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  • 1.
    Bergström, A.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Hsieh, C. C.
    Cancer Center, UMass Medical School, Worcester, MA, USA; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Lu, C. M.
    Cancer Center, UMass Medical School, Worcester, MA, USA; Department of Urology, Tian-Sheng Memorial Hospital, Pingtung, Taiwan.
    Cook, N. R.
    Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA.
    Wolk, A.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Obesity and renal cell cancer: a quantitative review2001In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 85, no 7, p. 984-990Article in journal (Refereed)
    Abstract [en]

    Obesity has been associated with an increased risk of renal cell cancer among women, while the evidence for men is considered weaker. We conducted a quantitative summary analysis to evaluate the existing evidence that obesity increases the risk of renal cell cancer both among men and women. We identified all studies examining body weight in relation to kidney cancer, available in MEDLINE from 1966 to 1998. The quantitative summary analysis was limited to studies assessing obesity as body mass index (BMI, kg m(-2)), or equivalent. The risk estimates and the confidence intervals were extracted from the individual studies, and a mixed effect weighted regression model was used. We identified 22 unique studies on each sex, and the quantitative analysis included 14 studies on men and women, respectively. The summary relative risk estimate was 1.07 (95% CI 1.05-1.09) per unit of increase in BMI (corresponding to 3 kg body weight increase for a subject of average height). We found no evidence of effect modification by sex. Our quantitative summary shows that increased BMI is equally strongly associated with an increased risk of renal cell cancer among men and women.

  • 2.
    Bergström, A.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Medical Epidemiology, Karolinska Institutet, Stockholm; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Birth weight and risk of renal cell cancer2001In: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, Vol. 59, no 3, p. 1110-1113Article in journal (Refereed)
    Abstract [en]

    Background: The prenatal period has been suggested to be important for future cancer risk. Conditions in utero are also important for the development of the kidney, and birth weight, a marker of fetal nutrition and growth, is linearly correlated with the number of nephrons and the structural and functional unit of the kidney. An association between birth weight and renal cell cancer, the major form of kidney cancer, is biologically plausible, but has never been studied.

    Methods: We conducted a population-based, case-controlled study in Sweden of men and women aged 20 to 79 years. We collected self-reported information on categories of birth weight from 648 patients with newly diagnosed renal cell cancer and from 900 frequency-matched control subjects. We used unconditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) as estimates of the relative risks.

    Results: An increased risk of renal cell cancer was observed among men with a birth weight of > or =3500 g (adjusted OR = 1.3, 95% CI, 1.0 to 1.8) compared with men with a birth weight between 3000 and 3499 g, especially in the subgroup without hypertension or diabetes (adjusted OR = 1.8, 95% CI, 1.2 to 2.6). No clear association among men with a birth weight <3000 g or among women was found.

    Conclusions: Our study shows that conditions in utero, reflected by birth weight, might affect the risk of renal cell cancer in adulthood. It is unclear why no association was found among women. Further studies, based on weight from birth certificates, are needed to clarify this relationship.

  • 3.
    Bergström, A.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Moradi, T.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Adami, H. O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Harvard Center for Cancer Prevention, Harvard School of Public Health, Boston, MA, USA.
    Wolk, A.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Occupational physical activity and renal cell cancer: a nationwide cohort study in Sweden1999In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 83, no 2, p. 186-91Article in journal (Refereed)
    Abstract [en]

    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.

  • 4.
    Bergström, A.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Terry, P.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Ahlbom, A.
    The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Feychting, M.
    The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wolk, A.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Physical activity and risk of renal cell cancer2001In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 92, no 1, p. 155-157Article in journal (Refereed)
    Abstract [en]

    The relation between physical activity and renal cell cancer is unclear. High occupational physical activity has been associated with a decreased risk of renal cell cancer among men-but not among women-in two previous studies, while no association has been found for leisure time physical activity. Our aim was to investigate the association between occupational and leisure time physical activity in a prospective cohort of 17,241 Swedish twins. Information on physical activity and a wide range of potential confounding factors was obtained through a mailed questionnaire. During follow-up from 1967 through 1997 we identified 102 cases of renal cell cancer. We found no evidence of an inverse association between either occupational or leisure time physical activity and risk of renal cell cancer in this prospective cohort.

