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

In Riyadh city 698 physicians were studied for their smoking habits, attitudes and behaviour; 48% were smokers and 34% are currently smoking. Males smoked significantly more than females currently and in the past. Smoking prevalence and intensity tended to decrease with age and quitting periods were longer. More than 60% of the physicians agreed that smoking is a major contributing factor in the causation of coronary artery disease, lung cancer and chronic bronchitis; less than 20% said the same for bladder cancer and neonatal death. Setting a good example for children was the most important reason for not smoking.
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PMID:Attitudes and behaviour of physicians towards smoking in Riyadh city, Saudi Arabia. 175 Jan 34

An historical cohort study was conducted among 4,213 men who worked for 5 or more years at a Soderberg aluminum reduction plant in British Columbia (BC), Canada. Standardized mortality and incidence ratios were used to compare the mortality and cancer incidence of the cohort with that of the BC population and to examine risk by cumulative exposure to coal-tar pitch volatiles (CTPV) and electromagnetic fields. Significantly elevated rates were observed for bladder cancer incidence (standardized incidence ratio [SIR] = 1.69) and brain cancer mortality (standardized mortality ratio = 2.17). The risk of bladder cancer was strongly related to cumulative exposure to CTPV (P less than .01). The risk for non-Hodgkin's lymphoma also increased with increasing exposure (P less than .05), although the overall rate was similar to that of the general population (SIR = 1.06). The lung cancer rate was as expected (SIR = 0.97), but showed a weak association with CTPV exposure that was not statistically significant. No individual cause of death or incident cancer site was related to exposure to electromagnetic fields. Analysis of the joint effect of smoking and CTPV exposure on lung and bladder cancer showed the exposure response relationships to be independent of smoking.
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PMID:Mortality and cancer incidence in aluminum reduction plant workers. 176 56

The rubber industry, acknowledged by the International Agency for Research on Cancer (IARC) to be a cancer risk technology is, because of difficulty in identifying causal factors, the subject of intensive epidemiological studies in many countries. In the presented study, cancer risk in the rubber industry was evaluated on the basis of long-term observation (1945-1985) of a cohort of 6978 male workers employed in a rubber goods factory, predominantly engaged in producing rubber footwear. The reference group was the general male population of Poland. Standardized mortality ratios (SMRs), calculated by means of the person-years method, were used in the evaluation of death risk. The observation of a whole cohort indicated an excess of cancer, in general (approx 12%), lung cancer (approx 40%) and gallbladder cancer (approx fourfold). In the subcohorts, distinguished according to peculiarities of individual production sections, cancer risk of the large intestine and larynx was significantly increased. The highest cancer risk was found in compounding, mixing, milling and vulcanizing sections. Hence, beta-naphthylamine, benzidine and solvents (benzene) were used in technological processes in the past, bladder cancer and leukemia were considered as most specific for the rubber industry. In the cohort observed, the risk of death from bladder cancer was significantly increased only in those who had been employed during the years 1945-1953, namely during the period when beta-naphthylamine was in use. No excess of deaths from leukemia was observed.
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PMID:Cancer mortality among male workers in the Polish rubber industry. 179 40

Molecular epidemiology approaches are being employed to examine the validity and elucidate the basis for hypothesized associations of genetic susceptibility factors with common malignancies due to carcinogen exposure. This approach integrates traditional epidemiologic study designs with state-of-the-art laboratory assays. Advantages of this strategy include the possibility of gaining insight into mechanisms and better exposure assessment. Disadvantages include added complexity and cost. Three examples of pharmacogenetic risk factors are discussed: the first two are p450 enzymes whose activity has been associated with susceptibility to lung cancer (debrisoquine hydroxylase, aryl hydrocarbon hydroxylase), and the last, N-acetyltransferase, a non-p450 enzyme, has been associated with bladder cancer susceptibility. In this context, a case-control study which examined the hypothesis of an association between the debrisoquine metabolic phenotype and lung cancer is discussed. While various studies from the molecular to the population level provide evidence to support each of these associations, methodologic problems exist and a causal association remains to be decisively demonstrated. New epidemiologic studies, the application of improved DNA based tests for the genotype, and further basic investigations regarding the mechanisms of the proposed associations continue, and progress is anticipated in the resolution of these questions with important consequences for our understanding of chemical carcinogenesis in these common malignancies. While these associations remain controversial, the existence of wide interindividual variation in the population in the ability to metabolize certain chemical carcinogens is certain and this argues for a conservative approach in the regulation of chemical carcinogens.
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PMID:Study design and genetic susceptibility factors in the risk assessment of chemical carcinogens. 182 Jul 35

Genetic modulation of environmental exposures associated with common malignancies (lung and bladder) is an attractive mechanism to explain differential susceptibility to tobacco or occupation related carcinogens in the population. Epidemiologic studies to test the hypothesis of such associations and to evaluate evidence for a causal role for genetic factors in the etiology of chemically-induced tumors are challenging and require the close collaboration of epidemiologists, clinicians and laboratory investigators. In this work we review the evidence for an association of three polymorphisms of drug or xenobiotic metabolism with human cancers. Methodologic considerations and data relevant to evaluating a causal role for each polymorphism are considered. Fair to good support for both an association of the acetylation phenotype with occupationally-related bladder cancer and for an association of the debrisoquine metabolic phenotype and lung cancer is found, although in neither case is the evidence completely convincing. Epidemiologic evidence for the association of aryl hydrocarbon hydroxylase and lung cancer is presently problematic because of difficulties in the assay and subsequent confounding factors. DNA based assays are at various stages of development for each of the genotypes and promise to simplify future studies while introducing new methodologic pitfalls. Further studies in all three areas are warranted as each has important implications for the understanding of the carcinogenic process, etiology and the public health aspects of common malignancies.
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PMID:Relevance of metabolic polymorphisms to human carcinogenesis: evaluation of epidemiologic evidence. 184 21

