| 1. |
- Wallin, H, et al.
(author)
-
Altered aromatic amine metabolism in epileptic patients treated with phenobarbital
- 1995
-
In: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. - 1055-9965. ; 4:7, s. 3-771
-
Journal article (peer-reviewed)abstract
- The fate of carcinogens differs among individuals who have different activities of drug-metabolizing enzymes that are important in activating and detoxifying carcinogens. A drug that profoundly alters the metabolism of the drugs and carcinogens is the anticonvulsive agent phenobarbital. To investigate why epileptic patients appear to have a low risk of cancer of the urinary bladder, and on the basis of the observation that levels of aromatic amine-hemoglobin adducts are strongly associated with various risk factors for cancer at that site, we determined aromatic amine-hemoglobin adducts in 62 epileptic patients as a surrogate measure of the reaction of carcinogenic metabolites with DNA in target tissue. Although adducts were detected in all subjects, the levels were proportional to daily tobacco consumption. When the subjects were stratified into groups smoking 20 g tobacco/day or more, smoking <20 g/day, and not smoking, an effect of medication was detected. Epileptic patients treated chronically with phenobarbital or primidone, which is effectively metabolized to phenobarbital, were found to have lower levels of 4-aminobiphenyl adducts than patients on the other treatment (P = 0.02; ANOVA). In nonsmokers, no effect of medication could be demonstrated above background variation; however, an increasing effect was seen with tobacco consumption with only one-half the increase in adducts per g of tobacco smoked as epileptic patients on other treatment. The difference in the increases (slopes of regression lines) was highly significant statistically. This reduction in the level of hemoglobin-aromatic amine adducts is probably due to induction of detoxification enzymes in the patients treated with phenobarbital.
|
|
| 2. |
- Voskuil, D W, et al.
(author)
-
Assessing the human intake of heterocyclic amines : Limited loss of information using reduced sets of questions
- 1999
-
In: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 8:9, s. 809-814
-
Journal article (peer-reviewed)abstract
- The aim of this study was to evaluate loss of information from a reduced food frequency questionnaire as compared with an extensive reference method developed to assess the intake of heterocyclic amines (HCAs), Food frequency data were linked to concentrations of HCAs in cooked foods to estimate the individual daily exposure to a combination of five HCAs. The number of food items in the questionnaire was reduced and selected in three ways: (a) according to the contribution to the estimated total intake; (b) the between-person variance; or (c) dishes included in other studies. The effect on sensitivity, specificity, concordance, the correlation coefficient, kappa, and simulated relative risks was determined using information from a population-based study conducted in Stockholm. Only a limited amount of misclassification was introduced when the number of dishes was reduced from 39 to 15 or 20, and no major difference was seen when dishes were selected according to the total intake or the between-person variance. Our data indicate that for a specific exposure, such as HCAs, the loss of accuracy in an analytical epidemiological study is small and may not be relevant when the number of dishes in a food frequency questionnaire is decreased, if the initially chosen dishes are carefully selected and cover a reasonable part of the total intake or between-person variance.
|
|
| 3. |
- Lindblad, Per, 1953-, et al.
(author)
-
Diet and risk of renal cell cancer : a population-based case-control study
- 1997
-
In: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia, USA : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 6:4, s. 215-223
-
Journal article (peer-reviewed)abstract
- In a few previous studies on diet and renal cell cancer, an inconsistent positive association with meat, milk, and protein and a negative association with vegetable and fruit consumption have been found. Whereas earlier studies have dealt with recent diet only, our study explored the effect of foods consumed both during the usual adult lifetime and 20 years prior to interview. The study included 379 individuals with incident histologically verified renal cell cancer and 350 control subjects residing in eight counties in Sweden between June 1989 and December 1991. Usual adult dietary intake and dietary habits 20 years prior to interview were assessed by a structured face-to-face interview and a self-administered questionnaire, respectively. Odds ratios were estimated through unconditional logistic regression. We have not observed an association of renal cell cancer with milk or total meat consumption per se; however, frequent intake of fried/sauteed meat increased the risk of renal cell cancer by about 60%; frequent consumption of poultry was also associated with an increased risk (P for trend, 0.05). A significantly protective effect on risk of renal cell cancer was observed with increasing consumption of fruit (P for trend, 0.05). When analyzed by smoking status, total fruit and especially citrus fruit consumption among nonsmokers showed an even stronger protective effect; the highest quartiles of total fruit, apple, and citrus fruit consumption entailed a 50-60% reduction in risk of renal cell cancer compared with the lowest quartiles. There was a suggestion of a protective effect of high total vegetable consumption. A protective effect of vitamin C and alpha-tocopherol was also more pronounced in nonsmokers (P for trend, 0.004 and 0.007, respectively). Our study adds to the evidence that diet may have an important role in the etiology of renal cell cancer.
