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

DNA was prepared from normal tissue and 19 lung cancer cell lines. Using probes which detect restriction fragment length polymorphisms at both the topoisomerase II alpha and beta loci, heterozygosity was detected at a frequency of 0.17 and 0.37 for the alpha and beta loci, respectively. Southern blot analysis of DNA extracted from lung cancer cell lines detected amplification of both the topoisomerase II alpha and ERBB2 genes in the adenocarcinoma line Calu3. These results indicate that topoisomerase II alpha and ERBB2 may be closely linked on chromosome 17 and coamplified during adenocarcinoma progression. Since topoisomerase II is a target for several anticancer drugs, it will be of interest to study alterations to topoisomerase II genes during tumour development, as these may in part determine the response of the tumour to chemotherapy.
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PMID:Amplification of the topoisomerase II alpha gene in a non-small cell lung cancer cell line and characterisation of polymorphisms at the human topoisomerase II alpha and beta loci in normal tissue. 137 18

Non-small-cell lung cancer (NSCLC) is one of the tumors that shows intrinsic drug resistance to various chemotherapeutic agents. We investigated a possible role of the multidrug resistance (mdr1) gene amplification using a DNA slot blot analysis in 23 untreated non-small-cell lung cancer tissues and 14 corresponding adjacent normal lung tissue samples. In all instances, whether tumors or adjacent normal tissue samples, DNA amplification was not detected except in 1 adenocarcinoma and 2 squamous cell carcinomas that had a low level of amplification of mdr1 gene. In addition, 6 untreated tumors and 7 normal tissue samples were examined for mdr1 RNA expression using RNA slot blot analysis. Only low levels of mdr1 expression were observed in all cases. We conclude that mechanisms other than mdr1 amplification or expression account for the intrisic drug resistance of non-small-cell lung cancers.
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PMID:Study of multidrug resistance (mdr1) gene in non-small-cell lung cancer. 137 98

On review of 115 poorly or undifferentiated lung cancers from 671 lung tumors resected over a 7-year period, we have found 38 cases of basaloid carcinoma. The cardinal histopathologic features distinguishing this tumor from other non-small cell lung cancers are a lobular growth pattern of small cells with moderately hyperchromatic nuclei, with no prominent nucleoli, and with scant cytoplasm, a high mitotic rate, and peripheral palisading. Basaloid carcinoma was present in a pure form in 19 cases and the other 19 tumors were of a mixed, but prominent, basaloid type associated with squamous cell carcinoma, large cell carcinoma, or adenocarcinoma. The immunophenotype of basaloid cancers was close to that of basal bronchial epithelial cells, with a low level of expression of low molecular weight cytokeratins. Staining for neuroendocrine markers was infrequent and inconsistent. Ultrastructural study showed an absence of neurosecretory granules and the presence of some squamous and/or glandular differentiation. This morphologic and immunologic phenotype suggests that basaloid carcinoma is derived from a pluripotent reserve cell or a basal bronchial epithelial stem cell. This unique histologic form of lung tumor has a poor prognosis, with a median survival rate of 22 months for stage I and II disease. This justifies classification of basaloid carcinoma as a distinct form of lung cancer, separate from small cell lung carcinoma.
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PMID:Basal cell (basaloid) carcinoma of the lung: a new morphologic and phenotypic entity with separate prognostic significance. 838 56

The fact that routinely effective treatments for disseminated lung cancer are not available has prompted the search for effective early detection systems. It is important to identify lung cancer while it is still confined to the bronchial epithelium and is potentially curable with local modalities. We have previously reported on an immunologically based assay to identify antigens expressed on shed bronchial epithelial cells. This assay resulted in a statistically significant correlation of immunostaining with the eventual development of lung cancer 2-4 years prior to routine clinical detection. Attempts to further improve this approach require an understanding of the basis for its success. Based on the work of Hakomori and coworkers, this difucosylated Lewis X structure would be a likely marker of carcinogenic transformation of the bronchial epithelium. In fact, an antibody to this structure was useful for sputum immunocytochemistry analysis for early lung cancer detection. Other carbohydrate structures would also be reasonable markers to evaluate for early detection application, based on the known pattern of expression of these structures in fetal, dysplastic, and neoplastic lung tissue. Another antibody used for sputum immunostaining recognizes a 31-kd protein structure; the antibody is not a known member of a likely class of early detection targets. The reported cases of lung cancer missed by the immunostaining approach included principally adenocarcinoma of the lung, suggesting that the addition of a marker(s) of that type of morphologic differentiation should be considered. Markers to dissect the various forms of lung adenocarcinoma are being characterized and are available for evaluation in early detection applications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rational targets for the early detection of lung cancer. 138 92

