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)

Major prognostic factors for early-stage non-small-cell lung cancer (NSCLC) are tumor size and nodal status. It has been suggested that HER2/neu overexpression may be related to poor prognosis in NSCLC. We evaluated the significance of HER2/neu overexpression on survival in patients with NSCLC. Data were collected on 239 patients treated surgically for stage I/II NSCLC between 1987 and 1996. None of the patients received adjuvant chemotherapy or radiation. Formalin-fixed, paraffin-embedded tumor tissue samples were stained with p185/HER2 receptor antibody. Results were reported as positive (2+, 3+) or negative (0, 1+) (Group A). A separate analysis considered only 3+ as positive (Group B). HER2/neu overexpression was seen in 18% in Group A (43 of 239) and 6% in Group B (15 of 239). HER2/neu overexpression was highest in bronchoalveolar cell carcinoma and adenocarcinoma. More stage I tumors were positive than stage II in both groups, but this was significant only in Group A (21% vs. 7%, P = 0.02). No difference was seen with age, gender, or grade for either group. In Group A, the relapse rate was 55% for HER2/neu-overexpressing tumors and 31% for HER2/neu-negative tumors (P = 0.003). Median time to relapse in patients with HER2/neu-positive tumors was 2.9 years; it was not reached in patients with HER2/neu-negative tumors. Median survival of patients with HER2/neu-positive tumors was 3.6 years compared to 5 years in patients with HER2/neu-negative tumors (P = 0.66). In Group B, the relapse rate was 60% for HER2/neu-overexpressing tumors and 33% for negative tumors (P = 0.036). Median time to relapse was 3.4 years in HER2/neu positive and had not been reached in negative tumors. There was no difference in 5-year survival rates for both groups (47% for HER2/neu positive and 50% for negative, P = 0.66).
Clin Lung Cancer 2001 Feb
PMID:Effect of HER2/neu expression on survival in non-small-cell lung cancer. 1470 Apr 81

Many studies have demonstrated how exposure to chemical pollutants in indoor air has adverse effects on health and comfort. Volatile organic compounds (VOCs), formaldehyde, ozone, particulates, fibres and environmental tobacco smoke have all been implicated. VOCs include a wide range of chemical substances which irritate mucosa. Many are neurotoxic and some are suspected or known to be carcinogenic e.g. benzene. Formaldehyde, the simplest and most common aldehyde in indoor air, is a powerful irritant to the skin, eyes, nose and upper airways. Given its close association with nasal-pharyngeal tumours, it has recently been classified as a certain carcinogen for humans. Exposure to ozone may cause airway irritation and inflammation, reduce the ventilation function and increase reversible bronchial reactivity. In the general population it increases the mortality rate and the number of hospital admissions for respiratory diseases. Airborne particles, a mixture of organic and inorganic substances, are powerful irritants for the eyes and mucosa and can cause adverse cardiovascular effects. Apart from indoor environments, exposure to asbestos fibres has been associated with an increased risk of respiratory diseases such as pneumoconiosis lung cancer and mesothelioma. Synthetic mineral fibres cause transient irritation and inflammation of the skin, eyes and upper airways. Recent observations have confirmed that exposure to environmental tobacco smoke, which is widespread in workplaces, increases the risk of lung cancer, irritative respiratory and ocular symptoms and cardiovascular diseases.
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PMID:[Chemical pollution of indoor air and its effects on health]. 1558 46

