Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of alveolar macrophage (AM) and activity of superoxide dismutase (SOD) and catalase (CA) in AM and obtained from bronchoalveolar lavage (BAL) were assayed in 11 lung cancer patients and 21 patients without lung cancer. The SOD, CA activities was lower in the patients with lung cancer than that in patients without lung cancer. The number of AM in BAL reduced too. It suggested that metabolism of AM was inhibited seriously in patients with lung cancer. The number of AM in BAL of smokers was significant higher than that of non-smokers, and it is postulated that the increase of AM is probably the result of stimulation induced by smoking.
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PMID:[Observation on the activity of superoxide dismutase and catalase of alveolar macrophage in patients with lung cancer]. 166 43

Forty-eight samples of primary non-small-cell lung cancer (NSCLC) and normal tissue from the same patients were analyzed for allelic deletions on chromosome 11p. Five polymorphic loci were assessed to determine the incidence of 11p sequence deletions and to define hot-spots of deletions. Information was obtained from all patients in at least one locus. Our data show that the deletions observed were not randomly scattered over the short arm of chromosome 11. Rather, 2 hot-spots of deletions were observed: one in the area of the genes for catalase and beta-FSH corresponding to band 11p13, the other close to the IGF-II locus corresponding to band 11p15. A high incidence of loss of heterozygosity (LOH) was found with the probe for catalase (21/29), a locus flanking the centromeric region of the Wilms' tumor locus. Most of the samples exhibiting LOH of one or more of the alleles analyzed remained heterozygous for at least one other chromosome 11p allele. Furthermore, duplication of the intensity of the remaining allele was rarely observed. Our results indicate that LOH on the short arm of chromosome 11 is a common event in NSCLC and that the chromosomal region containing the Wilms' tumor locus is most commonly involved.
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PMID:Allelic loss on the short arm of chromosome 11 in non-small-cell lung cancer. 168 78

A study was conducted to determine the bronchoscopic and chest roentgenographic findings associated with a positive TBNA. One hundred fifty-seven of 465 patients who were diagnosed for the first time as having carcinoma of the lung had a positive aspirate. Bronchoscopic findings associated with a positive TBNA of N2 nodes were carinal widening and endobronchial disease, especially of the right upper lobe. Mediastinal adenopathy noted on chest roentgenograms and subcarinal nodes on CAT scans were associated with a positive aspirate as well. In 34 of 465 patients, TBNA was the only means of establishing the diagnosis of pulmonary malignancy. A useful, simple and safe procedure, TBNA can be used to stage the mediastinum in patients with lung cancer and is most likely to be positive with endobronchial and nodal disease. It can also facilitate therapeutic decision-making in patients whose surgical candidacy is marginal.
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PMID:Bronchoscopic and roentgenographic correlates of a positive transbronchial needle aspiration in the staging of lung cancer. 195 1

Since 1987, 24 patients with inoperable non-small-cell lung cancer (NSCLC), stage T1-3 N0-2 M0, have undergone lymph node dissection and intraoperative radiation therapy (IORT) to the primary with 10-20 Gy. Patient selection criteria were nonresectability based on severe cardiorespiratory impairment, no radiological evidence of distant metastases and a Karnofsky performance status of greater than 80. In 18 patients the IORT procedure was followed by an external beam radiation series (EBR) including the tumor with 46 Gy and the regional lymph nodes with 46/56 Gy. The tumor response was assessed by CAT-scan volumetry before the institution of IORT, 4 weeks later, before the onset of EBR, 8 weeks after the combined treatment course and on a 3 months basis thereafter. Prospectively, MRI of the thorax with/without Gadolinium-DTPA was performed to examine contrast enhancement and signal behavior of the tumor, in an attempt to differentiate residual disease compared to therapy-related collateral damage. So far, 18 patients have completed the combined treatment course with a median follow-up of 11 months (range 4.5 to 25 months). The overall local response rate (CR and PR) was 88.2%. In detail, 11 complete responses, 6 partial responses and one minimal response were observed. The overall and recurrence-free survival at 25 months was 49.6% and 83.3%, respectively.
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PMID:Intraoperative plus external beam irradiation in nonresectable lung cancer: assessment of local response and therapy-related side effects. 217 42