An attempt was made to interpret the clinical significance of secondary infections associated with lung cancer. The incidence of secondary infections was 51.4% in 214 in-patients with lung cancer in our institution in 1988 and 1989, and almost all of them had respiratory infections caused by commonly encountered bacteria. The incidence of infection was high in lung cancer of cell types other than adenocarcinoma, and in those with hypoalbuminemia, impaired cellular immunity and obstruction of the airway. The prognosis in patients with infection was much poorer than that in patients without infection. Major pathogens responsible for infection were Staphylococcus aureus including methicillin-resistant S. aureus (MRSA), Haemophilus influenzae, Klebsiella spp. and Pseudomonas aeruginosa. These pathogens, except for H. influenzae, were isolated in the terminal stage in cases with airway obstruction and post cancer chemotherapy. The efficacy rate of 194 therapeutic regimens against infection was 57.7%. It was thus found that the efficacy rate in 1988 and 1989 exceeded that in the 1970s. The effectiveness was very poor for infections caused by S. aureus and P. aeruginosa, and for cases with airway obstruction and marked impairment of pulmonary blood flow. The efficacy rate of single-drug regimens was 57.1% (80/140) and that of combined regimens was 59.3% (32/54). The above results indicate that a new combined therapy which includes a beta-lactam antibiotic as well as measures to improve the general health of compromised hosts are required in the treatment of secondary infections in these patients.
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PMID:[Clinical significance of respiratory infections associated with lung cancer patients]. 140

To identify DNA sequences that are deleted in human lung cancer, genomic subtraction hybridization was used to construct plasmid libraries that are enriched for DNA sequences deleted in the small cell lung carcinoma cell line SK-LC-17. The clones of the libraries contained predominantly single copy sequences, allowing direct screening of normal and tumor DNA by genomic Southern blotting. Of 150 clones tested, three independent clones (del-27, del-118, and del-109) were identified that specifically hybridized with normal human DNA but not with tumor DNA from the cell line SK-LC-17. The corresponding DNA sequences are localized on human chromosomes 5, 8, and X/Y. The DNA regions identified by del-109 and del-118 were also found to be deleted in several other lung carcinoma cell lines. Moreover, del-118 was deleted in a freshly isolated lymph node metastasis of a human lung adenocarcinoma. It is therefore reasonable to speculate that the identified clones are derived from independent genetic loci encoding potential tumor suppressor genes.
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PMID:Isolation of DNA sequences deleted in lung cancer by genomic difference cloning. 140 87

Flow cytometry was used to detect platelet-associated fibrinogen (PA-Fbg), platelet-associated fibronectin (PA-FN) and platelet-associated thrombospondin (PA-TSP) on the surface membrane of platelets and plasma (P)-TSP in 30 patients with lung cancer (16 case of adenocarcinoma and 14 of squamous cell carcinoma). ELISA was used to analyze beta-TG and PF4. In the lung cancer group, beta-TG and PF4 were higher than those of a normal control group. PA-Fbg values were correlated with beta-TG and PF4 values. Each adhesive protein had a higher value in the patient than in the normal control group, and the degree of the increase was related to the progression of clinical disease stage. In the squamous cell carcinoma group, the P-TSP value was significantly elevated. Platelet size increased as the clinical stage of the disease progressed. These results suggest the following: 1. An increase in PA-Fbg can indicate the presence of activated platelets. 2. In patients with lung cancer, activated platelets appear in the blood, and their numbers increase as the clinical stage of the disease progresses. 3. Differences in histologic type led to differences in binding adhesive protein.
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PMID:[Analysis of adhesive proteins on the surface of platelets from the patients with lung cancer: studies in histological type and clinical stage]. 143 32

