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)

Extragenital choriocarcinoma in the male is known to occur in retroperitoneum, mediastinum and pineal body in a high proportion, and there have been no certain reports of lung origin. We studied two cases of choriocarcinoma arising from the lung in the male by histological, electronmicroscopical, immunofluorescent, and immunoenzyme methods. Histologically, characteristic changes of choriocarcinoma, composed of irregular complex of cytotrophoblasts and syncytiotrophoblasts with massive necrosis and hemorrhage were demonstrated. These two cell patterns, characteristic of choriocarcinoma, were also demonstrated electronmicroscopically and differed from giant cell carcinoma of the lung. By immunofluorescent and immunoenzyme methods, anti-HCG reactive particles were seen in the cytoplasm mainly of syncytiotrophoblasts and proved HCG production function of the tumor.
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PMID:Primary choriocarcinoma of the lung: case report of two male subjects. 55 68

The elevation in the serum level of CEA in cancer patients undergoing treatment with 5-FU and other antitumor drugs has been reported. In the present study, the ectopic synthesis of multiple carcinoplacental markers has been observed to be induced (10- to 264-fold) simultaneously in the same cervical carcinoma cells (HeLa65, HeLa71 and HeLa2.2) by hydroxyurea and sodium butyrate. Among the drug-induced biochemical markers observed in HeLa cells are four sialopeptides. Regan Isoenzyme (Placental Isoenzyme of Alkaline Phosphatase), HCT-Beta, FSH-Beta, HCG-Alpha and also a steroid hormone, Progesterone. The peptide and steroid hormones were quantitated by specific radioimmunoassays (RIA), in cultured cells, media, and homogenates of tumor tissues. The induction of biochemical markers was observed also with lung carcinoma cells. That multiple polypeptides, or steroids regulated by them, are simultaneously inducible in the same cancer cells, suggest the proximity on the DNA strand of several oncofetal and oncoplacental genes derepressed by antineoplastic drugs. This fundamental study has had important clinical ramifications. The results may be used to recognize the retention by cancer patients of occult malignancy after radiotherapy or surgery. The unsuspected metastasis may be reflected by a transient rise in the serum level of these markers during chemotherapy with anticancer drugs, which specifically inhibit DNA replication without interfering with the transcription of messenger-RNA and subsequent translation of proteins. The drug-induced protein-hormones, observed in this study, are the products of activated trophoblastic/pituitary genes in the nondividing DNA of neoplastic cells.
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PMID:Drug-induced biochemical markers of cancer in cervical carcinoma cells. 617 42

Two human cell lines have been established in vitro from patients with small cell carcinoma of the lung (SCC). The U-1285 line was derived from the classical small cell type of SCC while the U-1568 originated from a larger cell variant. The cell lines grow as suspension cultures and have been passaged continuously in vitro for 3 years (U-1285) and 2 years (U-1568), respectively. The malignant nature of the lines is suggested by their infinite growth potential, their capacity to form colonies in agarose and their aneuploidy. Both cell lines contain cytoplasmic electron dense particles indistinguishable from classical neurosecretory granules but only in U-1568 has hormone production (human chorion gonadotropin (alpha-HCG)) been proven. The U-1568 line produces carcino-embryonic antigen (CEA) while both U-1285 and U-1568 produce alpha-feto-protein (AFP). Chromosome analysis reveal aneuploidy of both lines. Among structural aberrations, involvement of chromosome 14 in U-1285 and chromosomes 1, 7 and 12 in U-1568 is interesting since alterations of these chromosomes have been described previously in other malignant conditions.
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PMID:Establishment and characterization of two neoplastic cell lines (U-1285 and U-1568) derived from small cell carcinoma of the lung. 628 65

In order to extend the usefulness of the quantitation of urinary nucleoside markers, studies were undertaken to explore the adaptability of such determinations for early detection in cancer-prone populations such as asbestos workers. Another study was aimed at exploring the usefulness of therapy in individual patients. During these studies, two heretofore unknown phenomena serendipitously emerged which expand the versatility of the marker determinations: (a) radiation damage in animals and humans causes an excretion of urinary BAIB which from preliminary studies appears to be proportional to the irradiation burden, and (b) lead poisoning in the human also produces BAIB excretion. Some of the practical uses of these determinations are self-evident. Among 13 asbestos workers without clinical symptoms, eight were found to have significant elevations of the marker levels. Nine asbestos workers with diagnosed mesothelioma all excreted two or more markers at high levels. Some of the psi levels were the highest seen. Currently the diagnosis of mesothelioma is difficult and painful, requiring a rib resection; however, an asbestos worker with such elevations--provided small cell carcinoma of the lung is ruled out--can be seriously suspected of having mesothelioma. In a study of the usefulness of the markers in following therapy of trophoblastic disease, these markers were determined in women with incipient invasive hydatidiform mole. After curettage, the nucleoside markers indicated absence of residual disease but the usual marker, HCG, was still markedly elevated. The women were followed up for 2 years and were found to remain symptom-free. Therefore the source of the nucleoside markers is cleared more rapidly than that of HCG.
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PMID:New applications of urinary nucleoside markers. 684 96

