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)

Peroxisome Proliferator Activated Receptor-gamma (PPAR-gamma) is a ligand-activated transcription factor belonging to the steroid receptor superfamily. It is a key regulator of adipogenic differentiation and glucose homeostasis, the ligands of which have also been demonstrated to induce differentiation in human breast, lung and colon cancer cell lines. In the present study, PPAR-gamma expression in cases of non-small cell lung carcinoma (NSCLC) was examined immunohistochemically and was correlated with tumor histological type and grade. Primary tumor samples from 147 patients with NSCLC were immunostained using a monoclonal antibody against PPAR-gamma. Positive PPAR-gamma immunostaining was prominent in 61 out of 147 cases (42%) and negative in the rest. PPAR-gamma positivity was prominent in 37 out of 79 cases (47%) of squamous cell lung carcinoma and in 24 out of 68 ones (35%) of lung adenocarcinoma. PPAR-gamma positivity was most frequently observed in squamous cell tumors (P=0.021) and in tumors of high histological grade of both histological types (P=0.041). Well-differentiated adenocarcinoma cases presented increased frequency for PPAR-gamma positivity compared with moderately and poorly differentiated ones (P=0.001). The intensity and pattern of PPAR-gamma staining in tumor cells were not correlated with histopathological parameters in PPAR-gamma positive cases of NSCLC examined. Our findings support evidence for participation of this protein in the biological mechanisms underlying the carcinogenic evolution in the lung, suggesting also the importance of specific PPAR-gamma ligands as future therapeutic approach in lung cancer.
Lung Cancer 2002 Jun
PMID:Expression of peroxisome proliferator activated receptor-gamma in non-small cell lung carcinoma: correlation with histological type and grade. 1200 33

The human U-1285 and GLC(4) cell lines, both derived from small cell carcinoma of the lung, are present in doxorubicin-sensitive (U-1285 and GLC(4)) and doxorubicin-resistant MRP-expressing (U-1285dox and GLC(4)/ADR) variants. These sublines were examined here with respect to their susceptibilities to the toxic effects of selenite and compared to the toxic effects of selenite on the promyelocytic leukemia cell line HL-60 and its doxorubicin-resistant P-glycoprotein expressing variant. The drug-resistant U-1285dox and GLC(4)/ADR sublines proved to be 3- and 4-fold, respectively, more sensitive to the cytotoxicity of selenite than the drug-sensitive U-1285 and GLC(4) sublines, whereas no difference was observed between the HL-60 sublines. The presence of doxorubicin at a concentration equal to the IC(10) did not significantly potentiate the toxic effects of selenite. The presence of selenite did not significantly affect the expression of the multi-drug resistant proteins (MRP1, LRP and topoisomerase IIalpha) in the drug-resistant cells. The activities of thioredoxin reductase (TrxR) were higher (50 and 25%, respectively) in the drug resistant cell sublines U-1285dox and GLC(4)/ADR compared to the drug-sensitive parental lines. The activity of glutathione reductase (GR) was essentially the same in the drug-sensitive and -resistant cell lines. Exposure to selenite resulted in a 4-fold increase in both TrxR and GR activities in U-1285 cells, an effect, which was less pronounced in the presence of doxorubicin. Under similar conditions the increase in the TrxR activity in the resistant U-1285dox cell line, was only 30% and the activity of GR was unaltered. Different responses in the activity of the key enzymes in selenium metabolism are one possible mechanism explaining the differential cytotoxicity of selenium in these cells.
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PMID:Drug-resistant human lung cancer cells are more sensitive to selenium cytotoxicity. Effects on thioredoxin reductase and glutathione reductase. 1203 72