  • 5.
    Cho, Eunyoung
    et al.
    Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA; Department of Nutrition, Harvard School of Public Health, Boston MA, USA.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston MA, USA.
    Lindblad, Per
    Department of Urology, Faculty of Medicine and Health, Örebro University Hospital, Örebro, Sweden.
    Epidemiology of renal cell cancer2011In: Hematology/Oncology Clinics of North America, ISSN 0889-8588, E-ISSN 1558-1977, Vol. 25, no 4, p. 651-665Article, review/survey (Refereed)
    Abstract [en]

    Renal cell cancer (RCC) is increasingly diagnosed at an early stage in many countries, which likely contributes to the recent leveling of RCC mortality in the United States and many European countries. However, over all stages nearly 50% of the patients die within 5 years after diagnosis. Smoking and obesity may account for approximately 40% of all incidental cases in high-risk countries. Besides obesity, rising prevalence of hypertension may play a growing role. Several other occupational and lifestyle factors may also affect the risk of RCC. Genetic variations may be an important factor in the differing incidence among populations.

  • 6.
    Chow, W. H.
    et al.
    Div. of Cancer Epidemiol. and Genet., National Cancer Institute, Bethesda, MD, United States; National Institutes of Health, Executive Plaza North, Bethesda, United States .
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institute; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Gridley, G.
    Div. of Cancer Epidemiol. and Genet., National Cancer Institute, Bethesda, MD, United States.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institute, Sweden.
    McLaughlin, J. K.
    International Epidemiology Institute, Rockville, MD, United States .
    Linet, M. S.
    Div. of Cancer Epidemiol. and Genet., National Cancer Institute, Bethesda, MD, United States.
    Pennello, G. A.
    Div. of Cancer Epidemiol. and Genet., National Cancer Institute, Bethesda, MD, United States.
    Adami, H. O.
    Department of Medical Epidemiology, Karolinska Institute, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States.
    Fraumeni, J. F.
    Div. of Cancer Epidemiol. and Genet., National Cancer Institute, Bethesda, MD, United States.
    Risk of urinary tract cancers following kidney or ureter stones1997In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 89, no 19, p. 1453-1457Article in journal (Refereed)
    Abstract [en]

    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.

  • 7.
    Dabestani, Saeed
    et al.
    Department of Urology, Skåne University Hospital, Malmö, Sweden.
    Thorstenson, Andreas
    Section of Urology, Department of Molecular Medicine and Surgery, Karolinska Institute Solna, Stockholm, Sweden.
    Lindblad, Per
    Örebro University, School of Medical Sciences. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Harmenberg, Ulrika
    Department of Oncology, Karolinska University Hospital, Solna, Stockholm, Sweden.
    Ljungberg, Börje
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Lundstam, Sven
    Department of Urology, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Renal cell carcinoma recurrences and metastases in primary non-metastatic patients: a population-based study2016In: World journal of urology, ISSN 0724-4983, E-ISSN 1433-8726, Vol. 34, no 8, p. 1081-1086Article in journal (Refereed)
    Abstract [en]

    Purpose: To present the occurrence of metastases and local recurrences in primary non-metastatic patients with renal cell carcinoma (RCC) in a contemporary Swedish population-based cohort.

    Methods: Between 2005 and 2009, a total of 4527 patients were included in the prospective National Swedish Kidney Cancer Register accounting for nearly all RCC patients in Sweden. Among M0 patients, 472 (13 %) had no follow-up data registered within 5-year follow-up time and were excluded from the analysis.

    Results: In total, 939 (21 %) had distant metastases at presentation with a decrease from 23 to 18 % during the inclusion period. Of 3107 patients with follow-up data and with M0 disease, 623 (20 %) were diagnosed with a tumor recurrence during 5-year follow-up. Mean time to recurrence was 24 months (SD ± 20 months). Among these, 570 patients (92 %) were at primary diagnosis treated with radical nephrectomy, 23 patients (3.7 %) with partial nephrectomy and 12 patients (1.9 %) with minimally invasive treatments. The most frequent sites of metastases were lung (54 %), lymph nodes (22 %) and bone (20 %). The treatment of recurrence was in 50 % systemic treatments, while metastasectomy was performed in 17 % of the patients, out of which 68 % were with a curative intention.

    Conclusions: In this population-based study, 21 % of the patients had metastatic disease at presentation, with a decreasing trend over the study period. During 5-year follow-up, 20 % of the primary non-metastatic patients had recurrent disease. Of the patients with recurrence, half were given systemic oncological treatment and 17 % underwent metastasectomy.

