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Query: UMLS:C0149925 (small cell lung cancer)
 6,491 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite disappointing results in the treatment of small cell lung cancer (SCLC), major progress in our understanding of SCLC biology has occurred in the past decade. Advances in the technique for culturing SCLC tumours in vitro have greatly facilitated the study of the biological properties of this tumour. The major progress in our understanding of SCLC includes: 1) the availability of nonspecific biological tumour markers such as neuron-specific enolase (NSE), the BB isoenzyme of creatine phosphokinase (CPKBB), bombesin/gastrin releasing peptide (GRP) and chromogranin A; 2) the generation of monoclonal antibodies raised against the neural and epithelial features of SCLC tumours; 3) the identification of several autocrine growth factors such as bombesin/GRP, insulin-like growth factor (IGF), transferrin and physalaemin; 4) the close study of cytogenetic abnormalities leading to the discovery of a unique chromosomal deletion of the short arm of chromosome 3 (del 3p 14-21), and to changes in oncogenic expression, e.g. c-myc, L-myc and N-myc, accounting for known biological and treatment results. These data suggest that all lung cancers arise from a common stem cell of endodermal origin. The information derived from these biological studies represents the most promising avenue towards new treatment strategies in SCLC.
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PMID:Biology of small cell lung cancer: an overview. 216 19

Immunocytochemical and immunochemical techniques were used to study the expression of the neural cell adhesion molecule (NCAM) by human lung cancer cell lines. Intense surface staining for NCAM was found at light and electron microscopic levels on small cell lung cancer cells. The NCAM polypeptide of Mr 140,000 (NCAM 140) was detected by immunoblotting in all of 7 small cell lung cancer cell lines examined and in one out of two of the closely related large cell cancer cell lines: it was not detected in cell lines obtained from one patient with a mesothelioma, in two cases of adenocarcinoma, nor in two cases of squamous cell cancer. In contrast, neuron-specific enolase was found by immunoblotting in all the lung cancer cell lines tested and synaptophysin in all but the adenocarcinoma cell lines. These antigens were localized intracellularly. The specific expression of NCAM 140 by human small and large cell lung carcinomas suggests its potential as a diagnostic marker.
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PMID:NCAM: a surface marker for human small cell lung cancer cells. 216 22

The respective pretreatment prognostic impacts of the following markers were evaluated in 125 patients with small cell lung cancer (SCLC): lactic dehydrogenase (LDH), serum thymidine kinase (S-TK), carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), and tissue polypeptide antigen (TPA). More traditional clinical and serologic markers were also evaluated. Univariate analysis showed that all of the biochemical markers mentioned above, the Karnofsky index (KI) and the patient's sex were related to both the stage of disease (limited/extensive disease: LD/ED) and to survival. The strongest marker for the clinical stage was S-TK, whereas TPA showed the strongest relationship with survival. Multivariate analyses produced a model consisting of S-TK, CEA, NSE, and the patient's sex for determining the clinical stage. To compare the prognostic capacity of easily determined biochemical and simple clinical variables to the more resource-demanding variable of the clinical stage, three multivariate analyses in relation to survival were performed: (1) biochemical markers and simple clinical variables; (2) LD/ED and simple clinical variables; and (3) all available variables. The model obtained from the first analysis included TPA, KI, age, and the patient's sex; the model from the second analyses included LD/ED, patient's age, and KI; and the model from the third analysis, TPA, KI, age, sex, and LD/ED. Indices based on these three multivariate models were calculated for each patient and the prognostic capacity of these indices was compared. Pretreatment serum marker levels also had the capacity to predict both the grade and the duration of the response to therapy.
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PMID:Clinical and serologic markers of stage and prognosis in small cell lung cancer. A multivariate analysis. 216 41

