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)

A case-control study involving interviews with 672 female lung cancer patients and 735 population-based controls was conducted to investigate the high rates of lung cancer, notably adenocarcinoma, among women in Shanghai. Cigarette smoking was a strong risk factor, but accounted for only about one-fourth of all newly diagnosed cases of lung cancer. Most patients, particularly with adenocarcinoma, were life-long non-smokers. The risks of lung cancer were higher among women reporting tuberculosis and other pre-existing lung diseases. Hormonal factors were suggested by an increased risk associated with late menopause and by a gradient in the risk of adenocarcinoma with decreasing menstrual cycle length, with a 3-fold excess among women who had shorter cycles. Perhaps most intriguing were associations found between lung cancer and measures of exposure to cooking oil vapors. Risks increased with the numbers of meals cooked by either stir frying, deep frying or boiling; with the frequency of smokiness during cooking; and with the frequency of eye irritation during cooking. Use of rapeseed oil, whose volatiles following high-temperature cooking may be mutagenic, was also reported more often by the cancer patients. The findings thus confirm that factors other than smoking are responsible for the high risk of lung cancer among Chinese women and provide clues for further research, including the assessment of cooking practices.
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PMID:Lung cancer among Chinese women. 282 85

In a population-based case-control study of lung cancer in Shanghai involving interviews during 1984-86 with 1,405 cancer patients and 1,495 controls, a significant 50% elevation in the risk of lung cancer, adjusted for cigarette smoking, was observed among persons who had a history of tuberculosis. Among those diagnosed with tuberculosis within the past 20 years, the risk exceeded 2.5-fold. In males the lung cancers tended to occur on the same side as the previous tuberculosis infection. For both sexes, the effect of recent tuberculosis was most apparent for adenocarcinoma and peripheral tumours. No relationship was found between lung cancer risk and the type of tuberculosis therapy, including use of isoniazid. The findings suggest that tuberculosis may predispose to lung cancer, with the association most apparent among recent survivors of the infection.
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PMID:Lung cancer and prior tuberculosis infection in Shanghai. 282 52

We determined the incidence of tuberculosis in lung cancer patients with known tuberculin status. All patients received chemotherapy with or without radiation therapy, corticosteroid therapy, or both, and none received isoniazid prophylaxis. Positive tuberculin reactivity was found in 89 of the 257 patients; among these 89, tuberculosis developed in one patient before and in one patient after chemotherapy. Among the other 168 patients, one case of tuberculosis developed after chemotherapy. For all lung cancer patients, the incidence of tuberculosis was higher than age-specific and race-specific rates in a control population. The risk of tuberculosis was judged to be significantly higher in patients with positive than with negative tuberculin reactivity; among tuberculin reactors, however, the risk of tuberculosis was estimated to be less than the potential risk of isoniazid hepatotoxicity reported in the literature for patients in a similar age group. The median survival for tuberculin-positive lung cancer patients was 9.6 months. Because of the limited survival in these patients, and because of the high risk of isoniazid hepatotoxicity for patients in this age group, we do not recommend isoniazid prophylaxis for tuberculin-positive patients receiving chemotherapy for lung cancer.
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PMID:Lung cancer, tuberculin reactivity, and isoniazid. 283 28

A cohort mortality study was carried out in Vermont granite workers who had been employed between the years 1950 and 1982. The cohort included men who had been exposed to high levels of granite dust prior to 1938-1940 (average cutters to 40 million parts/cubic foot), and those employed at dust levels after 1940, which on average were less than 10 million parts/cubic foot. Deaths were coded by a qualified nosologist and standardized mortality ratios were calculated. The results confirm previous studies that show that death rates from silicosis and tuberculosis, the major health threats in the years before 1940, were essentially eliminated after dust controls. However, we found excessive mortality rates from lung cancer in stone shed workers who had been employed prior to 1930, and hence had been exposed to high levels of granite dust. When information was available, 100% of those dying from lung cancer had been smokers.
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PMID:Vermont granite workers' mortality study. 283 46

