PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LUNG NEOPLASMS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1997

[Current capabilities and procedures for diagnosing lung neoplasms].

Lung cancer is the most common malignant cancer in males and it's incidence is rapidly rising in females. Factors linked to this are associated with cigarette smoking, urbanization along with atmospheric pollution. The lack of success in the treatment of lung cancer has to do with in many cases late diagnosis at the stage when surgical treatment is not possible and radio and chemotherapy being of minimal effectiveness. The WHO has proposed the following classification of lung cancer: 1. Squamous cell carcinoma; 2. Small cell carcinoma; 3. Adenocarcinoma; 4. Giant cell carcinoma; 5. Adeno-squamous cell carcinoma 6. Carcinoid. 7. Carcinoma of mucous gland. 8. Others. Early physical signs of lung cancer are: cough (50-80% of patients), dyspnea (10-15%), chest pain (15-20%), hemoptysis (20-50%), recurrent pneumonia and bronchitis (30-50%). More serious clinical signs associated with growth of the neoplasm are hoarseness, pleural effusion, vena cava superior syndrome, and Pancoast's syndrome. The growing neoplasm secrets many biochemical substances, which are them activity passed on the bloodstream or make their way into the blood as a result of degeneration of the tumor. These substances may then be detected in the patient's plasma and act as markers of malignant disease. The characteristics of these markers is varied, e.g.: hormones, enzymes and tissue antigens. Methods used in the diagnosis of lung-cancer which should be stressed, are apart from the obvious physical examination are chest x-rays, ultrasound, CAT scans, nuclear magnetic resonance, PET scans, and scintigraphy. Fine needle aspiration in changes in the peripheral regions, cytology of sputum, bronchial lavage, cytogenetic analysis. This underlines the need for prophylaxis, particularly the cessation of cigarette smoking.

Biomarkers, Tumor↗
PubMed2004

Discrimination of human lung neoplasm from normal lung by two target genes.

Simple tools for discrimination of lung tissues can be useful in a fast machine-aided diagnosis, for example, by tumor-specific microarrays. We demonstrate that an easy ratio technique, based on the expression levels of only two genes differentially expressed in lung tumor and normal lung samples, allows discrimination of normal and neoplastic lung with a sensitivity of 100% and specificity of 90.5%. DNA microarray analysis of 99 lung tumor samples and 15 normal lung tissues revealed that receptor for advanced glycation end products (RAGE) mRNA is reduced fourfold (p = 7.8 x 10(-11)) and cyclin-B2 mRNA is upregulated twofold (p = 5.9 x 10(-18)) in lung carcinoma compared with normal lung. The microarray-calculated expression ratio of RAGE to cyclin-B2 was used in polymerase chain reaction analysis of 84 independent blinded samples to discriminate tumor and corresponding normal lung tissues. In 94.7% of the samples this quotient correctly distinguished non-small cell lung cancer from normal lung tissue, suggesting the RAGE/cyclin-B2 quotient as a potential means for diagnosis of lung cancer.

Adenocarcinoma↗
PubMed1991

[Activity of angiotensin I converting enzyme in serum and bronchoalveolar lavage fluid of patients with sarcoidosis and lung neoplasms].

The lungs have an important role in the synthesis of angiotensin I converting enzyme (ACE). In BAL fluid and serum the ACE activity was determined in 18 patients with sarcoidosis (11 with high intensity and 7 with low intensity alveolitis), 14 patients with lung cancer and 16 with acute bronchitis. The activity of ACE was examined by a reagent set produced by Boehringer Mannheim Biochemica Test-Combination ACE cat. no. 789/011. The ACE activity in the high intensity alveolitis group of sarcoidosis patients was significantly increased in BAL fluid and serum in comparison to other observed patients. On the other hand, in patients with lung cancer the ACE activity was also increased in comparison to acute bronchitis and referred norms, especially in BAL fluid. This findings suggest a role of neoplastic process in ACE secretion in the airways. Very low correlation observed between ACE activity in serum and BAL fluid indicates a separate mechanism of secretion.

Acute Disease↗
PubMed1984

Distribution of the Ca (Oxford) antigen in lung neoplasms and non-neoplastic lung tissues.

The Ca (Oxford) antigen was originally isolated from a malignant neoplasm and with few exceptions was reported to discriminate between malignant and non-malignant neoplasms or normal tissues. Using the Ca 1 antibody we have studied the Ca distribution in 54 lung neoplasms and adjacent non-neoplastic lung tissue. Staining of tumours was very focal and the proportion of positive cells varied from about 50% for adenocarcinomas to less than 1% for oat cell carcinomas, which were often negative. Focal cytoplasmic staining can be seen in all neoplasms, whereas membrane staining is mainly seen in their areas of glandular and squamous differentiation. We found consistently strong membrane staining of alveolar type II pneumocytes in non-neoplastic lung. This staining may be useful in differentiating type II cells from alveolar macrophages which only occasionally showed granular cytoplasmic staining, probably due to phagocytosed Ca. Mucin from tumours and bronchi did not stain but there was consistent staining of alveolar serous exudate suggesting extracellular location of Ca.

Adenocarcinoma↗
PubMed1990

[Histochemical localization of glyco-conjugate and CEA-glycoprotein in human lung neoplasms].

Sixty-six human lung neoplasms of different histological types and normal bronchial epithelial cells of newborn babies and adults were studied histochemically using ConA and PSA and the result was compared with that of CEA. Normal mucosal epithelium could bind to ConA, and the location of ConA receptors was related to the maturation of mucosal epithelial cells. Normal mucosal epithelium in adult bronchi failed to be stained with PSA and anti-CEA, and most of lung neoplasms could bind to PSA and positive for CEA, indicating that new glycoconjugate and CEA-glycoprotein could be synthesized after malignant transformation of mucosal epithelium. The binding of ConA, PSA and anti-CEA to cell membrane and nucleus membrane was characteristic of squamous cell lung cancer while lung adenocarcinoma mainly showed cytoplasmic staining. The weak staining of ConA, PSA and anti-CEA in small cell carcinoma and negative staining in carcinoid and malignant melanoma help testify that their origin may differ from that of squamous cell carcinoma and adenocarcinoma.