  • 8.
    Ejerblad, E.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fored, C. M.
    Karolinska Institutet, Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fryzek, J.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Dickman, P. W.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Elinder, C. G.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Huddinge, Sweden.
    McLaughlin, J. K.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Nyren, O.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Association between smoking and chronic renal failure in a nationwide population-based case-control study2004In: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 15, no 8, p. 2178-2185Article in journal (Refereed)
    Abstract [en]

    For determining whether smoking is associated with an increased risk for chronic renal failure (CRF) overall and by type of renal disease, smoking data were analyzed from a nationwide population-based case-control study. Eligible as cases were native 18- to 74-yr-old Swedes whose serum creatinine for the first time and permanently exceeded 3.4 mg/dl (men) or 2.8 mg/dl (women). A total of 926 cases (78% of all eligible) and 998 control subjects (75% of 1330 randomly selected subjects from the source population), frequency matched to the cases by gender and age within 10 yr, were included. A face-to-face interview and a self-administered questionnaire provided information about smoking habits and other lifestyle factors. Logistic regression models estimated odds ratios (OR) as measures of relative risk for disease-specific types of CRF among smokers compared with never-smokers. Despite a modest and nonsignificant overall association, the risk increased with high daily doses (OR among smokers of >20 cigarettes/d, 1.51; 95% confidence interval [CI], 1.06 to 2.15), long duration (OR among smokers for >40 yr, 1.45; 95% CI, 1.00 to 2.09), and a high cumulative dose (OR among smokers with >30 pack-years, 1.52; 95% CI, 1.08 to 2.14). Smoking increased risk most strongly for CRF classified as nephrosclerosis (OR among smokers with >20 pack-years, 2.2; 95% CI, 1.3 to 3.8), but significant positive associations were also noted with glomerulonephritis. This study thus suggests that heavy cigarette smoking increases the risk of CRF for both men and women, at least CRF classified as nephrosclerosis and glomerulonephritis.

  • 9.
    Ejerblad, E.
    et al.
    Department of Medical Epidemiology and Biostatistic Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Fored, C. M.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute and Karolinsak University Hospital, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Fryzek, J.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    McLaughlin, J. K.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Nyren, O.
    Department of Medical Epidemiology and Biostatistic Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Obesity and risk for chronic renal failure2006In: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 17, no 6, p. 1695-1702Article in journal (Refereed)
    Abstract [en]

    Few large-scale epidemiologic studies have quantified the possible link between obesity and chronic renal failure (CRF). This study analyzed anthropometric data from a nationwide, population-based, case-control study of incident, moderately severe CRF. Eligible as cases were all native Swedes who were aged 18 to 74 yr and had CRF and whose serum creatinine for the first time and permanently exceeded 3.4 mg/dl (men) or 2.8 mg/dl (women) during the study period. A total of 926 case patients and 998 control subjects, randomly drawn from the study base, were enrolled. Face-to-face interviews, supplemented with self-administered questionnaires, provided information about anthropometric measures and other lifestyle factors. Logistic regression models with adjustments for several co-factors estimated the relative risk for CRF in relation to body mass index (BMI). Overweight (BMI>or=25 kg/m2) at age 20 was associated with a significant three-fold excess risk for CRF, relative to BMI<25. Obesity (BMI>or=30) among men and morbid obesity (BMI>or=35) among women anytime during lifetime was linked to three- to four-fold increases in risk. The strongest association was with diabetic nephropathy, but two- to three-fold risk elevations were observed for all major subtypes of CRF. Analyses that were confined to strata without hypertension or diabetes revealed a three-fold increased risk among patients who were overweight at age 20, whereas the two-fold observed risk elevation among those who had a highest lifetime BMI of >35 was statistically nonsignificant. Obesity seems to be an important-and potentially preventable-risk factor for CRF. Although hypertension and type 2 diabetes are important mediators, additional pathways also may exist.