The leukocyte adherence inhibition test (LAI) was used to study the cellular reactivity in 119 subjects: 48 were affected by lung cancer, 41 by non-malignant lung diseases, 10 by non-lung cancers and 20 were healthy volunteers. The LAI test is based on the observation that leukocytes do not adhere to glass when in the presence of an antigen against which a sensitization exists. Test selectivity was checked by the suppression technique: suppressed cells lose their competence to an antigen when incubated with it before testing. Peripheral blood leukocytes (PBLs) and bronchioloalveolar cells (BACs) were used. While controls showed no reactivity to lung cancer extracts, early cancer patients showed the highest reactivity and active cavitary tuberculosis patients gave false positive results. The blocking assay showed that patients with tuberculosis were sensitized to normal lung extracts. In lung cancer patients the blocking assay showed that a selective reactivity exists to cancer extracts derived from a histologically homologous cancer specimen.
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PMID:Leukocyte adherence inhibition test in lung cancer immunodiagnostic detection. 283 38

The most important demand the surgeon can make in respect of the radiologist's work is earliest possible diagnosis of lung cancer. Secondly, the surgeon is always grateful for any pointer leading to diagnosis of the type (and status) of the tumor. This supplies decisive information for both operative planning and perioperative technique. For example, it is essential to know, if x-ray reveals a circular focus, whether this represents tuberculosis of a carcinoma. In case of tuberculosis, drug treatment will be prescribed perioperatively, and the site of operation is limited as much as possible, whereas bronchial carcinoma requires immediate surgery which should be as radical as possible.
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PMID:[Surgery of bronchial cancer and demands on radiology]. 283 93

Sera from cancer patients specifically suppressed phosphofructokinase (fructose-6-phosphate kinase [PFK], EC 2.7.1.11), a rate-limiting enzyme in the glycolysis pathway. Among 418 cancerous sera, 68.7% evidence suppression; there was no organ specificity. Among 42 sera from early gastric cancer patients, 29 (69.0%) were positive, as were advanced gastric cancer, 14/19 (73.3%) pancreas cancer, and 75/101 (74.3%) lung cancer sera. In contrast 6/50 (12.0%) sera from patients with gastroduodenal ulcer, 3/23 (13.0%) with myoma uteri, and 0/6 with lung tuberculosis were positive. Patients with diabetes mellitus and those receiving steroid hormone therapy showed strong positive suppression. Comparative studies using other tumor markers (immunosuppressive acid protein, carcinoembryonic antigen, alpha-fetoprotein, beta 2-microglobulin, and ferritin) and the same sera used from PFK assay showed that the PFK method was two to three times more sensitive. Sephadex G-200 column chromatography revealed that the PFK-suppressive activity was retained in the postalbumin fraction. The PFK method may represent a promising new cancer screening method.
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PMID:A new cancer marker: a possible cancer screening method based on the suppression of phosphofructokinase by sera from cancer patients. 293 46

Mean values for serum angiotensin-I-converting enzyme (SACE), determined spectrophotometrically in 648 subjects, using the synthetic substrate hippuryl-L-histidyl-L-leucine, and expressed in units per milliliter, were: controls, 11.11 +/- 3.97 (n = 89); lung cancer, 6.50 +/- 3.26 (n = 87); tuberculosis of the lung, 8.93 +/- 4.60 (n = 68); pulmonary sarcoidosis, 21.18 +/- 14.93 (n = 48); pneumonia, 9.81 +/- 6.83 (n = 52); fibrosis, 11.18 +/- 8.26 (n = 34); diabetes mellitus, 10.90 +/- 7.51 (n = 29); ischemic heart disease, 8.98 +/- 6.19 (n = 42); pulmonary embolism, 13.20 +/- 3.91 (n = 5); and lymphomas, 11.66 +/- 5.44 (n = 36). The lowest values for SACE (5.92 +/- 1.95) were observed in 7 patients with pulmonary metastases. No relationship could be found between SACE and other laboratory parameters, nor between the enzyme activity in men and women. Evidence suggests that low SACE activity is often associated with extrapulmonary cancers of various organs. Levels were significantly decreased in cancer of the lung and pulmonary metastases and significantly (p less than 0.001) increased in sarcoidosis compared with other diseases, suggesting that SACE activity may be of value in the diagnosis and prognosis of cancer of the lung.
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PMID:The value of angiotensin-I-converting enzyme determinations in malignant and other diseases. 299 Jul 99