Inactivation of tumor suppressor genes by promoter methylation is an important mechanism of tumorigenesis. Increased expression of DNA methyltransferases has been commonly observed in cancer. A C/T polymorphism in the DNA methyltransferase 3b (DNMT3b) promoter region results in increased activity and has recently been identified as a risk factor for lung cancer. In this study, we examined the C/T polymorphism of the DNMT3b gene in specimens from 81 patients with prostate cancer and 42 controls selected from patients with benign prostatic hypertrophy (BPH). Genomic DNA was isolated from archived formaldehyde-fixed and paraffin-embedded tissue blocks. DNMT3b genotypes were determined by restriction-fragment-length-polymorphism polymerase chain reaction. The DNMT3b polymorphism frequencies in the prostate cancer and BPH specimens were, respectively, 20 and 26% for CC, 42 and 52% for CT, and 38 and 21% for TT. Although such differences fall within the realm of chance variation (P>0.05), the data suggest that the TT genotype may be associated with an increased risk of prostate cancer: the age-adjusted odds ratio (aOR) was 2.6 [95% confidence interval: 0.8-8.0]; the increase in odds ratio was seen in both blacks and whites (aOR=4.3 in blacks, and 2.0 in whites). The samples used in this study have previously been examined for methylation index (MI) based on the number of genes methylated, the range being 0 to 5. A trend toward an increase in MI was detected for the DNMT3b polymorphisms in prostate cancer patients but not for BPH subjects (mean MI 2.6, 2.9, 3.1 for CC, CT, and TT genotype in prostate cancer; 0.8, 0.8, 0.7 for CC, CT, and TT genotype in BPH subjects). These findings suggest that the DNMT3b polymorphisms may be associated with an increase in promoter methylation of tumor-suppressor genes related to the development of prostate cancer, and may thereby increase the risk of this disease.
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PMID:Polymorphisms in the DNA methyltransferase 3b gene and prostate cancer risk. 1601 46

Protein gene product 9.5 (PGP9.5) is a neurospecific peptide that removes ubiquitin from ubiquitinated proteins and prevents them being targeted for degradation by proteosomes. Its expression is a potential marker of non-small lung cancer, invasive colorectal cancer and esophageal squamous cell carcinoma. Gallbladder (GB) cancer is the most common malignant tumor of the biliary tract and is usually associated with gallstone disease, a late diagnosis, unsatisfactory treatment and a poor prognosis. To understand the role of PGP9.5 in GB cancer, we examined the methylation status of its promoter and its expression in surgical biopsy samples. Formalin-fixed, paraffin-embedded tumors and non-neoplastic GB tissues (22 carcinomas, eight adenomas, 26 normal epithelia) were collected from patients who had undergone surgical resection. The methylation status of the promoter region of the PGP9.5 gene was determined by methylation-specific polymerase chain reaction, and the expression of PGP9.5 was examined by immunohistochemistry using tissue microarrays. PGP9.5 promoter was methylated in 84.6% (22/26) of normal GB epithelium, 37.5% (3/8) of adenomas and 27.2% (6/22) of carcinomas. Most tumors with an unmethylated promoter exhibited positive staining for PGP9.5 in epithelial and neoplastic cells, but no PGP9.5 expression was observed in normal epithelia or in tumor tissues with a methylated promoter. No correlation was found between promoter hypomethylation of PGP9.5 and clinicopathological findings (i.e. age, sex, histological type or grade, N-status, invasion depth or tumor stage) whereas PGP9.5 hypomethylation was found to be inversely correlated with the presence of a gallstone (P = 0.015). These results suggest that PGP9.5 promoter hypomethylation could be a reliable marker for GB cancer and that DNA hypomethylation might play an important role in re-expression of the PGP9.5 gene in GB cancer.
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PMID:Hypomethylation of the protein gene product 9.5 promoter region in gallbladder cancer and its relationship with clinicopathological features. 1696 2

Exposure to certain industrial agents has been thought to have carcinogenic potential, both for employees who work closely with agents and for the general population that comes into contact with them. The objective of the present study is to evaluate the changes at the cellular level or at the level of cellular metabolism products present in the biological fluid, and to detect early stages of the carcinogenic process resulting from the exposure of industrial environmental hazards. Carcinoembryonic antigen (CEA), alpha-fetoproteins (AFP), and prostate-specific antigen (PSA) were measured in sera of workers (n = 51), who were divided into 4 groups: group I, workers exposed to phenol; group II, workers exposed to formaldehyde; group III, workers exposed to urea; and group IV, workers exposed to mixed vapor, plus a reference control healthy group (n = 15). The results showed that 75% of the workers exposed to phenol, 75% of the workers exposed to urea, 83.3% of workers exposed to formalin, and 92.3% of the workers exposed to mixed vapors had raised values of serum CEA (S-CEA) above normal value of the control group. Also, 23% of workers exposed to mixed vapors, 44% of workers exposed to formalin, 50% of workers exposed to phenol, and 62.5% of workers exposed to urea had raised values of serum AFP (S-AFP) above normal value of control group. Finally, 16.6% of workers exposed to phenol, 23% of workers exposed to mixed vapors, and 33.3% of workers exposed to formalin had raised values of serum PSA (S-PSA) above the normal value of control group; there were no raised values of S-PSA in workers exposed to urea. No significant difference was found in the activities of AST and ALT in group I, but a highly significant increase was found in the AST activities for groups II and IV and the ALT activities for groups III and IV. A significant difference was found in the activity of ALT in group II and in AST for group III. There was no significant difference in the levels of albumin in groups I, II, and III, whereas albumin levels were significantly decreased in group IV. No significant change was found in the level of urea and creatinine in all groups except for group III, where serum levels of creatinine were significantly decreased. From our findings, we concluded that S-CEA can be used as an important prognostic screening marker for early prediction for malignancy, and for management of workers with lung cancer who are exposed to the environmental hazards in industrial factories. Furthermore, S-AFP can be used also as a biomarker if it is carried out and correlated with S-CEA.
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PMID:Carcinoembryonic antigen, alpha-fetoprotein, and prostate-specific antigen in the sera of industrial workers exposed to phenol, formaldehyde, urea, and mixed vapors. 1696 4