The mechanism by which cigarette smoking and asbestos exposure synergistically increase the incidence of lung cancer is unknown. We hypothesized that cigarette smoke and asbestos might synergistically increase DNA damage. To test this hypothesis we exposed isolated bacteriophage PM2 DNA to cigarette smoke and/or asbestos, and assessed DNA strand breaks as an index of DNA damage. Our results supported our hypothesis. 78 +/- 12% of the DNA exposed to both cigarette smoke and asbestos developed strand breaks, while only 9.8 +/- 7.0 or 4.3 +/- 3.3% of the DNA exposed to cigarette smoke or asbestos, respectively, developed strand breaks under the conditions of the experiment. Our experimental evidence suggested that cigarette smoke and asbestos synergistically increased DNA damage by stimulating .OH formation. First, significant amounts of .OH were detected by electron paramagnetic resonance (EPR) in DNA mixtures containing both cigarette smoke and asbestos, but no .OH was detected in mixtures containing cigarette smoke alone or asbestos alone. Second, the .OH scavengers, dimethylsulfoxide (DMSO), mannitol, or Na benzoate decreased both .OH detection by EPR and strand breaks in DNA mixtures exposed to cigarette smoke and asbestos. Third, the H2O2 scavenger, catalase, and the iron chelators, 1,10-phenanthroline and desferrithiocin, decreased both .OH detection and strand breaks in DNA mixtures exposed to cigarette smoke and asbestos. These latter findings suggest that iron contained in asbestos may catalyze the formation of .OH from H2O2 generated by cigarette smoke. In summary, our study indicates that cigarette smoke and asbestos synergistically increase DNA damage and suggests that this synergism may involve .OH production.
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PMID:Role of oxidants in DNA damage. Hydroxyl radical mediates the synergistic DNA damaging effects of asbestos and cigarette smoke. 282 Oct 73

The high incidence of lung cancer in smokers is thought to be related to the direct exposure of bronchial and pulmonary cells to carcinogens in inhaled cigarette smoke. Using a 32P-postlabeling assay for chemically induced covalent DNA alterations, we found that unfractionated, relatively non-polar cigarette smoke components bound preferentially to lung and heart DNA in female ICR mice. After 6 days of topical treatment with cigarette smoke condensate (CSC) equivalent to a total of 4.5 cigarettes, covalent DNA damages was estimated to be 6.2, 5.7, 3.9 and 1.9 times higher, respectively, in lung, heart, skin and kidney than in liver, ranging from approximately 1 adduct in 5.4 +/- 0.7 X 10(6) DNA nucleotides in lung to 1 adduct in 3.3 +/- 0.6 X 10(7) DNA nucleotides in liver. Spleen DNA was virtually adduct-free. Adducts occupied two extensive zones, designated diagonal radioactive zone (DRZ) 1 and DRZ 2, on TLC fingerprints. Preference for lung and heart DNA was also observed in mice treated for 1 or 3 days. An inverse association appeared to exist between the tissue distribution of CSC-induced covalent DNA damage and the reported activity of enzymes catalyzing the metabolism of xenobiotics (cytochrome P-450 monooxygenases, phase II enzymes) and toxic oxygen species (superoxide dismutase, catalase). The results suggest that the well-known pulmonary and cardiovascular organotropism of cigarette-smoking-associated adverse health effects may, in part, have its origin in the inherent capacity of cigarette smoke components to induce lesions in lung and heart DNA in a tissue-specific manner. Possible mechanisms and health implications of the preferential binding of presumably aromatic CSC constituents to lung and heart DNA are discussed.
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PMID:Tissue distribution of covalent DNA damage in mice treated dermally with cigarette 'tar': preference for lung and heart DNA. 282 34

