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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new human cancer cell line was established from a metastatic lesion of a small cell lung carcinoma (SCLC-R1) and maintained in continuous culture with a doubling time of 62 h. The SCLC-R1 line, whose ultrastructural features are presented, showed a diploid DNA content, a translocation involving chromosome 16 [t(16;?)(q24;?)] and noticeable deletions in the FHIT (fragile histidine triad) region in the short arm of chromosome 3 [del(3)(p14)] and in the telomeric region of the short arm of chromosome 12 [del(12)(p13)]. The involvement of 12p in metastatic small cell lung cancer is reported here for the first time. No amplification or rearrangements were evident in the c-myc, L-myc, N-myc, int-2, c-erbB-2, H-ras, K-ras, c-mos, and hst-1 genes by Southern blot analysis. Wild-type p53, RB, K-ras and H-ras genes were evident by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis. The neuron specific enolase (NSE) level was much higher in the cell line's cytosol than in the patient's serum and the cell line also had high expression of chromogranin A and cytokeratin 19. SCLC-R1 cells were sensitive to cisplatin, carboplatin and doxorubicin. The clinical history of the patient from whom the cell line was derived is reported. The characteristics of this new cell line indicate it to be a useful experimental model to investigate lung cancer biology and anticancer drug response.
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PMID:Chromosomal alterations, biological features and in vitro chemosensitivity of SCLC-R1, a new cell line from human metastatic small cell lung carcinoma. 971 81

Gene amplification is a frequent event in lung cancer, specifically in squamous cell lung carcinoma. Recently, we reported amplifications on chromosomal bands 3q26.1-q26.3 with the genes BCHE and SLC2A2 amplified in 40% of squamous cell lung carcinomas. Here, we identified an amplified domain within chromosomal bands 1pter-p33 in squamous cell lung carcinoma using reverse chromosome painting. A panel of nine genes which have previously been assigned to region 1pter-p33 was tested for amplification using comparative PCR. The ENO1 gene that encodes enolase and the PAX7 gene that encodes a transcription factor were most frequently amplified. Specifically, the gene ENO1 was amplified in six and the gene PAX7 in five out of 37 cases which included both biopsies and paraffin-embedded tissues of squamous cell lung carcinomas. In total, we identified amplifications of at least one gene at bands 1pter-p33 in 10 out of 37 tumors (27%). Together, our data indicate that a novel and frequent amplification unit is present in squamous cell lung carcinoma with the center of the amplified domain in the vicinity of the genes PAX7 and ENO1.
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PMID:Gene amplification at chromosome 1pter-p33 including the genes PAX7 and ENO1 in squamous cell lung carcinoma. 1085 20

Carcinoembryonic antigen (CEA), cancer antigen 125 (CA 125), NCC-ST-439, carbohydrate antigen 19-9 (CA 19-9), cytokeratin 19 fragment (CYFRA 21-1), sialyl Lewis X-i antigen (SLX), progastrin-releasing peptide (ProGRP), squamous cell carcinoma antigen (SCC) and neuron specific enolase (NSE) were evaluated in the pleural effusion of 39 patients with lung cancer (29 adenocarcinomas, seven small-cell carcinomas, three squamous cell carcinomas) and 43 patients with tuberculous pleurisy. The levels of the tumor markers other than SCC and NSE were significantly higher in lung cancer than in tuberculosis. High levels of CYFRA 21-1 and SCC were observed in squamous cell carcinoma and high levels of ProGRP and NSE were observed in small-cell carcinoma. According to the validity score, sensitivity (%) + specificity (%) - 100, the optimal cut-off levels of pleural effusion were 8.1 ng/ml for CEA, 660 U/ml for CA 125, 2.6 U/ml for NCC-ST-439, 10 U/ml for CA 19-9, 65 ng/ml for CYFRA 21-1, 140 U/ml for SLX, 23.2 pg/ml for ProGRP, 0.6 ng/ml for SCC and 5 ng/ml for NSE. By comparison of validity scores for each optimal cut-off level and of receiver operating characteristic (ROC) curves, we suggest that a CEA assay is the most useful for pleural effusion. The combined assay of CEA + ProGRP and CEA + ProGRP + CYFRA 21-1 were considered to be useful.
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PMID:[Tumor markers in pleural effusion of patients with lung cancer and patients with tuberculous pleurisy]. 1197 64

