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 correlation between response to chemotherapy and the serum level of neuron specific enolase NSE as well as value of the test for predicting relapse has been evaluated in 41 patients with small cell lung carcinoma (SCLC). A significant decrease of the mean NSE level in comparison with the pretreatment value was observed (p = 0.01). At the time of relapse the mean level increased significantly (p = 0.005). In 9 out of 19 responders to chemotherapy (47.3%) increase of the NSE level above the normal value preceded clinically diagnosed relapse by 3-6 weeks. These results demonstrate the usefulness of the test in treatment monitoring of patients with SCLC.
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PMID:[Treatment monitoring of patients with small cell lung cancer by determining levels of serum neuron specific enolase]. 838 60

To evaluate the pronostic value of an elevated seric carcinoembryonic antigen (CEA > 10 ng/ml) at diagnosis, in patients with lung cancer, a pair study was done: couples of patients with same staging and histologic type were established, one patient with high CEA level compared to one patient with normal CEA level (< 5.5 ng/ml). Other markers were measured: neuron specific enolase (NSE), squamous cell carcinoma (SCC) or Cyfra 21-1. Survival was the end point of comparison. For 89 couples created, patients with low CEA level had a better survival rate at one year ( p = 0.02), this prognosis advantage was confirmed by a comparison of survival curves with Mantel-Cox and Breslow test (p = 0.01), but not by the signs test. These differences were also observed for the 71 couples of squamous cell carcinomas and adenocarcinomas, and the apparied signs test was still not significant. The poor prognosis persisted for patients with high CEA level, when one another marker's level (NSE or SCC or Cyfra 21-1) was increased, in comparison with patients with any marker increased. On 29 couples of all histological subtypes or on the 25 couples of non small cell lung cancer, the signs test and the comparison of survival curves were significant, but not the 1 year survival rate. This study shows that a CEA level greater than 10 ng/ml at diagnosis is a poor pronostic factor in patients with lung carcinoma, independent of the stage of disease and of the histologic type.
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PMID:[Prognostic value of pre-therapeutic levels of carcino-embryonic antigen in primary bronchial carcinoma]. 874 67

Three cases of peripheral small cell lung carcinoma (SCLC) with central fibrosis are presented. Central fibrosis is usually present in adenocarcinomas. Cases 1 and 2 are combined SCLCs with components of papillary adenocarcinoma, and case 3 is a mixed SCLC with a large cell component. Small cell components showed intermediate cell type in all cases. In cases 1 and 2, there was a gradual transition between small cell carcinoma and papillary adenocarcinoma. Small cell components showed Grimelius argyrophilia, but other neuroendocrine markers such as neuron specific enolase, chromogranin A, Leu-7 and synaptophysin were negative. The chest X-ray examination of case 1 demonstrated rapid enlargement of a tumor shadow, which was present two years before, for a recent year. Central fibrosis, coexistence of small cell carcinoma and papillary adenocarcinoma, and a change of growth rate in the chest X-ray may suggest that some SCLC derive from papillary adenocarcinomas.
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PMID:Peripheral lung carcinomas associated with central fibrosis and mixed small cell and other histologic components. 880 99

We report a case of paraneoplastic retinopathy in a patient who was found to have small cell carcinoma of the lung and was shown to have serum antibody against retinal soluble 70 kDa protein. A 71-year-old woman visited her ophthalmologist for gradual visual loss in both eyes. Although she underwent uncomplicated cataract surgery in her left eye, she was referred to our hospital because of progressive visual deterioration in November 1994. On admission, her corrected visual acuity was 0.3 OD and hand motion OS. Funduscopic examination showed narrowing retinal arteries, pigment epithelial mottling in the posterior retina bilaterally, and optic disc pallor in the left eye. An electroretinogram demonstrated marked reduction in the a and b waves. Bilateral central scotomas were detected by kinetic perimetry. We pursued further examination for systemic disease, and identified increased serum level of neuron specific enolase and radiographically abnormal shadow in the chest. Transcutaneous needle biopsy of the mediastinum confirmed small cell carcinoma. In western blot analysis the patient's serum reacted strongly with soluble retinal proteins of 70 kDa molecular weight, although the 26 kDa CAR antigen was not labeled. This patient was diagnosed as having paraneoplastic retinopathy due to small cell carcinoma and unusual serum protein which responded to an antigen with a molecular weight of 70 kilodaltons.
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PMID:[A case of paraneoplastic retinopathy with serum antibody against retinal soluble 70 kDa protein]. 902 14

A case of small cell carcinoma arising in the outer urethral orifice is presented. The resected tumor showed a proliferation of small round or fusiform neoplastic cells in the submucosa. Tumor cells were arranged in sheets or a trabecular manner and possessed markedly hyperchromatic nuclei with a high N:C ratio, closely resembling small cell carcinoma of the lung. Characteristically, pagetoid intraepithelial spreading could be identified. However, there was no evidence of in situ transitional cell carcinoma and adeno- or squamous cell carcinoma components anywhere. Ultrastructurally, each tumor cell contained only a few membrane-bound cored granules measuring 60-100 nm, which were compatible with neurosecretory granules, and desmosome-like intercellular attachments, but lacked aggregated microfilaments. By immunohistochemical examination, tumor cells were positive for epithelial markers, such as cytokeratin and epithelial membrane antigen, and neuron specific enolase, but negative for any other neuro-endocrine markers. Extensive systemic examination failed to show the primary site to be other than the outer urethral orifice. These findings indicate that the current tumor is a small cell carcinoma with neuro-endocrine differentiation arising from the outer urethral orifice.
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PMID:Small cell carcinoma arising from the outer urethral orifice: a case report examined by histologic, ultrastructural and immunohistochemical methods. 923 90