  • 10.
    Eunyoung, Cho
    et al.
    Channing Laboratory, Department of Medicine, Harvard Medical School, Brigham and Women’s Hospital; Department of Nutrition, Harvard School of Public Health, Boston, MA, USA.
    Lindblad, Per
    Örebro University, School of Medicine, Örebro University, Sweden. Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Kidney Cancer2008In: Textbook of cancer epidemiology / [ed] Hans-Olov Adam, David J. Hunter, Dimitrios Trichopoulos, Oxford, United Kingdom: Oxford University Press , 2008, 2nd ed.Chapter in book (Other academic)
    Abstract [en]

    Cigarette smoking and obesity may account for approximately 40% of cases in high-incidence countries. Continued research in kidney cancer is needed since nearly 50% of the patients die within five years after diagnosis. With the aim of prevention, the continued search for environmental causes should take into account the fact that kidney cancer consists of different types with specific genetic molecular characteristics. In some cases, these genetic alterations have been purportedly associated with specific exposures. Furthermore, genetic polymorphisms may have a modulating effect on metabolic activation and detoxification enzymes. Thus, better understanding of the genetic and molecular processes involved in kidney cancer may help with the analyzing exposure associations that are important in both its initiation and progression.

  • 11.
    Fored, C. M.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm; Department of Renal Medicine, Huddinge University Hospital, Huddinge, Sweden.
    Ejerblad, E.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Fryzek, J. P.
    The International Epidemiology Institute, Rockville, MD, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
    Lambe, M.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Elinder, C. G.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm; Department of Renal Medicine, Huddinge University Hospital, Huddinge, Sweden.
    Socio-economic status and chronic renal failure: a population-based case-control study in Sweden2003In: Nephrology, Dialysis and Transplantation, ISSN 0931-0509, E-ISSN 1460-2385, Vol. 18, no 1, p. 82-88Article in journal (Refereed)
    Abstract [en]

    Background: Low socio-economic status is associated with the occurrence of several different chronic diseases, but evidence regarding renal disease is scant. To explore whether the risk of chronic renal failure varies by socio-economic status, we performed a population-based case-control study in Sweden.

    Methods: All native residents from May 1996 to May 1998, aged 18-74 years, formed the source population. Cases (n = 926) were incident patients with chronic renal failure in a pre-uraemic stage. Control subjects (n = 998) were randomly selected within the source population. Exposures were assessed at personal interviews and relative risks were estimated by odds ratios (OR) in logistic regression models, with adjustment for age, sex, body mass index (BMI), smoking, alcohol consumption and regular analgesics use.

    Results: In families with unskilled workers only, the risk of chronic renal failure was increased by 110% [OR = 2.1; 95% confidence interval (CI), 1.1-4.0] and 60% (OR = 1.6; 95% CI, 1.0-2.6) among women and men, respectively, relative to subjects living in families in which at least one member was a professional. Subjects with 9 years or less of schooling had a 30% (OR = 1.3; 95% CI, 1.0-1.7) higher risk compared with those with a university education. The excess risk was of similar magnitude regardless of underlying renal disease.

    Conclusions: Low socio-economic status is associated with an increased risk of chronic renal failure. The moderate excess was not explained by age, sex, BMI, smoking, alcohol or analgesic intake. Thus, socio-economic status appears to be an independent risk indicator for chronic renal failure in Sweden.

  • 12.
    Fored, C. M.
    et al.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Huddinge, Sweden.
    Ejerblad, E.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Fryzek, J. P.
    International Epidemiology Institute, Rockville, MD, United States; Department of Medicine, Vanderbilt University Medical Center, Nashville, United States.
    Dickman, P. W.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Signorello, L. B.
    International Epidemiology Institute, Rockville, MD, United States; Department of Medicine, Vanderbilt University Medical Center, Nashville, United States.
    Lipworth, L.
    International Epidemiology Institute, Rockville, MD, United States; Department of Medicine, Vanderbilt University Medical Center, Nashville, United States.
    Elinder, C. G.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Huddinge, Sweden.
    Blot, W. J.
    International Epidemiology Institute, Rockville, MD, United States.
    McLaughlin, J. K.
    International Epidemiology Institute, Rockville, MD, United States; Department of Medicine, Vanderbilt University Medical Center, Nashville, United States.
    Zack, M. M.
    National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, United States .
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Acetaminophen, aspirin, and chronic renal failure2001In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 345, no 25, p. 1801-1808Article in journal (Refereed)
    Abstract [en]

    Background: Several epidemiologic studies have demonstrated an association between heavy consumption of nonnarcotic analgesics and the occurrence of chronic renal failure, but it is unclear which is the cause and which is the effect.

    Methods: In a nationwide, population-based, case-control study of early-stage chronic renal failure in Sweden, face-to-face interviews were conducted with 926 patients with newly diagnosed renal failure and 998 control subjects, of whom 918 and 980, respectively, had complete data. We used logistic-regression models to estimate the relative risks of disease-specific types of chronic renal failure associated with the use of various analgesics.