Large cell neuroendocrine carcinoma (LCNEC) is a rare type of lung cancer and it has the least favorable prognosis. We describe our experience with a patient in whom LCNEC was diagnosed. A 65-year-old man who was pointed out abnormal shadow on a chest X-ray film in the health screening was admitted to the hospital. Chest X-ray film and computed tomography (CT) scan showed a 4 x 3 cm mass in the left-S2. Poorly differentiated adenocarcinoma of the left lung was suspected based on CT guided cytology. An upper lobectomy of the left lung and dessection of the mediastinal lymph nodes were performed. This tumor showed light microscopic and immunohistochemical evidences of neuroendocrine differentiation. Further it showed positive responses in neuronspecific enolase (NSE), synaptophysin, and chromogranin-A stainings. Pathological diagnosis was stage IB (pT2N0M0) LCNEC. There have been no findings of tumor recurrence 22 months after the operation.
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PMID:[Large cell neuroendocrine carcinoma of the lung; report of a case]. 1536 78

The granular cell tumor (GCT) is a nodule that arises most commonly in the skin, the breast or the tongue. The vast majority are benign. Approximately 6-10% of granular cell tumors have been reported in the lower respiratory tract. The clinical, pathological and immunohistochemical findings of eleven cases are described in our material consisted of 6 males and 5 females aged from 35 to 58 years (median, 46 years). The GCT were solitary lesions in all our patients. The tumors were located in trachea (6 cases) and in bronchus (5 cases). They were found during bronchoscopy performed because of symptoms of pneumonia, lung cancer and hemoptysis or dyspnea alone. Diameter of the tumors ranged from 0.2-2.5 cm (median 1.2 cm). Six tumors were surgically excised and 5 were endoscopically removed. Pulmonary GCT behave in a benign fashion. It was observed that tumors of less than 8 mm were more amenable to endoscopic removal and larger tumors were more likely to infiltrate through the bronchial wall. Histologically, the GCT showed submucosal infiltrates of round or oval cells with abundant granular cytoplasm. The tumors cells were positive for S-100 protein, neuron specific enolase, CD68 and vimentin. Our immunohistochemical results are consistent with this concept.
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PMID:[Granular cell tumor--a rare, benign respiratory tract neoplasm in the material of the Institute of Tuberculosis and Lung Diseases]. 1575 56

Circulating autoantibodies are useful diagnostic markers of cancers and autoimmune diseases. Research over the past decade has resulted in some reports on the presence of autoantibodies against disease-related proteins such as annexin-I & II, recoverin and protein gene product 9.5 in the sera of patients with lung cancer, and also against calreticulin and alpha-enolase in autoimmune diseases. In this study, we first identified the a-enolase autoantibody in the sera of patients with lung adenocarcinoma by proteomics-based analysis. The comparison of two-dimensional polyacrylamide gel electrophoresis (2D-PAGE)/western blot (WB)/ECL detection revealed distinct distributions of antibodies in the sera of lung adenocarcinoma, tuberculosis and healthy subjects which reacted with soluble proteins derived from the adenocarcinoma A549 cell line. We found 16 spots in patients with adenocarcinoma by 2D-PAGE/WB/ECL detection and identified alpha-enolase, chaperonin, and other autoantibodies in the adenocarcinoma patients' sera. The specificities of an antibody against alpha-enolase was preliminarily observed in sera from 3 of 5 patients with adenocarcinoma, 0 of 10 patients with tuberculosis and 0 of 10 healthy subjects. In conclusion, we first identified alpha-enolase autoantibody in sera of lung adenocarcinoma and the autoantibody was seemed to be a specific marker of the lung adenocarcinoma. In addition, we also identified various autoantibodies in esophageal cancer, hepatocellular carcinoma, and non-Hodgkin's lymphoma. Moreover, we tried to identify the corresponding antigen of an unknown anti-cytoplasmic autoantibody, and an anti-red blood cell antibody by proteomics-based analysis. These antibodies might become new diagnosis markers.
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PMID:[Proteome analysis of autoantibodies in sera of patients with cancer]. 1596 8