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

Gastrin-releasing-peptide (GRP), the mammalian counterpart of amphibian bombesin, has been reported to be produced by cells of SCLC. Using recombinant ProGRP Yamaguchi et al developed an enzyme immunoassay for the measurement of this more stable precursor of GRP. We focused our interest on the comparability of ProGRP to neuron specific enolase (NSE), CYFRA 21-1 and CEA. For this purpose we investigated the sera of 272 patients with histologically proven carcinomas of the lung (87 SCLC, 185 NSCLC). The sera of 74 patients with benign diseases of the lung and smokers served as a reference group. At a specificity of 95% ProGRP and NSE possessed comparable sensitivities (47% versus 45%) in small cell lung carcinomas. ProGRP showed only a few more positive test results than NSE, but reached much higher value levels than NSE. ProGRP and NSE showed a clear additive sensitivity of about 20%. In NSCLC CYFRA 21-1 was the leading marker with 63% sensitivity, whereas ProGRP seldom showed a "false positive" test result. ProGRP proved a very high specificity and good sensitivity for small cell lung carcinomas and therefore enables diagnosis of small cell lung carcinoma in patients with lung tumours of unknown origin as well as good control of efficiency of therapy.
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PMID:Pro-gastrin-releasing peptide (ProGRP)--a useful marker in small cell lung carcinomas. 1047 Feb 18

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

Pleural effusion is a common diagnostic problem. The analysis of serum and body fluids for tumor markers has been intensively applied to clinical diagnosis. The aim of the present study was to determine the usefulness of simultaneous quantification of carbohydrate antigen 19.9, carbohydrate antigen 125, neuron specific enolase, mucinous-carcinoma-associated antigen, and ferritin in samples of pleural fluids in the malign pleural effusion and its differentiation from benign effusions. A total of 61 pleural effusions were collected from the patients, who were subjected either to simple needle aspiration or to tube drainage for the diagnosis of pleural effusion. Tumor markers were determined in benign patient groups with nonspecific pleurisy, tuberculous pleurisy, empyema, congestive heart failure and in malignancy groups consisting of adenocarcinoma, small cell lung carcinoma, mesothelioma, epidermoid lung cancer. The tumor markers CA-19.9, CA-125, NSE, and ferritin levels were quantified by the sandwich assay using the streptavidin technology of ELISA in an ES-300 Boehringer-Mannheim analyser. MCA was measured by employing a two-side solid phase EIA method. MCA measurements were done by the Cobas-Core. For all patients, the effusions correctly or incorrectly identified by the different procedures as being malignant or nonmalignant are defined as true positive, false positive, true negative, and false negative, the term 'positive' referring to histologically proven malignant pleural effusion while nonmalignant effusions are referred to as 'negative'. Therefore, sensitivity, specificity, positive predictive value, and negative predictive value were defined as diagnostic parameters. The cut-off values calculated were 352 U/ml for CA-125, 54 U/ml for CA-19.9, 555 for ferritin, 11.1 for MCA and 8.7 for NSE. In our study, the highest sensitivity is found to be MCA with 100%; specificity, CA-19.9 with 97%; PPV, CA-19.9 and MCA with 95% and NPV, MCA with 100%. Our data imply that the co-measurement of MCA+CA-19.9+CA-125 levels may further improve their diagnostic value in malignant pleural effusion compared with that of each tumour marker alone and may be useful in distinguishing malignant from benign pleural effusions.
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PMID:Diagnostic usefulness of tumour marker levels in pleural effusions of malignant and benign origin. 1095 62

To investigate the specific transduction of a suicide gene into human small cell lung carcinoma (SCLC) cells, we explored the promoter region of the neuron specific enolase (NSE) gene as a tumor-specific promoter. In Northern blot analysis, NSE mRNA was expressed more abundantly in the SBC3 human SCLC cell line than in the RERF human SCLC cell line, the A549 human lung adenocarcinoma cell line and the HeLa human uterine cervix epitheloid carcinoma cell line. A reporting vector containing the NSE promoter (pNSE-LUC) exhibited higher luciferase activity in SBC3 than in the other three cell lines. After transfecting an expression vector containing the NSE promoter-bound HSV-TK gene (pNSE-TK) into the cells, we measured their sensitivity to ganciclovir (GCV). In SBC3, pNSE-TK transfected cells showed about the same sensitivity to GCV as non-transfected (parental) cells. Though the NSE promoter itself is not optimal for use in suicide gene transfer to SCLC cells, it might be applied as a tumor-specific promoter after enhancement of its activity.
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PMID:Neuron specific enolase promoter for suicide gene therapy in small cell lung carcinoma. 1129 50


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