Biopsy specimens obtained from eight patients with lung cancer were tested for content of somatostatin receptors by autoradiography. Somatostatin receptors were detected in two of three patients with small cell lung cancer (SCLC) but in none of five patients with non-small cell lung cancer (NSCLC) including adenocarcinoma (two), squamous cell carcinoma (two), and bronchoalveolar carcinoma (one). In those with SCLC, specific somatostatin receptor binding was evidenced only in tumor foci and not in surrounding stroma or normal lung parenchyma. Further tissue characterization by immunoperoxidase staining with the pancytokeratin monoclonal antibody, mAB-lu-5, revealed labeling to all of the NSCLC but to none of the SCLC specimen. Selective immunoreactivity was detected in both the SCLC and the NSCLC specimen to chromogranin and neuron-specific enolase (NSE) whereas none of the specimen had detectable immunostaining to somatostatin, bombesin, serotonin, adrenocorticotropic hormone, neurofilament, calcitonin, and synaptophysin. The identification of somatostatin receptors in primary human lung cancer may have a bearing on the biology of this disease and perhaps on the clinical application of somatostatin analogues in patients with SCLC.
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PMID:Identification of somatostatin receptors in human small cell lung carcinoma. 217 45

Permanent human small cell lung cancer (SCLC) cell lines established in our laboratory were investigated for their expression of the enzymatic neuroendocrine markers L-DOPA decarboxylase (DDC), neuron-specific enolase (NSE), and creatine kinase (CK), including its BB isoenzyme (CK-BB), the classical tumor markers carcinoembryonic antigen (CEA), the alpha and beta subunits of human chorionic gonadotropin (alpha-HCG, beta-HCG), and alpha-fetoprotein (alpha-FP), and their chromosomal characteristics. DDC activities were detectable in 5/6 SCLC cell lines and absent in non-SCLC. NSE levels ranged from 160 to 1422 ng/mg soluble protein and were less than 290 ng/mg soluble protein in non-SCLC. Activities of CK and levels of CK-BB clearly distinguished SCLC from non-SCLC with CK activities greater than 1000 munits/mg soluble protein and CK-BB levels greater than 3000 ng/mg soluble protein in SCLC and less than 300 munits/mg soluble protein and less than 2000 ng/mg soluble protein in non-SCLC. CEA was detectable in 5/6 SCLC cell lines but absent in non-SCLC, and its level seemed to correlate with those of DDC, NSE, and CK. One cell line, SCLC-16H, lost some of its neuroendocrine properties and CEA after 1 year of in vitro cultivation. Generally, marker levels were low in fast growing cell lines and high in slow growing cell lines. HCG alpha and beta subunit and alpha-FP were not detectable in SCLC cell lines. All SCLC cell lines examined had near diploid DNA indices and modal chromosome numbers. Double minute chromosomes and homogeneously staining regions were found in 2/5 and 4/5 SCLC cell lines respectively. With respect to chromosomal aberrations, we found a deletion of the short arm of at least one chromosome 3 in all SCLC cell lines (5/5). These data show that SCLC expresses neuroendocrine markers and CEA; CK is the most sensitive marker, and DDC and CEA are the most specific markers for SCLC in vitro; individual marker levels correlate with each other and the in vitro malignancy of SCLC; and SCLC cell lines have relatively uniform chromosomal characteristics. Our results suggest that patients whose tumors have high levels of DDC, NSE, CK-BB, and CEA have a better prognosis than those with low marker levels. This hypothesis could be proved by comparing pairs of patients that are matched for all known prognostic parameters, in particular tumor spread, for their serum and tumor marker levels with respect to the patients' outcome and prognosis.
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PMID:Markers and characteristics of human SCLC cell lines. Neuroendocrine markers, classical tumor markers, and chromosomal characteristics of permanent human small cell lung cancer cell lines. 243 85

Three monoclonal antibodies (mAbs), NCC-LU-243, -244 and -246, detected three different epitopes on a 145-kDa cell membrane antigen, which had been designated as the cluster 1 antigen at the First International Workshop on Small Cell Lung Cancer (SCLC) Antigens. The distribution of the antigen in various tissues, cultured cells and sera was examined by immunohistochemistry and sandwich radioimmunoassay using these mAbs. The antigen is a normal differentiation antigen and is present in neuronal, neuroendocrine and cardiac muscle cells. The level of the antigen was highest in central nervous tissues, while it was undetectable in the liver, kidney and peripheral lung. Among tumor tissues, the antigen was detected only in SCLC, carcinoid tumor and neuroblastoma, indicating its usefulness as a marker for discriminating SCLC from non-SCLC. The level of the antigen varied among SCLC tissues and tended to be lower in variant-type cultured SCLC cells. Although an increase in the antigen level was observed in sera of some patients with advanced SCLC, the antigen did not possess any additional value over neuron-specific enolase as a serum tumor marker for monitoring SCLC patients.
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PMID:Quantitative distribution of cluster 1 small cell lung cancer antigen in cancerous and non-cancerous tissues, cultured cells and sera. 247 55

