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

Pulmonary resection was performed for primary lung cancer of a 72-year-old patient which was associated with diffuse panbrochiolitis that required home oxygen therapy. The preoperative total pulmonary vascular resistance at rest was 564 dyne.sec.cm-5/m2, but thoracotomy and reduction surgery were possible by strict respiratory and circulatory control. The troublesome postoperative pulmonary phthisis was dealt with through extended control by means of total parenteral nutrition and use of the Heimlich valve.
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PMID:[A case of primary lung cancer associated with diffuse panbronchiolitis]. 277 41

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

After presensitization with IV hematoporphyrin derivative (HpD), neoplasms in the tracheobronchial tree of 18 patients were treated by photodynamic therapy (PDT) with 630-nm light from a tunable dye argon laser system delivered through quartz fibers passed through the biopsy channel of a flexible bronchoscope under local anesthesia. Tumor effect was measured by complete response (CR)--no visible tumor in area treated, partial response (PR)--tumor size or degree of obstruction reduced by more than 50% and some response (SR)--tumor or degree of obstruction reduced by more than 20% but less than 50%. One month or less after 30 treatments to 26 areas in 18 patients, there was 40% CR, 57% PR, and 3% SR. All tumors showed at least some response. Since many of these patients had end-stage disease, the effect on the clinical condition and symptoms were evaluated using the Karnofsky Performance Status (KPS), oxygen requirements, and the presence or absence of respiratory symptoms. One month after treatment, 61% were clinically improved, with an increase of the average KPS from 48 to 61. Three patients with stage III primary lung cancer improved from being severely disabled requiring hospitalization to normal activity with effort and lived an average of 3.5 months. One patient with metastatic colon cancer was palliated from bedrest with continuous oxygen to normal activity with no oxygen for 12 months. A patient with hemoptysis and carcinoma in situ remains biopsy- and symptom-free for 34 months. A patient with hemoptysis and cough from breast cancer metastases maintained CR, biopsy- and symptom-free for 7 months. A patient with hemoptysis from recurrence at the bronchial stump maintained CR, biopsy- and symptom-free for 13 months. Six patients with Stage III primary lung cancer with average KPS of 27 (severe) died in the hospital and lived an average of 5 weeks (two CR, two PR, two SR). One patient with atelectasis of the right lower lobe re-expanded 14 days after treatments began.
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PMID:Photodynamic therapy of endobronchial tumors. 294 45

Epidemiological evidence suggests that smoking is a major cause of human lung cancer. However, the mechanism by which cigarette smoke induces the cancer remains obscure, although in tobacco carcinogenesis, promotion and/or co-carcinogenesis may have crucial roles. The epidemiological data show that if an individual stops smoking, the risk of his contracting lung cancer increases no further. Moreover, laboratory experiments show that cigarette smoke condensate (CSC) exhibits co-carcinogenic and promoting activities in tumour production and malignant transformation. Clastogenic action is thought to be intimately involved in tumour promotion, and it is therefore interesting that visible chromosome changes such as chromosome aberrations and sister chromatid exchanges are known to be caused by cigarette smoke. However, there has been no previous direct demonstration that cigarette smoke can cause single-strand breaks (SSB) in DNA. Here we report that cigarette smoke induces considerable numbers of DNA SSB in cultured human cells, and that such strand breaks may be ascribed to active oxygen generated from cigarette smoke.
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PMID:Cigarette smoke induces DNA single-strand breaks in human cells. 298 77

The ability of IgG and IgE immune complexes and of phorbol myristate acetate (PMA), a soluble membrane activator, to stimulate hydrogen peroxide (H2O2) release and to induce oxygen radical-mediated cytotoxic activity by human peripheral blood (PBL) eosinophils and by PBL neutrophils was evaluated in normal volunteers and patients with hypereosinophilic malignant pleural effusions due to lung cancer. PMA stimulated a significant respiratory burst. Similar results were obtained with IgG IC stimulation, although the levels of H2O2 were lower. Agg IgE induced H2O2 release only by PBL and PE eosinophils and not by neutrophils. PMA stimulation resulted in detectable cytotoxic activity. IgG IC generated both PBL and PE eosinophil and PBL neutrophil cytotoxicity. Agg IgE induced significant cellular cytotoxicity in both PBL and PE eosinophils. This study suggests that eosinophil oxidative metabolic burst and cytotoxic activity stimulated by IgG and IgE immune complexes could represent a possible mechanism of parenchymal injury in eosinophilic disorders.
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PMID:Human peripheral blood and pleural fluid eosinophils can be induced by immune complexes to release IgG immune complexes and aggregated IgE. 318 Aug 52