Lung cancer ranks top in both incidence and mortality in most part of the world. Scientists strive to explore biomarkers and their possible role in the diagnosis, treatment and prognosis of lung cancer. The ultimate goal is to discover biomarkers that can be tested in clinical trials and finally applied to patient care. Highly elevated concentrations of cytokeratin 19 fragment, tissue polypeptide antigen and squamous cell carcinoma antigen in non-small cell lung cancer particularly for squamous cell carcinoma, carcinoembryonic antigen and cancer antigen 125 in adenocarcinoma or non-small cell lung cancer, as well as progastrin-releasing peptide and neuron specific enolase in small cell lung cancer are suggestive biomarkers for the malignancy. Despite extensive studies, most results still remain controversial. Even with the report of high percent sensitivity and specificity, validation by clinical trials in large cohorts of patients is necessary before the cancer-related phenotypes can be translated into the clinic as reliable biomarkers. Nevertheless, identifications of biomarkers are leading to more understanding of the molecular pathways involved in lung cancer. It is hoped that understanding the connections between cellular pathways will help to reduce the suffering and loss of life caused by the lethal disease. This article summarizes the pre-clinical and translational researches against lung cancer in relation to biomarker discovery and validation. It is intended for policy makers, researchers, clinicians and other health professionals, offering a variety of useful biomarkers and updated data of clinical trials for lung cancer.
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PMID:Potentially useful biomarkers for the diagnosis, treatment and prognosis of lung cancer. 1791 44

Pulmonary neoplasm is a serious disease, often detected in its final stages. Tumor markers, although not a diagnosis method for pulmonary neoplasms, are useful in monitoring the response to treatment and the relapses, as follows: neuron specific enolase (NSE) increases in micro-cellular neoplasm, Cyfra 21-1 increases in non-micro-cellular neoplasm, while the increase of carcino-embryonic antigen (CEA) is non-specific, as it is high in both primary and secondary lung cancer
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PMID:[Tumor markers used in diagnosis and monitoring of primary bronchopulmonary carcinoma]. 1899 32

p19(ras) is an alternative splicing product of the proto-oncogene c-H-ras pre-mRNA. In this study, we identified a novel p19(ras)-binding protein, Neuron-Specific Enolase (NSE), using the yeast two-hybrid method. NSE is one of the enolase families that convert 2-phospho-d-glycerate (PGA) to phosphoenolpyruvate (PEP) in the glycolysis pathway. In both endogenous and over-expressed systems, we confirmed interactions between p19(ras) and NSE via co-immunoprecipitation assay. We also identified the interaction region of p19(ras), which is required for binding with NSE. When full-length p19(ras) and C-terminal region are bound to NSE, it inhibits the enzymatic activity of NSE. Furthermore, p19(ras) interacted with Enolase alpha (Enoalpha) and repressed its enzymatic activity in vitro. p19(ras) repressed lung cancer cell proliferation mostly increased by NSE in H1299 cells. Taken together, these results suggest that p19(ras) is a novel regulator to suppress cell proliferation in lung cancer through the interaction with NSE.
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PMID:p19(ras) Represses proliferation of non-small cell lung cancer possibly through interaction with Neuron-Specific Enolase (NSE). 1971 34

The development of rapid and sensitive methods for the detection of immunogenic tumor-associated antigen is important not only for understanding their roles in cancer immunology but also for the development of clinical diagnostics. Alpha-enolase (ENO1), a p48 molecule, is widely distributed in a variety of tissues, whereas gamma-enolase (ENO2) and beta-enolase (ENO3) are found exclusively in neuron/neuroendocrine and muscle tissues, respectively. Because ENO1 has been correlated with small cell lung cancer, nonsmall cell lung cancer, and head and neck cancer, it can be used as a potential diagnostic marker for lung cancer. In this study, we developed a simple, yet novel and sensitive, electrochemical sandwich immunosensor for the detection of ENO1; it operates through physisorption of anti-ENO1 monoclonal antibody on polyethylene glycol-modified disposable screen-printed electrode as the detection platform, with polyclonal secondary anti-ENO1-tagged, gold nanoparticle (AuNP) congregates as electrochemical signal probes. The immunorecognition of the sample ENO1 by the congregated AuNP@antibody occurred on the surface of the electrodes; the electrochemical signal from the bound AuNP congregates was obtained after oxidizing them in 0.1 M HCl at 1.2 V for 120 s, followed by the reduction of AuCl(4-) in square wave voltammetry (SWV) mode. The resulting sigmoidally shaped dose-response curves possessed a linear dynamic working range from 10(-8) to 10(-12) g/mL. This AuNP congregate-based assay provides an amplification approach for detecting ENO1 at trace levels, leading to a detection limit as low as 11.9 fg (equivalent to 5 microL of a 2.38 pg/mL solution).
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PMID:Diagnostic detection of human lung cancer-associated antigen using a gold nanoparticle-based electrochemical immunosensor. 2055 64


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