Diesel exhaust is a complex chemical mixture that has been linked to lung cancer mortality in a number of epidemiologic studies. However, the dose-response relationship remains largely undefined, and the specific components responsible for carcinogenicity have not been identified. Although previous focus has been on the particulate phase, diesel exhaust includes a vapor phase of numerous volatile organic compounds (VOCs) and aldehydes that are either known or suspected carcinogens, such as 1,3-butadiene, benzene, and formaldehyde. However, there are relatively few studies that quantify exposure to VOCs and aldehydes in diesel-heavy and other exhaust-related microenvironments. As part of a nationwide assessment of exposure to diesel exhaust in the trucking industry, we collected measurements of VOCs and aldehydes at 15 different U.S. trucking terminals and in city truck drivers (with 6 repeat site visits), observing average shift concentrations in truck cabs and at multiple background and work area locations within each terminal. In this paper, we characterize occupational exposure to 18 different VOCs and aldehydes, as well as relationships with particulate mass (elemental carbon in PM < 1 microm and PM2.5) across locations to determine source characteristics. Our results show that occupational exposure to VOCs and aldehydes varies significantly across the different sampling locations within each terminal, with significantly higher exposures noted in the work environments over background levels (p < 0.01). A structural equation model performed well in predicting terminal exposures to VOCs and aldehydes as a function of job, background levels, weather conditions, proximity to a major road, and geographic location (R2 = 0.2-0.4 work area; R2 = 0.5-0.9 background).
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PMID:Occupational exposure to volatile organic compounds and aldehydes in the U.S. trucking industry. 1799 62

Cigarette smoke is a complex chemical mixture that causes a variety of diseases, such as lung cancer. With the electrically heated cigarette smoking system (EHCSS), temperatures are applied to the tobacco below those found in conventional cigarettes, resulting in less combustion, reduced yields of some smoke constituents, and decreased activity in some standard toxicological tests. The first generation of electrically heated cigarettes (EHC) also resulted in increased formaldehyde yields; therefore, a second generation of EHC was developed with ammonium magnesium phosphate (AMP) in the cigarette paper in part to address this increase. The toxicological activity of mainstream smoke from these two generations of EHC and of a conventional reference cigarette was investigated in two studies in rats: a standard 90-day inhalation toxicity study and a 35-day inhalation study focusing on lung inflammation. Many of the typical smoke exposure-related changes were found to be less pronounced after exposure to smoke from the second-generation EHC with AMP than to smoke from the first-generation EHC or the conventional reference cigarette, when compared on a particulate matter or nicotine basis. Differences between the EHC without AMP and the conventional reference cigarette were not as prominent. Overall, AMP incorporated in the EHC cigarette paper reduced the inhalation toxicity of the EHCSS more than expected based on the observed reduction in aldehyde yields.
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PMID:Reduced toxicological activity of cigarette smoke by the addition of ammonia magnesium phosphate to the paper of an electrically heated cigarette: subchronic inhalation toxicology. 1846 53

