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 71 year-old male, with no recent history of travelling abroad and a past history of lung cancer two years prior to presentation, which had been successfully treated, developed a sudden onset of watery diarrhea more than ten times a day on February 26, 2001, which gradually became bloody. The next day he visited the Department of Integrated Medicine of the Tokyo Metropolitan Komagome Hospital by ambulance because his consciousness was deteriorating and he was hospitalized. He was hypotensive on admission, and a dopamine preparation was used throughout. The peripheral WBC was 3,800/microliter and the lymphocyte count was 76/microliter which thus suggested the presence of cellular immune suppression. HIV was not tested. He died seven hours after admission. His stool culture yielded a growth of Shigella flexneri 2a, and a blood culture on admission was sterile. No verocyte toxin-producing Esherichia coli was not detected. The causes of death in cases with shigellosis have been reported in the literature to be an electrolyte imbalance, septicemia and disseminated intravasucular coagulation (DIC) in developed countries. Our present case was considered to be a debilitated patient complicated with hemolytic uremic syndrome due to an infection with Shigella bacteria which resulted in death despite performing intensive treatments.
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PMID:[A fatal case of shigellosis in an elderly patient]. 1213 56

To investigate the role of microsomal epoxide hydrolase (mEH) polymorphisms in the aetiology of lung cancer and to assess the interaction between mEH polymorphisms and smoking, we performed a meta-analysis of seven published studies, which included 2078 cases and 3081 controls, and a pooled analysis of eight studies (four published and four unpublished at that time) with a total of 986 cases and 1633 controls. The combined meta-analysis odds ratios (ORs) were 0.98 (95% confidence interval [CI] = 0.72-1.35) for polymorphism at amino acid 113 in exon 3 (His/His versus Tyr/Tyr genotype) and 1.00 (95% CI = 0.71-1.41) for polymorphism at amino acid 139 in exon 4 (Arg/Arg versus His/His genotype). In the pooled analysis, we observed a significant decrease in lung cancer risk (OR = 0.70, 95% CI = 0.51-0.96) for exon 3 His/His genotype after adjustment for age, sex, smoking and centre. The protective effect of exon 3 polymorphism seems stronger for adenocarcinoma of the lung than for other histological types. The OR for high predicted mEH activity, compared with low activity, was 1.54 (95% CI = 0.77-3.07) in the meta analysis and 1.18 (95% CI = 0.92-1.52) in the pooled analysis. We did not find a consistent modification of the carcinogenic effect of smoking according to mEH polymorphism, although the risk of lung cancer decreased among never smokers with high mEH activity and among heavy smokers with the exon 3 His/His genotype. In conclusion, this study suggests a possible effect of mEH polymorphisms at exon 3 in modulating lung cancer. If present, this effect may vary among different populations, possibly because of interaction with genetic or environmental factors.
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PMID:Microsomal epoxide hydrolase polymorphisms and lung cancer risk: a quantitative review. 1214 Oct 66

This article presents a general review of the major trends in the conceptualization, development, and success of case-control methods for the study of disease causation and prevention. "Recent work on nested case-control, case-cohort, and two-stage case control designs demonstrates the continuing impact of statistical thinking on epidemiology. The influence of R. A. Fisher's work on these developments is mentioned wherever possible. His objections to the drawing of causal conclusions from observational data on cigarette smoking and lung cancer are used to introduce the problems of measurement error and confounding bias."
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PMID:Statistics in epidemiology: the case-control study. 1215 99

Lung cancer is a major cause of cancer-related death in the developed countries and the overall survival rate has still an extremely poor. Cigarette smoking is an established risk factor for lung cancer although a possible role for genetic susceptibility in the development of lung cancer has been inferred from familial clustering of the disease and segregation analyzes. Everyone may have a unique combination of polymorphic traits that modify genetic susceptibility and response to drugs, chemicals and carcinogens. Developments in molecular biology have led to growing interest in investigation of biological markers, which may increase predisposition to lung carcinogenesis. Therefore, the high-risk genotype of an individual could be determined easily. As there are the great number of carcinogen-activating and -detoxifying enzymes, the variation in their expression and the complexity of exposures to tobacco carcinogens, the existence of multiple alleles at loci of those enzymes may result in differential susceptibilities of individuals. This review summarize data addressing the relationships of lung cancer to markers of genetic susceptibility genes, including metabolic polymorphisms other than well-investigated cytochrome P450s or glutathione S-transferases, DNA repair genes and the p53 tumor suppressor gene. Among genetic polymorphisms reviewed here, myeloperoxidase gene (a G to A mutation) and microsomal epoxide hydrolase exon 4 polymorphism (substitution of Arg for His) were significantly associated with lung cancer risk. As lung cancer is a multifactorial disease, an improved understanding of the interplay of environmental and genetic polymorphisms at multiple loci may help identify individuals who are at increased risk for lung cancer. Hopefully, in the future we will be able to screen for lung cancer susceptibility by using specific biomarkers.
Lung Cancer 2002 Sep
PMID:Genetic polymorphisms and lung cancer susceptibility: a review. 1223 92