At the Veterans Administration Medical Center in Washington, DC, 73 patients with bronchogenic carcinoma had pulmonary wedge resection from February 1967 to March 1988, with a 1.4% perioperative mortality and a 4.1% morbidity. Mean age of the patients was 63 years. Patients were considered poor risk with a mean Goldman index of 9 +/- 4 (class II), mean ASA physical status classification II, mean 1-second forced expiratory volume (FEV1) of 1.25 liters (42% predicted), ratio of FEV1 to forced vital capacity 30% predicted, and maximum voluntary ventilation 24% predicted. Staging of the bronchogenic carcinomas indicated 68% stage I, 15% stage II, and 17% stage III, and histology showed 41% epidermoid, 40% adenocarcinoma, 12% bronchoalveolar, 3% large cell, and 4% small cell type. For the 72 patients eligible for follow-up, data were available on 62 for a period ranging from 4 months to 15 years. Survival was 94% at 1 year, 55% at 3 years, 29% at 5 years, 5% at 10 years, and 2% at 15 years. Within 5 years, 21% of the patients had died of causes other than bronchogenic carcinoma. The rate of recurrence was 16%. Analysis by each stage of lung cancer showed local recurrence in 4% of patients with stage I disease, in 9% of those with stage II disease, and in 59% of those with stage III disease. We conclude that wedge resection provided acceptable surgical treatment in a group of high-risk surgical patients.
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PMID:Wedge resection for bronchogenic carcinoma in high-risk patients. 143 44

Preexisting lung disease was examined as a risk factor for lung cancer in a population-based, case-control study of nonsmoking women in Missouri conducted between June 1, 1986, and April 1, 1991. A history of lung disease was reported by approximately 41% of 618 cases and 35% of 1,402 controls (odds ratio (OR) = 1.2; 95% confidence interval (Cl) 1.0-1.5. The risk was more pronounced when next-of-kin interviews were excluded (OR = 1.5). Previous lung disease was significantly related both to adenocarcinoma (OR = 1.4), which accounted for 62% of the cancers, and to all other cell types of lung cancer combined (OR = 1.8). Despite having discontinued smoking for more than 15 years, long-term ex-smokers were at a 2.2-fold risk of lung cancer compared with lifetime nonsmokers. Among lifetime nonsmokers, significant risks were noted for asthma (OR = 2.7) and pneumonia (OR = 1.5). Emphysema (OR = 2.6) and tuberculosis (OR = 2.0) were also significantly related to lung cancer, but only among former smokers. Chronic bronchitis was linked to elevated risks of nonadenocarcinomas only (OR = 2.3). Pleurisy was not reported more frequently by cases than by controls. Approximately 16% of all lung cancers among nonsmoking women could be attributed to previous lung diseases, most notably asthma, pneumonia, emphysema, and tuberculosis.
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PMID:Preexisting lung disease and lung cancer among nonsmoking women. 144 29

Carbohydrate antigen 19-9 (CA19-9) was measured in bronchial lavage fluid in 21 patients with lung cancer and 4 patients with benign lung diseases (2 patients with DPB, 2 patients with BE). Bronchial lavage of the tumor-related bronchus was performed. In normal subjects, levels of CA19-9 in lavage fluid were less than 1000 IU/ml. On the other hand, in 6 patients with lung cancer, levels of CA19-9 were higher than 1000 IU/ml, and in 3 of these cases, CA19-9 levels were higher than 8000 IU/ml. All six three cases were histologically diagnosed as adenocarcinoma. Tumor resected at operation was then stained by antibody recognizing CA19-9. Tumor in cases with high levels of CA19-9 was stained immunohistochemically. These results indicate that measurement of CA19-9 in bronchial lavage fluid of the tumor-related bronchus is a useful auxiliary method in the diagnosis of lung cancer.
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PMID:[Measurement of CA19-9 in bronchial lavage fluid from patients with lung cancer]. 144 44


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