There is experimental evidence that volatile substances in human breath can reflect presence of neoplasma. Volatile aldehydes were determined in exhaled breath of 12 lung cancer patients, 12 smokers and 12 healthy volunteers. Alveolar breath samples were collected under control of expired CO(2). Reactive aldehydes were transformed into stable oximes by means of on-fiber-derivatization (SPME-OFD). Aldehyde concentrations in the ppt and ppb level were determined by means of gas chromatography-mass spectrometry (GC-MS). Exhaled concentrations were corrected for inspired values. Exhaled C(1)-C(10) aldehydes could be detected in all healthy volunteers, smokers and lung cancer patients. Concentrations ranged from 7 pmol/l (161 pptV) for butanal to 71 nmol/l (1,582 ppbV) for formaldehyde. Highest inspired concentrations were found for formaldehyde and acetaldehyde (0-55 nmol/l and 0-13 nmol/l, respectively). Acetaldehyde, propanal, butanal, heptanal and decanal concentrations showed no significant differences for cancer patients, smokers and healthy volunteers. Exhaled pentanal, hexanal, octanal and nonanal concentrations were significantly higher in lung cancer patients than in smokers and healthy controls (p(pentanal) = 0.001; p(hexanal) = 0.006; p(octanal) = 0.014; p(nonanal) = 0.025). Sensitivity and specificity of this method were comparable to the diagnostic certitude of conventional serum markers and CT imaging. Lung cancer patients could be identified by means of exhaled pentanal, hexanal, octanal and nonanal concentrations. Exhaled aldehydes reflect aspects of oxidative stress and tumor-specific tissue composition and metabolism. Noninvasive recognition of lung malignancies may be realized if analytical skills, biochemical knowledge and medical expertise are combined into a joint effort.
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PMID:Breath gas aldehydes as biomarkers of lung cancer. 1983 51

A pilot study has been carried out to define typical characteristics of the trace gas compounds in exhaled breath of non-smokers and smokers to assist interpretation of breath analysis data from patients who smoke with respiratory diseases and lung cancer. Exhaled breath was analyzed using proton transfer reaction-mass spectrometry (PTR-MS) for 370 volunteers (81 smokers, 210 non-smokers, 79 ex-smokers). Volatile organic compounds corresponding to product ions at seven mass-to-charge ratios (m/z 28, 42, 69, 79, 93, 97, 123) in the PTR-MS spectra differentiated between smokers and non-smokers. The Youden index (= maximum of sensitivity + specificity - 1, YI) as a measure for differentiation between smokers and non-smokers was YI = 0.43 for ions at the m/z values 28 (tentatively identified as HCN), YI = 0.75 for m/z = 42 (tentatively identified as acetonitrile) and YI = 0.53 for m/z = 79 (tentatively identified as benzene). No statistically significant difference between smokers and non-smokers was observed for the product ions at m/z = 31 and 33 (compounds tentatively identified as formaldehyde and methanol). When interpreting the exhaled breath of lung cancer or COPD patients, who often smoke, compounds appearing at the above-mentioned seven mass-to-charge ratios should be considered with appropriate care to avoid misdiagnosis. Validation studies in larger numbers of patients with more precise delineation of their smoking behavior and using additional analytical techniques such as GC/MS and SIFT-MS should be carried out.
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PMID:Compounds enhanced in a mass spectrometric profile of smokers' exhaled breath versus non-smokers as determined in a pilot study using PTR-MS. 2138 43

Nearly one third of the world's population use biomass fuels such as coal, wood, animal dung, and crop residues as their primary source of domestic energy. Due to their incomplete combustion, a multitude of pollutants associated with high levels of indoor air pollution (IAP) are released which include suspended particulate matter (SPM), carbon monoxide, formaldehyde, nitrogen dioxide, polycyclic aromatic hydrocarbons (PAH), etc. There is a line of evidence that exposure to those pollutants can lead to increased risk of diseases including respiratory infections (e.g., pneumonia, tuberculosis and chronic obstructive pulmonary disease (COPD), lung cancer, and asthma), low birth weight, cataracts, and cardiovascular events. It is one of the major global public health threats that require greater efforts for prevention through research and policy-making. This review summarizes the available information on potential health risks associated with biomass fuel use.
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PMID:A review of diseases associated with household air pollution due to the use of biomass fuels. 2170 40


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