    Results: Aspirin and acetaminophen were used regularly by 37 percent and 25 percent, respectively, of the patients with renal failure and by 19 percent and 12 percent, respectively, of the controls. Regular use of either drug in the absence of the other was associated with an increase by a factor of 2.5 in the risk of chronic renal failure from any cause. The relative risks rose with increasing cumulative lifetime doses, rose more consistently with acetaminophen use than with aspirin use, and were increased for most disease-specific types of chronic renal failure. When we disregarded the recent use of analgesics, which could have occurred in response to antecedents of renal disease, the associations were only slightly attenuated.

    Conclusions: Our results are consistent with the existence of exacerbating effects of acetaminophen and aspirin on chronic renal failure. However, we cannot rule out the possibility of bias due to the triggering of analgesic consumption by predisposing conditions.

  • 13.
    Fored, C. M.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
    Nise, G.
    Division of Occupational Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
    Ejerblad, E.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Fryzek, J. P.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    McLaughlin, J. K.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Elinder, C. G.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Absence of association between organic solvent exposure and risk of chronic renal failure: a nationwide population-based case-control study2004In: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 15, no 1, p. 180-186Article in journal (Refereed)
    Abstract [en]

    Exposure to organic solvents has been suggested to cause or exacerbate renal disease, but methodologic concerns regarding previous studies preclude firm conclusions. We examined the role of organic solvents in a population-based case-control study of early-stage chronic renal failure (CRF). All native Swedish residents aged 18 to 74 yr, living in Sweden between May 1996 and May 1998, formed the source population. Incident cases of CRF in a pre-uremic stage (n = 926) and control subjects (n = 998), randomly selected from the study base, underwent personal interviews that included a detailed occupational history. Expert rating by a certified occupational hygienist was used to assess organic solvent exposure intensity and duration. Relative risks were estimated by odds ratios (OR) in logistic regression models, with adjustment for potentially important covariates. The overall risk for CRF among subjects ever exposed to organic solvents was virtually identical to that among never-exposed (OR, 1.01; 95% confidence interval [CI], 0.81 to 1.25). No dose-response relationships were observed for lifetime cumulative solvent exposure, average dose, or exposure frequency or duration. The absence of association pertained to all subgroups of CRF: glomerulonephritis (OR, 0.96; 95% CI, 0.68 to 1.34), diabetic nephropathy (OR, 1.02; 95% CI, 0.74 to 1.41), renal vascular disease (OR, 1.16; 95% CI, 0.76 to 1.75), and other renal CRF (OR, 0.92; 95% CI, 0.66 to 1.27). The results from a nationwide, population-based study do not support the hypothesis of an adverse effect of organic solvents on CRF development, in general. Detrimental effects from subclasses of solvents or on specific renal diseases cannot be ruled out.

  • 14.
    Grabowska, Beata
    et al.
    Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Ulvskog, Emma
    Örebro University, School of Medical Sciences. Department of Oncology, University Hospital Örebro, Örebro, Sweden.
    Carlsson, Jessica
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Urology.
    Fiorentino, Michelangelo
    Department of Pathology, F. Addari Institute of Oncology, S. Orsola Hospital, Bologna, Italy.
    Giunchi, Francesca
    Department of Pathology, F. Addari Institute of Oncology, S. Orsola Hospital, Bologna, Italy.
    Lindblad, Per
    Örebro University, School of Medical Sciences. Department of Urology.
    Sundqvist, Pernilla
    Örebro University, School of Medical Sciences. Department of Urology.
    Clinical outcome and time trends of surgically treated renal cell carcinoma between 1986 and 2010: results from a single centre in Sweden2018In: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 52, no 3, p. 206-212Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The aims of this study were to create a cohort of retrospectively collected renal cell carcinoma (RCC) specimens to be used a basis for prognostic molecular studies, and to investigate the outcome and time trends in patients surgically treated for RCC in a single-centre cohort.

    MATERIALS AND METHODS: Patients undergoing surgery for RCC between 1986 and 2010 were included in the study. Medical records were reviewed, and the diagnostic tissue was re-evaluated according to a modern classification. The change in patient and tumour characteristics over time was analysed.