To evaluate the diagnostic usefulness of simultaneous determinations of carcinoembryonic antigen (CEA), neuron specific enolase (NSE), chorionic gonadotrophin (HCG) and carbohydrate antigenic determinant 19-9 (CA 19-9), we studied 48 patients with small cell lung carcinoma (SCLC) and 15 with nonmalignant lung disease. The combination of CEA-BAL, NSE-BAL, and NSE-serum taken together with results of bronchoscopy (histologic and cytologic) showed the highest discriminating power between malignant (SCLC) and nonmalignant lung disease. The sensitivity of bronchoscopy alone was 35%. However, when bronchoscopy results were combined with 3 positive markers, the sensitivity increased to 71%, with at least 2 positive markers to 94%, and with at least 1 positive marker to 100%. When both bronchoscopy and all 3 markers were negative, the results showed a negative predictive value of 100%.
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PMID:Usefulness of a multiple biomarker assay in bronchoalveolar lavage (BAL) and serum for the diagnosis of small cell lung cancer. 827 60

Multiple and bilateral oncocytomas are rare. There are only ten cases that have been previously described. Three of these displayed multiple and bilateral oncocytomas and microoncocytomas, a so-called oncocytomatosis. This report describes a case of renal oncocytomatosis found at autopsy. In addition, we found an adrenal adenoma, a pheochromocytoma and thoracic cicatrices 4 years after curatively resected large cell carcinoma of the lung. In the distal renal tubules we found oncocytic epithelial cells, with partial transition into microoncocytomas. Immunohistochemically, these and the main oncocytomas were CD 10 negative. These findings support the origin of oncocytoma from oncocytically transformed distal tubular epithelium. CGH analysis of the different tumors revealed no common cytogenetic changes. Coexistence of renal oncocytoma with other tumors is rare. Hitherto, coexistence of a renal oncocytomatosis with multiple tumors has not been described.
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PMID:[Renal oncocytomatosis]. 1041 79

Genomic alterations have been identified in lung cancer tissues and reported in numerous studies. To analyze genomic aberrations in lung cancer patients, we used array comparative genomic hybridization (array CGH) in 14 squamous cell lung carcinoma (SqC) tissues. Copy number gain and loss in chromosomal regions were detected, and the corresponding genes were confirmed by real time PCR. Several frequently altered loci, including gain of 3q (36% of samples), were found. The most frequently identified losses were found at 14q32.33 (21% of samples). The relative degree of chromosomal change was analyzed using log2 ratios. High-level DNA amplifications (>0.8 log2 ratio) were detected at 20 regions in 1p, 2q, 3q, 4q, 6q, 7p, 8q, 9p, 10q, 12q, 14q and 19p. We found that the fold change levels were highest at EVI1 (3q26.2), LPP (3q27-28) and FHF-1 (3q28) gene loci. Our results show that array CGH is a useful tool for identification of gene alteration in lung cancer, and that the above-mentioned genes might represent potential candidate genes for pathogenesis and diagnosis of lung cancer.
Lung Cancer 2007 Jan
PMID:Comparative genomic hybridization array analysis and real time PCR reveals genomic alterations in squamous cell carcinomas of the lung. 1710 92

Alterations in genomic content and changes in gene expression levels are central characteristics of tumors and pivotal to the tumorigenic process. We analyzed 23 non-small cell lung cancer (NSCLC) tumors by array comparative genomic hybridization (array CGH). Aberrant regions identified included well-characterized chromosomal aberrations such as amplifications of 3q and 8q and deletions of 3p21.31. Less frequently identified aberrations such as amplifications of 7q22.3-31.31 and 12p11.23-13.2, and previously unidentified aberrations such as deletion of 11q12.3-13.3 were also detected. To enhance our ability to identify key acting genes residing in these regions, we combined array CGH results with gene expression profiling performed on the same tumor samples. We identified a set of genes with concordant changes in DNA copy number and expression levels, i.e. overexpressed genes located in amplified regions and underexpressed genes located in deleted regions. This set included members of the Wnt/beta-catenin pathway, genes involved in DNA replication, and matrix metalloproteases (MMPs). Functional enrichment analysis of the genes both overexpressed and amplified revealed a significant enrichment for DNA replication and repair, and extracellular matrix component gene ontology annotations. We verified the changes in expressions of MCM2, MCM6, RUVBL1, MMP1, MMP12 by real-time quantitative PCR. Our results provide a high resolution map of copy number changes in non-small cell lung cancer. The joint analysis of array CGH and gene expression analysis highlights genes with concordant changes in expression and copy number that may be critical to lung cancer development and progression.
Lung Cancer 2007 May
PMID:Chromosomal aberrations and gene expression profiles in non-small cell lung cancer. 1725 48