Early hilar lung cancer is rare. It is usually curable if properly diagnosed and treated. We recently encountered two cases of early stage squamous cell carcinoma of the left upper division bronchus, which responded well to left upper division sleeve segmentectomy. Case 1 was a 74-year-old man, a heavy smoker, who was referred to our hospital after sputum cytology had resulted in a positive diagnosis while receiving inpatient care for heart failure at another hospital. Bronchoscopy revealed a thickened tumor at the spur between left B(1+2) and B(3). Squamous cell carcinoma was diagnosed by forceps biopsy via bronchoscopy. Left upper division sleeve segmentectomy with lymph node dissection was performed. Since the bronchi to be anastomosed to each other were greatly different in diameter, telescoped anastomosis was used. His postoperative course was uneventful, and he continues to show good respiratory condition, without any evidence of recurrence 25 months after surgery. Case 2 was a 60-year-old man, a heavy smoker, who was identified by sputum cytology as needing detailed examination during a mass screening of high-risk groups for early detection of lung carcinoma. Bronchoscopy revealed a nodular tumor at the orifice of the left upper division bronchus. Squamous cell carcinoma was diagnosed by forceps biopsy via bronchoscopy. Left upper division sleeve segmentectomy with lymph node dissection was performed. During surgery for this case, the lingular bronchus was dissected obliquely to make its cross-section wide enough to match the diameter of the left upper lobe bronchus to which the former was anastomosed. His postoperative course was uneventful, and he shows good respiratory condition, without any evidence of recurrence five months after surgery. The pathological stage was TisN0M0 (stage 0) in both patients, and their tumors were confirmed as early hilar lung cancer. Sleeve segmentectomy, aimed at radical resection of cancer while preserving lung function, can serve as a standard procedure for surgical treatment of cases of early hilar lung cancer confined to the segmental bronchi.
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PMID:Left upper division sleeve segmentectomy for early stage squamous cell carcinoma of the segmental bronchus: report of two cases. 1266 32

Mr. C. was diagnosed with lung cancer seven months ago. The cancer then spread to his brain. He was fully aware that the physicians were treating his symptoms, not the disease, however, discussions regarding the goals of treatment did not occur. He continued the treatment regimen of chemotherapy and radiation therapy. While at home one evening, he fell and fractured his femur. His mobility and independence were at once greatly compromised. While recovering in the hospital, he made the decision to opt out of curative treatment. He stated, "I want to go home, play with my cat, smoke cigarettes, and be with my friends when they can visit." What are the processes by which adults with life-threatening conditions make decisions about their care? What is the context of these decisions? The purpose of this study was to describe the process of decision making for adults with a terminal illness.
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PMID:The contextual nature of decision making near the end of life: hospice patients' perspectives. 1269 44

A 69 year-old [correction of 63] man who had had a radical cystectomy for bladder cancer was admitted to our hospital because of hemosputum and right femoral pain. His chest radiograph and computed tomogram showed a mass shadow with a cavity in the left upper lung field. Sputum cytology showed class V squamous cell carcinoma and a bone scintigram showed right femoral metastasis. Despite radiotherapy to the left upper lung and the right femur, the patient's condition worsened, and he died of respiratory failure after hospitalization for about 1 month. At autopsy, pathologic studies of lung cancer revealed mixed-type transitional cell carcinoma, squamous cell carcinoma and adenocarcinoma. A diagnosis of metastatic lung cancer from bladder cancer was made. Cavitating pulmonary metastasis is uncommon. We report a rare case of pulmonary metastasis from bladder cancer, with mixed-type histopathology at both primary and metastatic sites.
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PMID:[Cavitary pulmonary metastasis from bladder cancer: a case report]. 1272 27