|
|
| 4. |
- Pero, Ronald W., et al.
(author)
-
Quality control program for storage of biologically banked blood specimens in the Malmo diet and cancer study
- 1998
-
In: Cancer Epidemiology Biomarkers and Prevention. - 1055-9965. ; 7:9, s. 803-808
-
Journal article (peer-reviewed)abstract
- A biological bank has been developed to extend the biochemical and molecular research base for a prospective study on diet and cancer in the city of Malmo, Sweden. The study entered individuals 45-69 years of age, of which 30,382 individuals (45%) participated. Each individual entering the bank has stored samples of viable mononuclear leukocytes (MNLs; -140°C) and granulocytes (GRANs; -80°C) or buffy coats (-140°C), erythrocytes (- 80°C), and plasma/serum (-80°C). The bioassays developed to monitor the quality of storage conditions were: (a) viability and growth response to phytohemagglutinin for MNLs; (b) DNA strand breakage for GRANs; (c) NAD content for erythrocytes; and (d) thiol status for plasma/serum. The yield, purity, and storage conditions were all quality controlled, and the samples were determined to be of high standard after 137-190 weeks of storage. No differences in yield and purity were found in samples banked by different laboratory technicians. Growth responses of MNLs were severely reduced (90%) after 40 weeks of storage, which justified switching from the storage of purified MNLs and GRANs to the more cost-effective banking of buffy coats. We conclude that the quality of the banked material, based on the biochemical analysis done, indicate that the storage conditions are optimal at least up to 3.5 years, except for the growth response of MNLs.
|
|
| 5. |
- Yngveson, A, et al.
(author)
-
p53 Mutations in lung cancer associated with residential radon exposure.
- 1999
-
In: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 8:5
-
Journal article (peer-reviewed)abstract
- Unusual mutation patterns in lung tumors among underground miners have been indicated, suggesting radon-specific alterations in the genome, but the data are not consistent. To investigate the association between residential radon exposure and p53 mutations in lung tumors, we performed a study on cases from a nation-wide population-based investigation in Sweden. Our study included 83 nonsmoking lung cancer cases and 250 smoking lung cancer cases, diagnosed 1980-1984, with a time-weighted average radon exposure over 140 Bq/m3 or up to 50 Bq/m3. Radon was measured in dwellings occupied by the study subjects at some time since 1947. Information on smoking habits and other risk factors was obtained from questionnaires. After exclusions because of the initiation of treatment or insufficient material, the p53-status of 243 tumors was determined using PCR-single-stranded conformation polymorphism analysis and sequencing determination of exons 5-8. The overall mutation prevalence was 23.9%. An increased mutation prevalence was suggested among those with high exposure to residential radon [odds ratio (OR), 1.4; 95% CI, 0.7-2.6], especially among nonsmokers (OR, 3.2; 95% CI, 0.7-15.5), but no specific mutational pattern was indicated. Furthermore, the mutation prevalence seemed to be higher among smoking lung cancer cases than among nonsmoking cases (OR, 2.1; 95% CI, 0.9-5.0), and particularly among those smoking less than 10 cigarettes per day. It may be concluded that residential exposure to radon seems to contribute to a higher mutation prevalence of the p53 gene in lung tumors.
|
|