Lung cancer is one of the most common malignant tumors in humans. Metastasis is the basic biological feature of malignant tumors, which is the main cause of death. Molecular mechanism of metastasis is still unclear, although lots of studies have been done in tumor metastasis. To study and explore the molecular basis of metastasis in lung cancer, and isolate tumor metastasis-related genes, two human lung adenocarcinoma cell lines AGZY 83-a and Anip 973 were chosen as research materials. The Anip973 was derived from AGZY83-a, but manifested much higher metastasis potential than the parent line. Using mRNA differential display technique, an unknown cDNA fragment, OPB7-1, which is over-expressive in Anip973 cell line, was obtained. It was used as a template to isolate its corresponding cDNA through dbEST searching and PCR. To search and clone lung adenocarcinoma metastasis-related candidate gene, and to explore the molecular basis of development of lung carcinoma, differential expression of OPB7-1 cDNA fragment among 9 human lung adenocarcinoma cell lines and 12 normal human tissues were detected using cell culture, cDNA clone, Northern blot analysis and bioinformation technology. Results showed that there were significant differences in OPB7-1 expression among 9 human lung adenocarcinoma cell lines. High expression tendency was observed in Anip973 cell line with high metastasis potential, TKB-18 cell line with high invasion potential and GLC-82 cell line with low differentiation potential. Besides, a bigger fragment can be found in Anip973 cell line on the Northern blot hybridization. The 3.0 kb transcriptions were found in various tissues. Over-expression in heart and skeletal muscle could be observed, whereas expression in spleen, liver, kidney, placental and lung could be found except colon, thyroid gland and small intestine. These manifests indicate that OPB7-1 gene has a wide-rage expression in human multiple tissues. A 1.0 kb cDNA fragment was acquired by linking up EST fragments homologous match 5' end and PCR. BLAST analysis revealed that OPB7-1 gene has extremely low sequence identity with any known genes from GenBank and any sequences from EST database. The chromosomal localization of it was determined by RH location method. The OPB7-1 fragment was localized to chromosome 1p31-34. That OPB7-1 gene has an extensive expression pattern, may be a novel tumor gene related to lung carcinoma. Further research needs to be done to obtain the full-length cDNA of OPB7-1 gene. It will be helpful to investigate the expression in lung cancer cases and other tumor tissues for further determining the function of OPB7-1 gene in development of tumor.
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PMID:[Mapping and expression analysis of a different expression cDNA fragment from lung adenocarcinoma cell line]. 1209 22

Glycolysis is known to be the primary energy source in most cancer cells. We investigated here the effect of clotrimazole (1-(alpha-2-chlorotrityl)imidazole), the antifungal azole derivative, which was recently recognized as calmodulin antagonist, on the levels of glucose 1,6-bisphosphate and fructose 1,6-bisphosphate, the two stimulatory signal molecules of glycolysis, and on ATP content and cell viability in LL/2 Lewis lung carcinoma cells and CT-26 colon adenocarcinoma cells. We found that clotrimazole induced a significant, dose- and time-dependent reduction in the levels of glucose 1,6-bisphosphate, fructose 1,6-bisphosphate, ATP, and cell viability. These findings suggest that clotrimazole causes a reduction in glycolysis and ATP levels, which eventually leads to cell destruction after 3 h of treatment. Since cell proliferation was also reported to be inhibited by calmodulin antagonists, this substance is most promising agent in treatment of cancer by inhibiting both cell proliferation and the glycolytic supply of ATP required for cancer cell growth.
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PMID:Clotrimazole decreases glycolysis and the viability of lung carcinoma and colon adenocarcinoma cells. 1224 83

Anthracyclines are included in clinical treatments against various malignancies, but severe cardiotoxic side-effects and the development of resistance mechanisms limit their usefulness. Many aspects of the cellular response to anthracyclines remain debated. The status of the main regulator of iron homeostasis, namely the RNA-binding activity of iron regulatory proteins (IRPs), has been assessed herein for two types of human tumor cells and their derived doxorubicin-resistant sublines. IRPs were always fully activated in the latter, whereas only partial activation occurred in the former. Doxorubicin exposure reversibly inactivated IRP1 in small cell lung carcinoma (GLC(4)) and myelogenous leukemia (K562) cell lines, but was without effect in their derived doxorubicin-resistant sublines. In contrast, adding doxorubicin to cytosolic fractions of untreated cells or to purified IRPs led to the irreversible alteration of the RNA-binding activity of IRP1. In these different conditions, interaction between doxorubicin and the iron regulatory system disturbs iron metabolism, and cells having developed a resistance mechanism are tuned to maximize the iron supply. The results reported herein may lead the path toward a better therapeutic management of cancer patients receiving doxorubicin by discriminating between the antiproliferative and cardiotoxic properties of this anthracycline.
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PMID:Interactions between doxorubicin and the human iron regulatory system. 1258 65

The aim of this study was to investigate the effect of adriamycin (ADR) in signaling activation of NF-kappaB in ADR-sensitive and -resistant GLC(4) human small-cell lung carcinoma. ADR activated NF-kappaB only in ADR-sensitive GLC(4) cells in a time- and dose-dependant manner by stimulating IkappaBalpha degradation after 4h. Activation of NF-kappaB in response to tumor necrosis factor was intact in both cell lines. Topoisomerase II, a target for a number of chemotherapeutic agents, was depleted in both types of GLC(4) cells after ADR treatment, suggesting the stabilization of transient DNA-topoisomerase II complexes. Another transcription factor, Sp1, was activated by ADR, demonstrating the nonspecificity of NF-kappaB activation in ADR-sensitive GLC(4) cells. These findings indicated that resistance to ADR in ADR-sensitive GLC(4) cells did not involve the NF-kappaB transcription factor.
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PMID:Adriamycin activates NF-kappaB in human lung carcinoma cells by IkappaBalpha degradation. 1270 43