Our method to evaluate acetylator phenotype and N-oxidation phenotype with a single caffeine dose and a single urine specimen collection has enabled us to examine acetylation and N-oxidation by two enzyme systems that have a known genetic polymorphism and are important in aromatic amine metabolism. Based on available data, we have hypothesized patients with urinary bladder cancer will have a higher frequency of rapid N-oxidation and slow acetylation phenotypes when compared to controls. On the other hand, patients with colorectal cancer should contain a higher proportion of both rapid N-oxidation phenotype and rapid acetylation phenotype when compared to the control group. In contrast, lung cancer patients, should contain an increased frequency of rapid arylamine N-oxidation phenotypes with the frequency of acetyltransferase phenotype being greater or perhaps the same as in the control group.
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PMID:Aromatic and heterocyclic amine metabolism and phenotyping in humans. 195 28

This paper describes the cellular and tissue distribution of P-glycoprotein (P-GP) (mdr1 gene product), the role of P-GP in vivo and immunodiagnosis of multi-drug-resistant cancers. We mainly used MRK 16 monoclonal antibody (MAb) reactive with P-GP. P-GP was found to be expressed very strongly in the adrenal cortex of adults and strongly in the renal tubules of the kidney, capillary blood vessels of the brain, and also in placenta. Interestingly, P-GP was not distributed in fetal and neonatal adrenals, and thus may be closely related to adrenal maturation. A high level of P-GP expression was also seen in all cases of functional hormone-producing adrenal tumor, one case of insulinoma, two cases of untreated colonic cancer, one case each of untreated lung cancer, gastric cancer and breast cancer, six cases of renal cell carcinoma and 17 cases of bladder cancer. Using flow cytometry and immunocytochemistry, we investigated the reactivity of MRK 16 MAb with peripheral human mononuclear cells (mainly blastic cells and lymphocytes) from 31 patients with leukemia or malignant lymphoma. Reactivity with MRK 16 MAb was observed in five cases. Some cases reflected the prior administration of adriamycin, vincristine and VP-16, which are known to induce P-GP expression. P-GP-MRK 16-protein A-Sepharose complex derived from human adrenal possessed marked ATPase activity. These data suggest that P-GP may play a physiological role in the human adrenal. Finally, diagnostic criteria of multi-drug-resistant cancers are presented.
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PMID:Expression and functions of P-glycoprotein (mdr1 gene product) in normal and malignant tissues. 197 61

In 1974 and 1975, serum specimens were collected from 25,802 volunteers in Washington County, Maryland. The serum was kept frozen at -73 degrees C until the time of assay. Prediagnostic samples from 436 cancer cases and 765 matched control subjects have been assayed. Nine sites have been studied: colon, rectum, pancreas, lung, melanoma, basal cell of skin, breast, prostate, and bladder. Serum beta-carotene levels showed a strong protective association with lung cancer, suggestive protective associations with melanoma and bladder cancer, and a suggestive but nonprotective association with rectal cancer. Serum vitamin E levels had a protective association with lung cancer; none of the other sites showed impressive associations. Low levels of serum lycopene were strongly associated with pancreatic cancer and less strongly associated with cancer of the bladder and rectum.
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PMID:Prediagnostic serum levels of carotenoids and vitamin E as related to subsequent cancer in Washington County, Maryland. 198 96

Radiation-induced cancers after radiation therapy for cancer of the uterine cervix were investigated on 11,855 patients including 5725 patients treated with radiation therapy alone, 1969 postoperative radiation therapy and 4161 surgery alone. The observed-to-expected ratios of the second primary cancer was 0.933 for the patients with radiation therapy alone and 1.074 for the patients with postoperative radiation therapy, respectively. No significant increase was observed in the risk of second primary cancers when all sites were combined. However, assessing on site by site basis, significant excess was noted for the rectum cancer, leukemia, and bladder cancer for the radiation therapy group but not for the surgery group. A significant excess of lung cancer was observed in both radiation therapy and surgery groups, which was attributed to some other causative factors. Radiation-induced cancers were suggested to develop apparently in organs involved in the irradiated field.
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PMID:Second cancer after radiation therapy for cancer of the uterine cervix. 198 34

Vital statistics were examined for the years 1955 through 1985 for Japanese natives and United States whites to elucidate changes in cancer mortality and related antecedent patterns of life-style in these two populations. Results show that lung cancer rates are rapidly accelerating among Japanese males as a consequence of their prior history of heavy cigarette smoking. Oropharyngeal cancer rates are also rising in Japan paralleling increases in alcohol and tobacco utilization. As the Japanese life-style and diet continue to become more "westernized," the rates of malignancies of the breast, ovary, corpus uteri, prostate, pancreas, and colon also continue to rise. Nevertheless, the mortality patterns of certain malignancies, viz., laryngeal, esophageal, and urinary bladder cancer, are discrepant with their established risk factor associations, suggesting the existence of other differences in risk factor exposure between the two countries. Epidemiologists and health educators need to develop innovative international programs of investigation and health promotion with preventive impact on common malignancies associated with risk factors of life-style.
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PMID:Comparative epidemiology of cancer between the United States and Japan. A second look. 198 68


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