This case study centers on a seventy-eight-year-old man with triple malignancies, namely, gastric cancer, lung cancer and malignant pleural mesothelioma, all of which developed at different times. The histological types were adenocarcinoma of the stomach, squamous cell carcinoma of the lung and sarcomatous malignant pleural mesothelioma. Gastric cancer was treated by endoscopic mucosal resection 2 years ago. The patient presented with a chief complaint of dyspnea, and right pleural effusion was found on chest radiography. The right-side effusion disappeared spontaneously, but a small mass on the left side was diagnosed as lung cancer, and so left inferior lobe resection was performed. Malignant pleural mesothelioma appeared after one year of pleural effusion and the patient died of mesothelioma one year after diagnosis. At autopsy, the gastric cancer and lung cancer had not relapsed and malignant pleural mesothelioma had metastasized to the lung, liver, adrenal gland and small intestine. He was a sailor by profession and it was obvious that he had been exposed to asbestos, because 538 asbestos bodies per 5 g of wet lung tissue were detected. His advanced age was one of the risk factors for the multiple malignancies, and the asbestos exposure was considered to have compounded these hazards to cause the triple malignancies. It is well known that lung cancer and malignant mesothelioma are induced by asbestos exposure, but multiple cancers including lung cancer and malignant mesothelioma are extremely rare.
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PMID:[A case of triple malignancies (gastric cancer, lung cancer and malignant pleural mesothelioma) after asbestos exposure]. 1279 87

DNA repair plays a critical role in protecting the genome from insults of cancer-causing agents, such as those found in tobacco smoke. Therefore, reduced DNA repair capacity can increase the susceptibility to smoking-related cancers. Recently, several polymorphisms have been identified in the xeroderma pigmentosum group G (XPG) gene, and it is possible that these polymorphisms may affect the DNA repair capacity, thereby modulating cancer susceptibility. We investigated the relationship between the His1104Asp polymorphism in the XPG gene and the risk of lung cancer. The study population consisted of 310 lung cancer patients and 311 healthy controls who were frequency (1:1) matched based on age and sex. The Asp/Asp genotype was more frequent in the controls (28.9%) than in the cases (18.7%) and associated with a significantly decreased risk of lung cancer [adjusted odds ratio (OR) = 0.54, 95% confidence interval (CI) = 0.37-0.80] when the combined His/His and His/Asp genotype was used as the reference. The protective effect of the Asp/Asp genotype against lung cancer was statistically significant in the older subjects (adjusted OR = 0.51, 95% CI = 0.37-0.80), males (adjusted OR = 0.54, 95% CI = 0.35-0.83), and lighter smokers (adjusted OR = 0.48, 95% CI = 0.25-0.94) in a stratification analysis. When the lung cancers were analyzed by histologic type, the Asp/Asp genotype was associated with a significantly decreased risk of squamous cell carcinoma (adjusted OR = 0.55, 95% CI = 0.34-0.88) and small cell lung cancer (adjusted OR = 0.44, 95% CI = 0.20-0.97), but non-significant decreased risk of adenocarcinoma (adjusted OR = 0.64, 95% CI = 0.36-1.12). These results suggest that the XPG codon 1104 polymorphism contributes to genetic susceptibility to lung cancer.
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PMID:Relationship between XPG codon 1104 polymorphism and risk of primary lung cancer. 1286 23

Microsomal epoxide hydrolase (mEH) plays a dual role in the detoxification and activation of tobacco procarcinogens. Two polymorphisms affecting enzyme activity have been described in the exons 3 and 4 of the mEH gene, which result in the substitution of amino acids histidine to tyrosine at residue 113, and arginine to histidine at residue 139, respectively. We performed a hospital-based case-control study consisting of 277 newly diagnosed lung cancer patients and 496 control subjects to investigate a possible association between these two polymorphisms and lung cancer risk. The polymorphisms were determined by polymerase chain reaction/restriction fragment length polymorphism and TaqMan assay using DNA from peripheral white blood cells. Logistic regression was performed to calculate odds ratios (ORs), confidence limits (CL) and to control for possible confounders. The exon 3 polymorphism of the mEH gene was associated with a significantly decreased risk of lung cancer. The adjusted OR, calculated relative to subjects with the Tyr113/Tyr113 wild type, for the His113/His113 genotype was 0.38 (95% CL 0.20-0.75). An analysis according to histological subtypes revealed a statistically significant association for adenocarcinomas; the adjusted OR for the His113/His113 genotype was 0.40 (95% CL 0.17-0.94). In contrast, no relationship between the exon 4 polymorphism and lung cancer risk was found. The adjusted OR, calculated relative to the His139/His139 wild type, was for the Arg139/Arg139 genotype 1.83 (0.76-4.44). Our results support the hypothesis that genetically reduced mEH activity may be protective against lung cancer.
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PMID:Association of microsomal epoxide hydrolase polymorphisms and lung cancer risk. 1291 82


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