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Träfflista för sökning "AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Cancer och onkologi) srt2:(1995-1999);pers:(Adami H O)"

Sökning: AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Cancer och onkologi) > (1995-1999) > Adami H O

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1.
  • Bergström, A., et al. (författare)
  • Occupational physical activity and renal cell cancer : a nationwide cohort study in Sweden
  • 1999
  • Ingår i: International Journal of Cancer. - New York, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 83:2, s. 186-91
  • Tidskriftsartikel (refereegranskat)abstract
    • The causes of renal cell cancer remain incompletely understood. In one previous retrospective case-control study, high occupational physical activity has been associated with a decreased risk among men, but not among women. Our aim was to investigate the association between occupational physical activity and renal cell cancer in a large cohort in Sweden. A cohort of Swedish men and women was identified in the nationwide censuses in 1960 and 1970, and the reported occupations were classified into 4 levels of physical demands. Follow-up from 1971 through 1989 was accomplished through record linkages to the Swedish Cancer Registry. Multivariate Poisson regression models were used to estimate relative risk (RR) and 95% confidence intervals (CI). We found a monotonic increase in risk of renal cell cancer with decreasing level of occupational physical activity among men (p for trend <0.001). After adjustment for socio-economic status, place of residence, and calendar year of follow-up, men with long-term sedentary jobs had a 25% (RR = 1.25, 95% CI 1.02-1.53) increased risk compared to men with physically demanding occupations. Among women there was no association, the dose-risk trend was not significant (p for trend >0.50). Occupational physical activity was inversely associated with renal cell cancer among men. The absence of association among women might be due to smaller range of exposure, confounding by household work or reproductive factors, or to a difference in biological response to physical activity in men and women.
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2.
  • Chow, W. H., et al. (författare)
  • Risk of urinary tract cancers following kidney or ureter stones
  • 1997
  • Ingår i: Journal of the National Cancer Institute. - Oxford, United Kingdom : Oxford University Press. - 0027-8874 .- 1460-2105. ; 89:19, s. 1453-1457
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: A relationship has been suggested between kidney or ureter stones and the development of urinary tract cancers. In this study, a population-based cohort of patients hospitalized for kidney or ureter stones in Sweden was followed for up to 25 years to examine subsequent risks for developing renal cell, renal pelvis/ureter, or bladder cancer.Methods: Data from the national Swedish In-patient Register and the national Swedish Cancer Registry were linked to follow 61,144 patients who were hospitalized for kidney or ureter stones from 1965 through 1983. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were computed on the basis of nationwide cancer incidence rates, after adjustment for age, sex, and calendar year.Results: Risk of renal cell cancer was not elevated in this cohort. Significant excesses of renal pelvis/ureter cancer (SIR = 2.5; 95% CI = 1.8-3.3) and bladder cancer (SIR = 1.4; 95% CI = 1.3-1.6) were observed, but the SIRs for women were more than twice those for men. Risks varied little by age or duration of follow-up. Risks of renal pelvis/ureter cancer and bladder cancer among patients with an associated diagnosis of urinary tract infection were more than double those among patients without such infection, although the risks were significantly elevated in both groups.Conclusions: Individuals hospitalized for kidney or ureter stones are at increased risk of developing renal pelvis/ureter or bladder cancer, even beyond 10 years of follow-up. Chronic irritation and infection may play a role, since kidney or ureter stones were located on the same side of the body as the tumors in most patients with renal pelvis/ureter cancer evaluated in our study.
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3.
  • Hunter, D J, et al. (författare)
  • Non-dietary factors as risk factors for breast cancer, and as effect modifiers of the association of fat intake and risk of breast cancer
  • 1997
  • Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 8:1, s. 49-56
  • Tidskriftsartikel (refereegranskat)abstract
    • To assess more precisely the relative risks associated with established risk factors for breast cancer, and whether the association between dietary fat and breast cancer risk varies according to levels of these risk factors, we pooled primary data from six prospective studies in North America and Western Europe in which individual estimates of dietary fat intake had been obtained by validated food-frequency questionnaires. Based on information from 322,647 women among whom 4,827 cases occurred during follow-up: the multivariate-adjusted risk of late menarche (age 15 years or more compared with under 12) was 0.72 (95 percent confidence interval [CI] = 0.62-0.82); of being postmenopausal was 0.82 (CI = 0.69-0.97); of high parity (three or more births compared with none) was 0.72 (CI = 0.61-0.86); of late age at first birth (over 30 years of age compared with 20 or under) was 1.46 (CI = 1.22-1.75); of benign breast disease was 1.53 (CI = 1.41-1.65); of maternal history of breast cancer was 1.38 (CI = 1.14-1.67); and history of a sister with breast cancer was 1.47 (CI = 1.27-1.70). Greater duration of schooling (more than high-school graduation compared with less than high-school graduation) was associated significantly with higher risk in age-adjusted analyses, but was attenuated after controlling for other risk factors. Total fat intake (adjusted for energy consumption) was not associated significantly with breast cancer risk in any strata of these non-dietary risk factors. We observed a marginally significant interaction between total fat intake and risk of breast cancer according to history of benign breast disease; with fat intake being associated nonsignificantly positively with risk among women with a previous history of benign breast disease; no other significant interactions were observed. Risks for reproductive factors were similar to those observed in case-control studies; relative risks for family history of breast cancer were lower. We found no clear evidence in any subgroups of a major relation between total energy-adjusted fat intake and breast cancer risk.