    RESULTS: The study included 345 patients. Smaller tumours, as indicated by primary tumour diameter, tumour (T) stage and American Joint Committee on Cancer (AJCC) stage, were found more frequently in later years compared to the early 1990s. No changes in the clinical outcome for the patients were seen among the time periods investigated. Increasing T stage, AJCC stage, primary tumour diameter and decreasing haemoglobin levels were associated with cancer-specific mortality in univariate analysis. A high calcium level was significantly associated with increased cancer-specific mortality (hazard ratio = 4.25, 95% confidence interval 1.36-13.28) in multivariate analysis.

    CONCLUSIONS: This study on patients who underwent surgery for RCC from 1986 to 2010 at a single institution in Sweden indicates that there has been a change in tumour characteristics of patients diagnosed with RCC over time. It was also shown that calcium levels were an independent prognostic factor for cancer-specific mortality in this cohort. This cohort could provide a valuable basis for further molecular studies.

  • 15.
    Greving, J. P.
    et al.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lee, J. E.
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
    Wolk, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lukkien, C.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Bergström, A.
    Division of Environmental Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Alcoholic beverages and risk of renal cell cancer2007In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 97, no 3, p. 429-433Article in journal (Refereed)
    Abstract [en]

    Using a mailed questionnaire, we investigated the risk of renal cell cancer in relation to different types of alcoholic beverages, and to total ethanol in a large population-based case-control study among Swedish adults, including 855 cases and 1204 controls. Compared to non-drinkers, a total ethanol intake of >620 g month(-1) was significantly related to a decreased risk of renal cell cancer (odds ratio (OR) 0.6, 95% confidence interval (CI) 0.4-0.9; P-value for trend=0.03). The risk decreased 30-40% with drinking more than two glasses per week of red wine (OR 0.6, 95% CI 0.4-0.9), white wine (OR 0.7, 95% CI 0.4-1.0), or strong beer (OR 0.6, 95% CI 0.4-1.0); there was a clear linear trend of decreasing risk with increasing consumption of these beverages (P-values for trends <0.05).

  • 16.
    Hemminki, K.
    et al.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Jiang, Y.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Ma, X.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Yang, K.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Egevad, L.
    Department of Pathology and Cytology, Karolinska Hospital, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Molecular epidemiology of VHL gene mutations in renal cell carcinoma patients: relation to dietary and other factors2002In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 23, no 5, p. 809-815Article in journal (Refereed)
    Abstract [en]

    Carcinogenic chemicals act through DNA damage and mitogenic effects. No established mechanism explains the cancer preventive effects, if any, of food items, such as vegetables and fruit. If such data were available, preferably on tumor-initiating genes, the evidence for the protective effects would become stronger. The von Hipple-Lindau (VHL) gene is the tumor suppressor gene predisposing to both sporadic renal cell carcinoma (RCC) and von Hippel-Lindau disease. We have earlier analyzed VHL mutations in RCCs from 102 Swedish patients identified in a case-control study and here examine associations between patient characteristics, including dietary habits and mutations, considering the type of mutation. The results are given as odds ratios (OR), separately for smokers and all patients. In univariate analysis, consumption of vegetables and citrus fruit decreased the frequency of VHL mutations among smokers and citrus fruit among all patients. In multivariate analysis of smokers' characteristics, welding fumes showed a risk of 5.63 for multiple VHL mutations. In smokers, citrus fruit decreased the OR of GC to AT mutations to 0.13 and that of multiple mutations to 0.17; vegetables decreased the OR for single mutations to 0.22. Among all subjects, welding fumes were a risk factor and citrus fruit a protective factor. Additionally, an intake of selenium protected against multiple mutations. The present results provide evidence that the intake of vegetables, selenium and particularly of citrus fruit protects the renal VHL gene from mutational insults that may be endogenous or common in a population. Even though most of the associations are biologically plausible, and vegetables and fruit were an a priori hypothesis, fortuitous results cannot be ruled out in this relatively small study.

  • 17.
    Lambe, M.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wuu, J.
    Cancer Center, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
    Remler, R.
    Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
    Hsieh, C. C.
    Cancer Center, University of Massachusetts Medical School, Worcester, Massachusetts, USA; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA.
    Pregnancy and risk of renal cell cancer: a population-based study in Sweden2002In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 86, no 9, p. 1425-1429Article in journal (Refereed)
    Abstract [en]