Selection modes for surgery were studied in a group of lung cancer patients. Selection is based: on the certain diagnosis of the disease, its histological classification and stage respiratory function tests and the assessment of any surgical indications. A total of 714 lung cancer cases were examined. Of these, 28.4% were at stage 1, 19.8% at stage 2 and 51.8% at stage 3. Only 141 patients or 19.8% of all cases examined were judged fit for radical exeresis. In the absence of metastasis all three stages of epidermoid carcinomas and adenocarcinomas were judged operable. In the case of microcytomas indication to surgery was limited to very few cases and only those in the first two stages. In the presence of metastasis to the hilar lymph nodes, surgery was only indicated where the metastasis was small. Exeresis was also indicated in the presence of single metastases to mediastinal lymph nodes on the same side as the neoplasia especially if these were considered intranodal. The difficulty of precise assessment of metastases to the hilar and mediastinal lymph nodes even with the aid of modern techniques like CAT scanning and mediastinoscopy was also noted. In 87 of 141 patients operated it was possible to check the result which was radical in 84 cases. In all, 19 pneumonectomies, 49 lobectomies and 16 bilobectomies were performed. The operative mortality rate was 3.4%. The various surgical indications were also examined in relation to the diverse clinical situations presented by lung cancers. In conclusion the modalities to be followed in order to enhance the value of radical resections in lung cancer are outlined. Above all diagnostic means must be refined to a point where the disease can be staged with maximum precision, patients for surgery must be selected with the utmost care and diagnosis must be as early as possible.
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PMID:[Indications for surgical intervention in patients with pulmonary cancer. Observations on 714 cases]. 370 28

The activity of erythrocyte superoxide dismutase (SOD) and catalase was determined in 38 patients with lung cancers (n = 15), malignant lymphoma (n = 11) and acute myeloid leukemia (n = 12). The patients with malignant lymphoma and acute myeloid leukemia showed a significant decrease in both enzyme activities (P less than 0.01) while the patients with lung cancer (9 squamous cell carcinomas and 6 small cell carcinomas) showed normal values of SOD and catalase activities. Furthermore, the patients with malignant lymphoma and acute myeloid leukemia, in remission, but not treated with anticancer drugs, also showed a significant decrease in SOD and catalase activity. These observations therefore indicate that a deficiency of erythrocyte SOD and catalase activities is caused by cancer and varies with the type of the cancer.
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PMID:Deficiency of erythrocyte superoxide dismutase and catalase activities in patients with malignant lymphoma and acute myeloid leukemia. 609 9

The evaluation of size and histological type of primary tumors of the lung and of the draining regional lymph nodes needs a very extensive diagnostic program. This means a standardized basic program (case history, physical examination, laboratory diagnosis, X-rays of the chest, cytologic evaluation of the sputum, and bronchoscopy), and further examination depending on the findings in the individual patients (lung scan, mediastinoscopy, needle biopsy, angiography, thoracoscopy, and sometimes diagnostic thoracotomy). Looking for distant metastases it is necessary to investigate the most frequently involved organs: the liver (sonography, scan, CAT scan, laparoscopy), the skeleton (scan, X-ray, biopsy), the central nervous system (CAT scan, electroencephalogram, liquor cytology, myelography), and the retroperitoneal space (sonography, CAT scan). It is absolutely necessary to follow this program in patients with small cell carcinoma. Contrary, in patients with other types of lung cancer the whole diagnostic program is indicated when clinical signs evoke suspicion of metastases. The limits of the different diagnostic procedures are discussed.
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PMID:[Methods and problems in staging bronchial carcinomas]. 625 17

The aim of this study was to examine antitumorigenic Cis DDP properties in metastatic brain tumors. Thirty-four untreated patients with brain metastases recorded by CAT scans or radionuclide scans plus neurological examinations underwent the treatment. Pathohistology of primary tumors mainly showed breast [8] and lung [8] carcinomas and melanomas [10]. Other localizations of primary tumors were infrequent. Cis DDP was administered in doses of 30 mg/m2 body surface daily over 4 days. All the patients received at least two cycles and 33 have been evaluated. No corticosteroids were administered concurrently. An objective response (seven complete and seven partial remissions) was observed in 14 out of 33 patients (42%). Six stable disease cases were also noted. A complete response (5-14 months) was observed in breast cancer [4], lung cancer [1], and melanoma [2]. Seven partial responses lasted 2-5 months. Antitumorigenic activity of Cis DDP was also noted in extracerebral tumor lesions, especially in breast cancer patients. Toxicity was moderate but tolerable. The results of this study have shown Cis DDP to possess antitumorigenic properties also in patients with metastatic brain tumors, a point that has not been proved so far.
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PMID:Phase II clinical trial of cis dichlorodiammine platinum (Cis DDP) in metastatic brain tumors. 676 44


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