The current standard of practice for the detection of osseous metastatic disease is the conventional bone scan of the entire body using technetium-99m methylene diphosphonate (Tc-99m MDP). Although Tc-99m MDP scintigraphy is sensitive for the detection of advanced skeletal metastatic lesions, early involvement may be missed because this technique relies on the identification of the osteoblastic reaction of the involved bone rather than the detection the tumor itself. Positron emission tomography (PET) has proven to be the gold standard in metabolic imaging. Fluorine -18 deoxyglucose (FDG) provides a means of quantitating the glucose metabolism, with the amount of tracer accumulation reflecting the glucose metabolism: high-grade malignancies tend to have higher rates of glycolysis than do low-grade malignancies and benign lesions; therefore, high-grade malignancies have greater uptake of FDG than that of low-grade or benign lesions. Positron emission tomography has been shown to be superior to scintigraphy in the detection of metastases because it detects the presence of tumor directly by metabolic activity, rather than indirectly by showing tumor involvement due to increased bone mineral turnover. This has allowed the detection of metastatic foci earlier with PET than with bone scintigraphy. Although the spectrum of PET applications is unknown, it now is approved for the diagnosis, staging and restaging of many common malignancies and has shown efficacy for the detection of osseous metastasis from several malignancies including lung carcinoma, breast carcinoma, and lymphoma.
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PMID:Diagnosis of occult bone metastases: positron emission tomography. 1460 Jun 1

Over the past several years, positron emission tomography (PET) has become a clinically useful, noninvasive study which complements conventional imaging (chest radiographs, computed tomography [CT], and magnetic resonance imaging [MRI]) in the evaluation of patients with lung cancer. PET imaging of lung cancer is typically performed with the radiopharmaceutical 18F-2-deoxy-D-glucose (FDG), a d-glucose analog. Increased glucose metabolism by malignant cells results in increased uptake and accumulation of FDG, which serves as the basis for tumor detection. This review will focus on the current applications of FDG-PET in lung cancer patients including evaluation of focal pulmonary abnormalities, staging lung cancer, determining tumor recurrence, and in assessing prognosis.
Clin Lung Cancer 1999 Aug
PMID:Positron emission tomography imaging in lung cancer. 1472 48

Accurate staging of cancer has a critical role in optimal patient management. Fluorine-18 fluorodeoxyglucose positron emission tomography (FDG PET) is superior to CT in the detection of local and distant metastases in patients with non-small cell lung cancer. Although Tc-99 m methylene diphosphonate (MDP) bone scanning is well established in the evaluation of bone metastases, there are conflicting reports on the use of FDG PET in the evaluation of skeletal metastases. We report on a patient with locally advanced lung carcinoma in whom FDG PET accurately identified previously unsuspected widespread asymptomatic bone metastases (bone scan and X-rays negative, confirmed on MRI). Assessment of glucose metabolism with FDG PET might represent a more powerful tool to detect bone metastases in lung cancer compared with conventional bone scans.
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PMID:Detection of occult bone metastases of lung cancer with fluorine-18 fluorodeoxyglucose positron emission tomography. 1523 Jul 58

The increasing incidence of malignant pleural mesothelioma has led to the development of new treatment strategies and a need for new diagnostic techniques to identify the extent of the disease at an early stage and to evaluate treatment. Computed tomography (CT) and magnetic resonance imaging (MRI) are helpful in identifying the location and extent of the involved areas but cannot always differentiate between benign and malignant processes. Fluorodeoxyglucose (FDG)-positron emission tomography (PET) imaging, which in oncology, is based on changes in metabolic pathways of glucose, has been shown in a number of studies to differentiate malign and benign lesions in patients with asbestos exposure. FDG-PET images were also found to provide excellent delineation of the active tumour sites. Further evaluations of this technique included a combined experimental/clinical study to investigate the difference in rates of FDG uptake between malignant and inflammatory cells and processes.
Lung Cancer 2004 Aug
PMID:Positron emission tomography in the diagnosis of mesothelioma. 1526 38


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