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4.
  • Lindblad, Per, 1953-, et al. (författare)
  • Diet and risk of renal cell cancer : a population-based case-control study
  • 1997
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia, USA : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 6:4, s. 215-223
  • Tidskriftsartikel (refereegranskat)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.
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5.
  • Lindblad, Per, 1953-, et al. (författare)
  • International renal-cell cancer study. V. Reproductive factors, gynecologic operations and exogenous hormones
  • 1995
  • Ingår i: International Journal of Cancer. - Hoboken, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 61:2, s. 192-198
  • Tidskriftsartikel (refereegranskat)abstract
    • The relationships between reproductive factors, exogenous hormones and renal-cell cancer were examined in an international, multicenter, population-based, case-control study undertaken in 1989-1991. Data from 5 centers situated in Australia, Denmark, Germany, Sweden and the United States included for analysis 608 women with renal-cell cancer and 766 female controls. A significant trend in risk (p = 0.002) was associated with number of births, with an 80% excess risk for 6 or more births [RR = 1.8, 95% confidence interval (CI) = 1.1 to 2.9] compared with one birth. A decreasing risk was seen for increasing age at first birth, although this was confounded by body-mass index and number of births. A suggestive reduction of risk was also seen for increasing age at menarche. Age at menopause was unrelated to risk of renal-cell cancer. An increased risk was observed for women having had both a hysterectomy and an oophorectomy. Use of oral contraceptives in non-smoking women reduced the risk of renal-cell cancer (RR = 0.5, 95% CI = 0.4 to 0.8); this reduction increased with longer duration of use. No association was observed for estrogen replacement therapy. Our results indicate that certain hormonal and reproductive variables may be related to risk of renal-cell cancer and deserve further investigation, both epidemiologically and experimentally.
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6.
  • Lindblad, Per, 1953-, et al. (författare)
  • The role of diabetes mellitus in the aetiology of renal cell cancer
  • 1999
  • Ingår i: Diabetologia. - New York, USA : Springer. - 0012-186X .- 1432-0428. ; 42:1, s. 107-12
  • Tidskriftsartikel (refereegranskat)abstract
    • To investigate the relation between diabetes mellitus and the risk of renal cell cancer we carried out a population-based retrospective cohort study. Patients identified in the Swedish Inpatient Register who were discharged from hospitals with a diagnosis of diabetes mellitus between 1965 and 1983 formed a cohort of 153852 patients (80005 women and 73847 men). The cohort members were followed up to 1989 by record linkage to three nation-wide registries. Standardized incidence ratios (SIRs) and standardized mortality ratios (SMRs) were computed using age-specific sex-specific and period-specific incidence and mortality rates derived from the entire Swedish population. After exclusion of the first year of observation, a total of 267 incidences of renal cell cancer (ICD-7:180.0) occurred in diabetic patients compared with the 182.4 that had been expected. Increased risks were observed in both women (SIR = 1.7, 95% confidence interval, CI = 1.4-2.0) and men (SIR = 1.3; 95 % CI = 1.1-1.6) throughout the duration of follow-up (1-25 years). A higher risk was seen for kidney cancer (ICD-7:180) mortality (SMR = 1.9; 95% CI = 1.7-2.2, women; SMR 1.7, 95% CI = 1.4-1.9, men). In comparison with the general population, patients with diabetes mellitus have an increased risk of renal cell cancer.
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7.
  • Mandel, J. S., et al. (författare)
  • International renal-cell cancer study. IV. Occupation
  • 1995
  • Ingår i: International Journal of Cancer. - New York, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 61:5, s. 601-605
  • Tidskriftsartikel (refereegranskat)abstract
    • The relationship between renal-cell cancer (RCC) and occupation was investigated in an international multicenter population-based case-control study. Study centers in Australia, Denmark, Germany, Sweden and the United States interviewed 1732 incident RCC cases and 2309 controls. Significant associations were found with employment in the blast-furnace or the coke-oven industry [relative risk (RR), 1.7; 95% confidence interval (CI), 1.1-2.7], the iron and steel industry (RR, 1.6; 95% CI, 1.2-2.2) and exposure to asbestos (RR, 1.4; 95% CI, 1.1-1.8), cadmium (RR, 2.0; 95% CI, 1.0-3.9), dry-cleaning solvents (RR, 1.4; 95% CI, 1.1-1.7), gasoline (RR, 1.6; 95% CI, 1.2-2.0) and other petroleum products (RR, 1.6; 95% CI, 1.3-2.1). Asbestos, petroleum products and dry-cleaning solvents appear to merit further investigation, in view of the relationship between risk and duration of employment or exposure and after adjustment for confounding. There was a negative association between RCC and education, but it was not consistent across all centers. Overall, the results of our multicenter case-control study suggest that occupation may be more important in the etiology of RCC than indicated by earlier studies.