Adenocarcinoma↗
PubMedDate not supplied

Unusual primary lung neoplasms: spindle cell and undifferentiated lung carcinomas expressing only vimentin.

Two unusual primary carcinomas of the lung are described. One occurred in a 31-year-old man and was composed of large, undifferentiated, ovoid to polygonal cells. The other occurred in a 72-year-old man, was composed of spindle-shaped cells, and was initially diagnosed as a localized fibrous mesothelioma. The neoplastic cells of these tumors expressed only vimentin intermediate filaments and showed no other immunohistochemical features of epithelial neoplasms, although they exhibited a metastatic pattern characteristic of lung carcinomas. These two malignant neoplasms further expand the spectrum of unusual lung neoplasms, and suggest that there are pulmonary carcinomas that contain only vimentin intermediate filaments.

Adult↗
PubMedDate not supplied

The unusual spectrum of neuroendocrine lung neoplasms.

Neoplasms of the lungs showing neuroendocrine differentiation are classified histologically into the following groups: (1) carcinoid, (2) atypical carcinoid (well-differentiated neuroendocrine carcinoma and malignant carcinoid, (3) small cell neuroendocrine carcinoma (small cell undifferentiated carcinoma and oat cell carcinoma), and (4) large cell neuroendocrine carcinoma (atypical endocrine tumor of the lung and intermediate neuroendocrine carcinoma). Nine examples of neuroendocrine lung carcinomas are discussed that have unusual histologic features that make it difficult to assign them to one of the above groups, have unusual immunohistochemical features, have unusual ultrastructural features, or exhibit a biologic behavior different from what one would have predicted from their morphologic appearance. The findings in these nine cases suggest that the present classification of neuroendocrine lung neoplasms may be too precise and that these neoplasms, like other nonneuroendocrine pulmonary tumors, exhibit a wider morphologic and biologic spectrum than previously appreciated.

Adenocarcinoma↗
PubMedDate not supplied

Predominant K-ras codon 12 G --> A transition in chemically induced lung neoplasms in B6C3F1 mice.

Based on long-term toxicity and carcinogenicity studies in B6C3F1 mice conducted by the National Toxicology Program, 2,2-Bis(bromomethyl)-1,3-propanediol (BMP) and tetranitromethane (TNM) have been identified as carcinogens. Following 2 yr of exposure to 312, 625, or 1,250 ppm BMP in feed, or exposure to 0.5 or 2 ppm TNM by inhalation, increased incidences of lung neoplasms were observed in B6C3F1 mice at all exposure concentrations compared to unexposed mice. The present study characterizes genetic alterations in the K-ras protooncogene in BMP- and TNM-induced lung neoplasms, respectively, and compares the findings to spontaneous lung neoplasms from corresponding control mice. The frequencies of the K-ras mutations were 57% (29/51) in BMP-induced lung neoplasms compared to 15% (3/20) in lung neoplasms from dosed feed control mice, and 54% (14/26) in TNM-induced lung neoplasms compared to 60% (3/5) in lung neoplasms from inhalation control mice. G --> A transitions at the second base of the K-ras codon 12 (GGT --> GAT) were the most frequent pattern of K-ras mutations identified in BMP-induced (20/29) and TNM-induced lung neoplasms (13/14), which differed from the mutational patterns identified in the lung neoplasms from unexposed control mice. These results indicate that mutations in the K-ras gene are involved in B6C3F1 lung carcinogenesis following BMP- and TNM-exposure, and the high frequency and specificity of the ras mutation profile in lung neoplasms (G --> A transition) may be due to in vivo genotoxicity by the parent compounds or their metabolites.

Animals↗
PubMed1995

Increased frequency of K-ras mutations in lung neoplasms from female B6C3F1 mice exposed to ozone for 24 or 30 months.

The National Toxicology Program recently completed long-term ozone inhalation studies in B6C3F1 mice and F344/N rats. Mice and rats were exposed to 0, 0.5 or 1.0 p.p.m. ozone by inhalation for 24 or 30 months. There was an increased incidence of lung neoplasms in B6C3F1 mice. However, there was no evidence of carcinogenicity in F344/N rats. The objectives of this study were to (i) evaluate benign and malignant lung neoplasms from B6C3F1 mice for mutations in the K-ras gene at codons 12, 13 and 61, (ii) determine if the frequency and spectra of K-ras mutations were unique for ozone-induced lung neoplasms, (iii) determine if specific K-ras mutations were associated with the size and morphological patterns of lung neoplasms or ozone exposure concentrations and (iv) screen lung neoplasms by immunohistochemical methods for the p53 protein. K-ras mutations were detected by single-strand conformation analysis and identified by direct sequencing of polymerase chain reaction-amplified DNA isolated from formalin-fixed, paraffin-embedded neoplasms. K-ras mutations were detected in 73% of ozone-induced neoplasms, as compared with 33% of lung neoplasms from controls. The predominant mutations consisted of A-->T transversions at codon 61 (8/19) and G-->T transversions at codon 12 (7/19). Specific K-ras mutations in lung neoplasms were not associated with various morphological patterns. Our data suggests that ozone may cause direct and/or indirect DNA damage in the K-ras proto-oncogene of B6C3F1 mice.

Adenocarcinoma, Bronchiolo-Alveolar↗