A total of 49 consecutive specimens of lung cancer were collected prospectively at surgical resection or autopsy from 40 men and nine women, aged 40-74 years. Of the 49 tumors, the gross appearance of 22 fitted the description of a scar cancer, i.e., a tumor with pleural puckering and central pigmentation. Nineteen of the "scar cancers" were peripheral (17 adenocarcinomas and two squamous cell carcinomas); three were central (one squamous cell carcinoma and two adenocarcinomas). In the 19 peripheral "scar cancers," elastic stains demonstrated the presence of collapsed, unfibrosed lung tissue at the center with traction of the overlying pleura toward it. Elsewhere in the tumor, the elastic framework was either destroyed or expanded by tumor filling the alveolar spaces. None of the "scar cancers" had a significant desmoplastic reaction that might otherwise explain the scarred appearance. It appeared that local atelectasis was solely responsible for the pleural puckering and central pigmentation. On the other hand, atelectatic lung tissue was not seen in the 27 cancers that did not have the appearance of a scar cancer. Tuberculosis was found in 10 of the 49 lung specimens. In only one specimen was the tuberculous lesion anatomically associated with the tumor. There was no evidence of pulmonary infarct in any of the specimens. The term "scar cancer" was considered inappropriate as there was no preformed fibrous tissue. The scarred appearance was thought to be the result of localized pulmonary atelectasis owing to small airways obstruction by tumor. Association with tuberculosis was considered incidental.
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PMID:Pulmonary scar cancer. A pathologic reappraisal. 300 43

Lung cancer is the predominant fatal neoplasm of our time, and SCLC, which accounts for about 25% of all lung cancer, if untreated results in death in about 3 months. Currently employed aggressive combination chemotherapy has allowed a 4- to 5-fold improvement in median survival over untreated patients. Ten to 20% of patients with limited disease can be expected to have a long-term (2-yr) survival. The majority of patients, however, have extensive disease. For these patients the median survival is about 7 months. Less than 2% survive 2 yr. During the last 10 yr, experience in the treatment of thousands of patients has been reported. These trials, using a large variety of drug combinations, doses, and schedules as well as multiple modalities including radiotherapy, surgery, and bone marrow transplantation, demonstrate that a plateau has been reached with our present therapeutic approach. The development of new effective therapeutic strategies as well as prevention of SCLC require a better basic understanding of the cellular pathophysiology of the disease. A consistent chromosomal abnormality has been associated with SCLC. This may provide new insight into predisposition and pathogenesis of SCLC. How this chromosomal abnormality relates to loss of control of cell growth is under intense investigation. Similarly, during the past 3 yr, the identification of growth regulatory oncogenes has greatly improved our understanding of malignancy. The discovery that metastatic cells escape immune surveillance has led to attempts at modulating antigenic expression. The modulation of cellular antigenic expression may facilitate the destruction of tumor cells by host defense mechanisms. The understanding of the genetic basis of drug resistance may lead to approaches that prevent or delay resistance. This century has witnessed the emergence of SCLC as an important fatal neoplasm. It has also been during this time that another, formerly dominant pulmonary condition, tuberculosis, has been controlled. The reduction of tuberculosis was accomplished by a combination of scientific understanding, beginning with the discovery of Koch's bacillus, and public health measures. Perhaps a similar parallel for SCLC as well as other forms of cancer will be written. Basic cellular investigations with the new tools of molecular biology as well as measures to control exposure to predisposing environmental factors such as component of cigarette smoke may one day lead to control of SCLC.
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PMID:Small cell lung cancer. 301 96


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