    Epidemiological findings indicate that hormonal influences may play a role in the etiology of renal cell cancer (RCC). The possible effect of childbearing remains enigmatic; while some investigators have reported a positive association between number of births and renal cell cancer risk, others have not. A case-control study, nested within a nation-wide Fertility Register covering Swedish women born 1925 and later, was undertaken to explore possible associations between parity and age at first birth and the risk of renal cell cancer. Among these women a total of 1465 cases of RCC were identified in the Swedish Cancer Register between 1958 and 1992 and information on the number of live childbirths and age at each birth was obtained by linkage to the Fertility Database. For each case, five age-matched controls were randomly selected from the same register. Compared to nulliparous women, ever-parous women were at a 40% increased risk of RCC (Odds Ratio [OR]=1.42; 95% CI 1.19-1.69). The corresponding OR for women of high parity (five or more live births) was 1.91 (95% CI 1.40-2.62). After controlling for age at first birth among parous women, each additional birth was associated with a 15% increase in risk (OR=1.15; 95% CI 1.08-1.22). The observed positive association between parity and renal cell cancer risk is unlikely to be fully explained by uncontrolled confounding, but warrants further evaluation in large studies, with allowance for body mass index.

  • 18.
    Lee, Jung Eun
    et al.
    Sookmyung Women's University, Seoul, Republic of Korea.
    Kim, Nayeon
    Sookmyung Women's University, Seoul, Republic of Korea.
    Adami, Hans-Olov
    Harvard School of Public Health, Boston MA, USA.
    Lindblad, Per
    Örebro University, School of Medical Sciences.
    Body mass, smoking habit, and hypertension and renal cell cancer survival2015In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 75, article id 883Article in journal (Other academic)
  • 19.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Epidemiology of renal cell carcinoma2004In: Scandinavian Journal of Surgery, ISSN 1457-4969, E-ISSN 1799-7267, Vol. 93, no 2, p. 88-96Article, review/survey (Refereed)
    Abstract [en]

    The increasing incidence of RCC in most populations may in part be due to increasing numbers of incidentally detected cancers with new imaging methods. Further, the increase is not only limited to small local tumours but also includes more advanced tumours, which may to some part explain the still high mortality rates. The variation in incidence between populations may have several other explanations. Traditionally the starting point has included thoughts of environmental exposures, which so far have only in part explained the causes of RCC, by means of cigarette smoking and obesity, which may account for approximately 40% of cases in high-risk countries (Table 2). Further, the genetic variations may be of importance as a cause of the difference between populations. Continued research in RCC is needed with the knowledge that nearly 50% of patients die within 5 years after diagnosis. The further search for environmental exposures should take in account the knowledge that RCC consists of different types with specific genetic molecular characteristics. These genetic alterations have in some cases been suggested to be associated with specific exposures. Furthermore, there might exist a modulating effect of genetic polymorphisms among metabolic activation and detoxification enzymes. Hence, a further understanding of the genetic and molecular processes involved in RCC will hopefully give us a better knowledge how to analyse and interpret exposure associations that have importance for both initiation and progression of RCC.

  • 20.
    Lindblad, Per
    et al.
    Örebro University, School of Medical Sciences.
    Adami, Hans-Olov
    Institutionen för medicinsk epidemiologi och biostatistik, Karilinska Institute, Stockholm, sweden.
    Kidney Cancer2002In: Textbook of Cancer Epidemiology, New York NY USA: Oxford University Press, 2002Chapter in book (Other academic)
  • 21.
    Lindblad, Per
    et al.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Chow, W. H.
    National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, Maryland, USA.
    Chan, J.
    Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA.
    Bergström, A.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Wolk, A.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Gridley, G.
    National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, Maryland, USA.
    McLaughlin, J. K.
    International Epidemiology Institute, Rockville, Maryland, USA.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Adami, H. O.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    The role of diabetes mellitus in the aetiology of renal cell cancer1999In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 42, no 1, p. 107-12Article in journal (Refereed)
    Abstract [en]

    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.

