tolerated and the delivered dose intensity was 83% of that projected. Median survival was 54 weeks, with 4 patients (17%) being alive 2 years after the completion of therapy.
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PMID:Sequential chemotherapy in good-prognosis patients with small-cell lung cancer. 164 92

Imipenem/cilastatin sodium (IPM/CS) was used to treat respiratory tract infections (RTI) in 54 patients with lung cancer. Out of the 54 patients studied, 53 were evaluable for the utility of IPM/CS; 42 had pneumonia, 9 had obstructive pneumonia, 1 had a lung abscess and 1 had acute bronchitis. The efficacy rate was 71.7%. Seventeen causative organisms were isolated from 14 patients. They included Staphylococcus aureus 5 strains, Staphylococcus epidermidis 4 strains, Staphylococcus sp. 2 strains, Enterococcus faecalis 1 strain, Pseudomonas aeruginosa 2 strains, Pseudomonas fluorescens 2 strains, Acinetobacter sp. 1 strain, and the eradication rate was 81.8%. Clinical adverse effects (nausea and vomiting) were observed in 1 patient. Abnormalities in laboratory test results were observed in 3 patients. They disappeared or returned to normal values after completion of therapy or discontinuation of IPM/CS administration. IPM/CS appears to be a useful antibiotic for RTI in patients with lung cancer.
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PMID:[Therapeutic efficacy of imipenem/cilastatin sodium on respiratory tract infections in lung cancer patients]. 165 53

Intravenous administration of sodium benzylideneascorbate (SBA) rapidly necrotized inoperable human lung cancer, and induced degeneration of 3'-methyl-4-dimethylaminoazobenzene-induced rat hepatocellular carcinoma (vacuolar, eosinophilic degeneration, nuclear debris) without affecting the serum glutamic oxaloacetic transaminase, gamma-glutamyl transpeptidase and total protein levels. Cultured normal human lung and skin fibroblasts, and human glioma and glioblastoma cell lines were relatively resistant to SBA, when compared to human myelogenous leukemic cell lines. SBA had no apparent host immunopotentiation activity such as stimulation of cytokine action or production; activation of monocyte or polymorphonuclear cells; or modulation of poly (ADP-ribose) glycohydrolase activity. The data suggest that the antitumor activity of SBA might be produced by direct action of authentic SBA or its metabolized form(s), rather than by immunopotentiation of the hosts.
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PMID:Induction of tumor degeneration by sodium benzylideneascorbate. 174 10

A new cell line (LC-1/sq) of human lung squamous-cell carcinoma was established from a surgically resected specimen of primary lung cancer. Upon continuous propagation in serum-free culture medium, it secreted trypsin inhibitors into the conditioned medium. The major fraction of the trypsin inhibitor (T1-1) was purified to apparent homogeneity by anion-exchange and gel-filtration high-performance liquid chromatography (HPLC) and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) followed by transblotting to Immobilon. T1-1 effectively inhibited trypsin. Chymotrypsin, plasmin and kallikrein were inhibited to a lesser extent, but urokinase-type plasminogen activator, elastase, thrombin and papain were not inhibited. The activity of T1-1 was acid-stable and heat-resistant, and its molecular weight was 115 kDa by SDS-PAGE. It exhibited single NH2-terminal sequence, and its first 20 NH2-terminal amino-acid residues were identical with those of protease nexin-II (PN-II)/amyloid beta-protein precursor (APP). These characteristics of T1-1 suggest that the major trypsin inhibitor secreted by LC-1/sq is indistinguishable from PN-II/APP. LC-1/sq is the first lung squamous carcinoma cell line that secretes functionally active trypsin inhibitor, PN-II/APP, in vitro and is useful for studying its biological significance in malignant tumor.
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PMID:Establishment of a new human cancer cell line secreting protease nexin-II/amyloid beta protein precursor derived from squamous-cell carcinoma of lung. 191 42

Several studies of small cell lung cancer (SCLC) treatments have been performed in the United Kingdom. In some, prognostic factor analyses were carried out but the results were not entirely consistent. The Lung Cancer Subcommittee of the United Kingdom Coordinating Committee on Cancer Research (UKCCCR) consequently initiated an overview of these studies with the aim of identifying the important prognostic factors using a large number of patients. Information on almost 4,000 patients was available, but it was necessary to perform analyses on smaller subsets because the variables recorded in individual studies were inconsistent. A number of variables contributed significantly to the prediction of likely survival over the 6 months after starting treatment, but performance status (PS), alkaline phosphatase (AlkP) and disease stage were shown to be the most important; aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) may also be useful. A prognostic index was devised for this initial period and validated using independent data. For patients who survived the first 6 months, the pre-treatment variables important for prognosis in the 6-24 month period were stage, PS and plasma sodium (Na). The Subcommittee recommends that performance status, disease stage, AlkP, Na, AST and LDH should be measured in all future SCLC studies to assist comparisons between studies and possibly the selection of patients for different treatment strategies. The additional recording of five other variables would allow a more definitive overview to be performed at some future date.
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PMID:An overview of prognostic factors in small cell lung cancer. A report from the Subcommittee for the Management of Lung Cancer of the United Kingdom Coordinating Committee on Cancer Research. 215 8


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