The authors report two cases of apparent adult respiratory distress syndrome (ARDS) following limited thoracic irradiation for lung cancer. Respiratory failure followed rapidly after irradiation with diffuse bilateral infiltrates, both in and out of the irradiated volume along with progressive hypoxemia unresponsive to oxygen management. Other potential causes of lung injury such as lymphangitic tumor, cardiac failure, and infections were excluded by both premortem and postmortem examination. Autopsy findings in both irradiated and unirradiated volumes of lung were consistent with hyaline membrane changes. The possible relationship between radiation therapy to limited lung volumes and the development of adult respiratory distress syndrome is discussed.
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PMID:The association of adult respiratory distress syndrome (ARDS) with thoracic irradiation (RT). 319 41

Neuroendocrine lung cancer is among the most common types of lung tumor in man and demonstrates a strong etiological association with cigarette smoking. However, despite numerous efforts, this cancer type has never been induced in animals. This report describes, for the first time, the reproducible induction of pulmonary neuroendocrine cancer in a readily available hamster model. The data provide evidence that deviations from pre-existing normal pulmonary oxygen levels may be an essential factor for the induction of this malignancy. This new model should greatly facilitate studies of the pathophysiology, biochemistry and therapy of neuroendocrine cancer of the lung.
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PMID:An animal model for neuroendocrine lung cancer. 333 13

We studied the effect of a decrease in vital capacity (VC) on the blood lactate threshold detected during exercise in 16 preoperative (PRE) and 10 postoperative (POST) lung cancer patients who had undergone lobectomy or pneumonectomy. The PRE patients were selected on the basis of having normal preoperative pulmonary function. The POST patients were selected on the basis of having normal preoperative pulmonary function and a postoperative VC of less than 80%. The oxygen consumption/body surface area at a 2.2 m.mol.l-1 arterial lactate concentration (VO2/BSA at La-2.2) was adopted as the blood lactate threshold. VC/BSA in the POST group significantly correlated with VO2/BSA at La-2.2 (r = 0.85, P less than 0.01), but not in the PRE group. SaO2 at La-2.2 was 95.4 +/- 1.5% in the PRE group and 95.2 +/- 1.3% in the POST group. SaO2 at La-2.2 did not correlated with VC/BSA in either group. The hemoglobin concentration (Hb) in the arterial blood correlated significantly with VC/BSA in the POST group (r = 0.65, P less than 0.05) but not in the PRE group. These results indicate that VO2/BSA at La-2.2 was restricted by VC in patients with restrictive pulmonary function disorder. Of the three elements of oxygen delivery, Hb was a limiting factor for VO2/BSA at La-2.2 but SaO2 was not. Cardiac output, which was not measured in our study, was speculated to be another limiting factor for VO2/BSA at La-2.2.
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PMID:Effect of lung resection on blood lactate threshold in lung cancer patients. 339 52

To evaluate the significance of the blood lactate threshold as a predictor of postthoracotomy hospital mortality resulting from pulmonary complications, a 3-minute incremental exercise test was administered to 33 lung cancer patients who underwent thoracotomy between October, 1981, and May, 1984. The oxygen consumption/body surface area at an arterial lactate level of 20 mg/dl (VO2/BSA at La-20) was adopted as the blood lactate threshold. Age and pulmonary function parameters such as forced expiratory volume in one second (FEV1)/body surface area (BSA), FEV1/forced vital capacity, diffusing capacity for the carbon monoxide/lung volume, and maximum ventilatory volume/BSA revealed significant differences between patients with postthoracotomy pulmonary complications and those without such complications. However, there was no difference in pulmonary function test results between the surviving and deceased patients. In contrast, although VO2/BSA at La-20 did not differ between the patients with and without pulmonary complications, it differed significantly between the surviving and deceased patients. We concluded that postthoracotomy pulmonary complications depended on the severity of preoperatively associated pulmonary function disorders and that the blood lactate threshold expressed by VO2/BSA at La-20 was an important indicator of the risk of hospital mortality.
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PMID:Exercise tolerance test in lung cancer patients: the relationship between exercise capacity and postthoracotomy hospital mortality. 367 52

We have carried out a comparison of two different methods for cloning human lung cancer cells. The method of Courtenay & Mills (1978) generally gave higher plating efficiencies (PE) than the method of Carney et al. (1980). The number of colonies increased with incubation time in both methods and the weekly medium replenishment in the Courtenay method was advantageous for longer incubation times of several weeks. In the Courtenay method, the use of August rat red blood cells (RBC) and low oxygen tension were both found to be necessary factors for maximum plating efficiency. The usefulness of heavily irradiated feeder cells in improving PE is less certain; each cell type may have its own requirement.
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PMID:Cloning of human lung cancer cells. 390 99


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