Chromosomal aberrations of malignant cells from pleural effusions of 31 cases of lung adenocarcinoma were analyzed. Pooled CGH results showed frequent amplifications on chromosome arms 1p (22.6%), 1q (35.5%), 2q (25.8%), 3q (38.7%), 4q (41.9%), 5p (41.9%), 5q (51.6%), 6p (19.4%), 6q (25.8%), 7p (41.9%), 7q (35.5%), 8q (32.3%), 12q (38.7%), 13q (22.6%), 14q (35.5%), 17q (19.4%), Xp (22.6%), and Xq (38.7%). Frequent deletions were found on 1p (19.4%), 3p (16.1%), 4q (16.1%), 8p (25.8%), 9p (22.6%), 9q (29.0%), 10q (22.6%), 13q (22.6%), 16p (19.4%), 16q (22.6%), 17p (29.0%), 18q (16.1%), 19p (41.9%), 19q (32.3%), 20p (19.4%) and 22q (29%). These genomic changes were generally found consistent with previous reports of CGH analysis of primary tumors of lung adenocarcinoma. Loss of 19q and 22q were more frequently found in our studies (32.3% and 29.0%, respectively) than studies of primary tumors (less than 7% for both genetic changes). Gain of 11p, although not a frequent finding, was relatively more common in this (16%) than other studies (range, 2.9-11.8%). Interestingly, occurrences of 3p loss and 11p gain were higher in smokers than non-smokers, and deletion of 3p and increased copy number of 11p and Xp appeared more often in male than female patients. Among 17 male patients, gain of chromosomal 11p was a frequent aberration in tumors of smokers, while gain of Xp was more easily found in tumors of non-smokers. One candidate gene located within 11p15, lactate dehydrogenase C (LDHC), was selected for further study. Three cases with 11p gain had amplified FISH signals of LDHC. Also tumors from smokers or male had significantly higher transcript level of LDHC than non-smokers or female, respectively. The results demonstrate that different cytogenetic changes of malignant pleural effusions from lung adenocarcinoma are correlated with genders and smoking habits. The role of LDHC in the carcinogenesis of smoking-related lung adenocarcinoma, especially in male patients with pleural effusions, deserves further investigations.
Lung Cancer 2007 Sep
PMID:Chromosomal aberrations of malignant pleural effusions of lung adenocarcinoma: different cytogenetic changes are correlated with genders and smoking habits. 1755 91

The epidemiological relationship between squamous cell lung cancer (SCC) and chronic obstructive pulmonary disease (COPD), both smoking-related diseases, suggests that they have also a genetic basis. We compared 35 SCC patients with and without COPD with whole-genome gene expression profiles of laser microdissected tissue. Validation of differential expression was performed for 25 genes using quantitative (q)RT-PCR. Subsequently, we performed array-based CGH on the same tumor samples. We found that 374 probes were differentially expressed in SCC from patients with and without COPD. Forty-four probes were derived from genes with mitochondrial functions and 34 probes were located on 5q. All these probes showed a lower expression level in SCC from non-COPD patients. For a random selection of 25 mitochondrial and 5q genes, we confirmed the differential expression by qRT-PCR. Loss of 3p, 5q and 9p was observed, via array-CGH, to be more frequent in SCC from non-COPD patients as compared to SCC from COPD patients. Combination of chromosomal aberrations and the location of the differentially expressed genes showed significant association for loss of the 5q31.2-31.3 region and reduced expression of the 5q genes. In conclusion, a more frequent loss of 5q and a low expression of genes located on 5q in SCC tumors of non-COPD patients compared to tumors from COPD patients was identified suggesting that different oncogenetic pathways are operational in patients with and without COPD.
Lung Cancer 2011 May
PMID:A chronic obstructive pulmonary disease related signature in squamous cell lung cancer. 2083 96


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