We studied the value of pleural fluid neuron-specific enolase as a possible diagnostic marker for pleurisy of small cell lung cancer by using enzyme immunoassay. Pleural fluid NSE levels in 12 patients with carcinomatous pleurisy due to small cell lung cancer were compared with those in 37 patients with carcinomatous pleurisy due to non-small cell lung cancer and 39 patients with tuberculous pleurisy. The pleural fluid NSE level was elevated in nine of 12 (75 percent) patients with SCLC. However, only two of 37 (5 percent) patients with NSCLC and two of 39 (5 percent) patients with tuberculous pleurisy had an elevated pleural fluid NSE level. Moreover, none of ten SCLC patients with cytology-negative pleural effusions showed elevated pleural fluid NSE level. Thus, determination of pleural fluid NSE levels seems to be an effective means to differentiate carcinomatous pleurisy due to SCLC from that due to NSCLC, tuberculous pleurisy and cytology-negative pleural effusion in SCLC.
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PMID:Pleural fluid neuron-specific enolase. A useful diagnostic marker for small cell lung cancer pleurisy. 253 10

Neuron-specific enolase (NSE) was purified from human brain to a specific activity of 91 U/mg with no demonstrable impurities. The enzyme has a molecular weight of 96,000, consists of two subunits of 47,000, and has an isoelectric point at pH 4.5. A radioimmunoassay based on antibody raised in sheep was established. The assay has a sensitivity of 2 micrograms/l, and an interassay coefficient of variation of 6.4% at 10 micrograms/l. The reference limit was defined as 10 micrograms/l, as found in sera from a population of 389 persons. Of 50 untreated patients with small cell lung cancer (SCLC), 70% had NSE levels above 10 micrograms/l. None of 170 patients with non-SCLC neoplasms had elevated enzyme levels.
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PMID:Establishment and evaluation of a radioimmunoassay for neuron-specific enolase. A marker for small cell lung cancer. 253 16

Small cell lung cancer (SCLC) is histologically simple and looks undifferentiated, but possesses cytoplasmic dense-cored granules resembling neuroendocrine granules, and frequently produces amine and peptide hormones, occasionally presenting related symptoms. Among these bioactive substances, gastrin releasing peptide (GRP) is most important, which is known as autocrine growth factor and one of the useful monitoring markers for SCLC together with neuron-specific enolase. Aromatic L-amino acid decarboxylase is another important enzyme in SCLC. Abnormality of myc family oncogenes is occasionally noted in SCLC, which appears related to proliferative activity of the tumor rather than development. Deletion of chromosomes 3p, 13q and 17p is noted in almost every SCLC, where antioncogene is suspected to be present, and inactivation of antioncogene may play an important role in development of SCLC. Nucleolar size is the important parameter for proliferative potential of SCLC. The larger the nucleoli, the faster is the growth of SCLC. Phenotypes of SCLC in vitro may be altered by change of microenvironment, although it may be due to the selective growth of a certain clone. SCLC and nervous tissue specific membrane antigen is named cluster 1 SCLC antigen, the monoclonal antibody to which will be utilized for immunohistological diagnosis, imaging and treatment of SCLC. Accumulation of basic knowledge is now leading to reconsideration of histological subtyping of SCLC.
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PMID:[Recent advances in pathology and biology of small cell lung cancer]. 254 78

This study analyses retrospectively the plasma level of neuron-specific enolase (NSE) performed in 236 patients presenting for the diagnosis of a bronchopulmonary disease. Taking a cut off on 15 micrograms/L, 61 (64%) of the 95 patients sharing a small cell lung cancer (SCLC) (45% of those with a limited disease and 90% with an extensive disease) but 8 (13%) of 60 with a non small cell lung cancer patients and 0% of those with a benign bronchopulmonary disease showed an abnormal value of NSE. Therefore in this group of patients, the diagnosis of SCLC could be assessed with a sensitivity of 64% and a specificity of 94% in patients with an NSE plasma level above 15 micrograms/L. In addition, the interest of sequential dosages of NSE for the monitoring of SCLC patients is also stressed.
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PMID:[Serum level of neuron-specific enolase: value as tumor marker of microcellular bronchial cancer]. 255 29


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