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8.
  • McLaughlin, J. K., et al. (författare)
  • International renal-cell cancer study. I. Tobacco use
  • 1995
  • Ingår i: International Journal of Cancer. - New York, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 60:2, s. 194-198
  • Tidskriftsartikel (refereegranskat)abstract
    • The relationship between renal-cell cancer (RCC) and tobacco use was investigated in an international, multicenter, population-based case-control study. Coordinated studies were conducted in Australia, Denmark, Germany, Sweden and the United States using a shared protocol and questionnaire. A total of 1,732 cases (1,050 men, 682 women) and 2,309 controls (1,429 men, 880 women) were interviewed for the study. No association was observed between risk and use of cigars, pipes or smokeless tobacco. A statistically significant association was observed for cigarette smoking, with current smokers having a 40% increase in risk [relative risk (RR) = 1.4, 95% confidence interval (CI) 1.2-1.7]. Risk increased with intensity (number of cigarettes) and duration (years smoked). Among current smokers the RR for pack-years rose from 1.1 (95% CI 0.8-1.5) for < 15.9 pack years to 2.0 (95% CI 1.6-2.7) for > 42 pack years (p for trend < 0.001). Long-term quitters (> 15 years) experienced a reduction in risk of about 15-25% relative to current smokers. Those who started smoking late (> 24 years of age) had about two-thirds the risk of those who started young (< or = 12 years of age). Overall, the findings of this pooled analysis confirm that cigarette smoking is a causal factor in the etiology of RCC.
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9.
  • McLaughlin, J. K., et al. (författare)
  • International renal-cell cancer study. VIII. Role of diuretics, other anti-hypertensive medications and hypertension
  • 1995
  • Ingår i: International Journal of Cancer. - New York, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 63:2, s. 216-221
  • Tidskriftsartikel (refereegranskat)abstract
    • Risk of renal-cell cancer in relation to use of diuretics, other anti-hypertensive medications and hypertension was assessed in a multi-center, population-based, case-control study conducted in Australia, Denmark, Germany, Sweden and the United States, using a shared protocol and questionnaire. A total of 1,732 histologically confirmed cases and 2,309 controls, frequency-matched to cases by age and sex, were interviewed. The association between renal-cell cancer and the drugs was estimated by relative risks (RRs) and 95% confidence intervals (CIs). Risks were increased among users of diuretics and other anti-hypertensive medications. After adjustment for hypertension, risk for diuretics was reduced to unity, except among long-term (15+ years) users. Risk for use of non-diuretic anti-hypertensive drugs remained significantly elevated and increased further with duration of use. Overall risk was not enhanced when both classes of medications were used. Excess risk was not restricted to any specific type of diuretic or anti-hypertensive drug and no trend was observed with estimated lifetime consumption of any particular type of product. The RR for hypertension after adjustment for diuretics and other anti-hypertensive medications was 1.4 (95% CI = 1.2-1.7), although among non-users of any anti-hypertensive medications, there was little excess risk associated with a history of hypertension. Exclusion of drug use that first occurred within 5 years of cancer diagnosis or interview did not alter the associations. Our findings suggest small effects on renal-cell cancer risk associated with hypertension and use of diuretics and other anti-hypertensive medications. However, because of potential misclassifications of these highly correlated variables, it is difficult to distinguish the effect of treatment from its indication, hypertension.
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10.
  • Wolk, A., et al. (författare)
  • International renal cell cancer study. VII. Role of diet
  • 1996
  • Ingår i: International Journal of Cancer. - Hoboken, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 65:1, s. 67-73
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated the role of diet in the etiology of renal cell cancer (RCC) in a multi-center, population-based case-control study conducted in Australia, Denmark, Sweden and the United States, using a shared protocol. A total of 1,185 incident histopathologically confirmed cases (698 men, 487 women) and 1,526 controls (915 men, 611 women) frequency-matched to cases by sex and age were included in the analyses. The association between RCC and diet was estimated by relative risks (RR) and 95% confidence intervals (CI) adjusted for age, sex, study center, body mass index and smoking. A statistically significant positive association was observed for total energy intake (RR = 1.7, 95% CI = 1.4-2.2 for the highest vs. lowest quartile, p value for trend < 0.00001), while the hypothesis that protein and fat are risk factors independent of energy was not supported. Fried meats were associated with increased RCC risk, while vegetables and fruits were protective, with the strongest effect observed for the highest quartile of consumption of orange/dark green vegetables but not vitamin C or beta carotene. Increased risk was associated with low intake (lowest decile) of vitamin E and magnesium. We observed an apparent protective effect of alcohol confined to women and probably due to chance. Our findings indicate an important role of nutrition in the development of RCC. The apparent positive association of energy intake with risk of RCC needs further investigation in a prospective cohort study to exclude the possible impact of differences in recall between cases and controls.
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