  • 22.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    McLaughlin, J. K.
    National Cancer Institute, Bethesda, Maryland, United States.
    Mellemgaard, A.
    Danish Cancer Society, Danish Cancer Registry, Copenhagen, Denmark .
    Adami, H. O.
    Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States.
    Risk of kidney cancer among patients using analgesics and diuretics: a population-based cohort study1993In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 55, no 1, p. 5-9Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to determine the risk of kidney cancer in 2 cohorts defined on the basis of hospital discharge diagnoses associated with analgesic or diuretic use during the period 1965 to 1983. Patients were followed up through 1984 for cancer incidence. After excluding cancers in the first year of observation, 161 kidney cancers were observed vs. 138 expected among 54,662 patients in the analgesics cohort. The relative risk was higher for women than for men. When examined by sub-site within the kidney, risk for cancer of the renal pelvis was similar in magnitude to that for the renal parenchyma. Among 115,616 patients in the diuretics cohort, 278 kidney cancers occurred vs. 209 expected. The risk for women was higher than for men. This elevation in risk was confined to cancer of the renal parenchyma, with no significantly increased risk seen for cancer of the renal pelvis. Although we observed little excess risk among members of the analgesics cohort, the significantly elevated risk among patients using diuretics supports a number of recent studies, but inability to adjust for confounding factors such as obesity preclude drawing any conclusion regarding diuretics. Further research is warranted to assess in detail the relationship between diuretic use and cancer of the renal parenchyma.

  • 23.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark .
    Schlehofer, B.
    Deutsches Krebsforschungszentrum, Heidelberg, Germany.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States.
    McCredie, M.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia.
    McLaughlin, J. K.
    International Epidemiology Institute, Rockville, Maryland, United States.
    Mandel, J. S.
    Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States .
    International renal-cell cancer study. V. Reproductive factors, gynecologic operations and exogenous hormones1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 61, no 2, p. 192-198Article in journal (Refereed)
    Abstract [en]

    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.

  • 24.
    Lindblad, Per
    et al.
    Department of Urology, Sundsvall Hospital, Sweden.
    Rentzhog, L.
    Department of Urology, Sundsvall Hospital, Sweden.
    Sundström, G.
    Department of Urology, Sundsvall Hospital, Sweden.
    Åberg, J.
    Department of Urology, Sundsvall Hospital, Sweden.
    Classical urethral resistance compared with Schäfer concept1988In: Scandinavian Journal of Urology and Nephrology, Supplementum, ISSN 0300-8886, E-ISSN 1651-2537, Vol. 110, p. 225-229Article in journal (Refereed)
  • 25.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Bergstrom, R.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Statistics, Uppsala University, Uppsala, Sweden.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States .
    Diet and risk of renal cell cancer: a population-based case-control study1997In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 6, no 4, p. 215-223Article in journal (Refereed)
    Abstract [en]

    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.

  • 26.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Bergström, R.
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden; Department of Statistics, Uppsala University, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Persson, I.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Adami, H. O.
    Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    The role of obesity and weight fluctuations in the etiology of renal cell cancer: a population-based case-control study1994In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 3, no 8, p. 631-9Article in journal (Refereed)
    Abstract [en]

    The causes of renal cell cancer (RCC) are poorly understood. Besides smoking, obesity remains the only risk factor that is fairly well established. The association between obesity and RCC appears stronger and more consistent in women than in men. We investigated the question of whether this apparent sex difference could be explained by repeated weight changes (weight cycling), less physical exercise, or pharmacological treatment of obesity in women. Structured face-to-face interviews were carried out with 379 (70% of all eligible) incident cases of RCC and 353 (72% of eligible) controls. The relationships between RCC and adult height, weight, and body mass index (BMI), defined as weight/height, were analyzed. Odds ratios (ORs) were estimated through logistic regression. No association was found between adult height and RCC. In men, weight and BMI appeared at most to be weakly related to risk of RCC. In women, higher adult weight and BMI (usual, highest, and lowest) and also high BMI at ages 30, 40, and 50 years were consistently associated with a significantly increased risk of RCC. Women with an usual adult BMI in the top 5% had a nearly 3-fold increased risk of RCC [OR, 2.67; 95% confidence interval (CI), 1.02-7.01]. Compared with individuals with no weight-loss periods, 2 or more such periods implied an OR of 0.96 (95% CI, 0.32-2.90) in men and 3.87 (95% CI, 1.20-12.45) in women. Physical activity at work reduced the risk of RCC in men but not women. Regular use of diet pills containing amphetamine was associated with an increased risk of RCC (OR, 4.06; 95% CI, 1.35-12.22).(ABSTRACT TRUNCATED AT 250 WORDS)

  • 27.
    Lindblad, Per
    et al.
    Department of Urology Epidemiology Unit, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Zack, M.
    Centers for Disease Control, Atlanta, United States.
    Adami, H. O.
    Department of Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden.
    Ericson, A.
    National Board of Health and Welfare, Stockholm, Sweden.
    Maternal and perinatal risk factors for Wilms' tumor: a nationwide nested case-control study in Sweden1992In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 51, no 1, p. 38-41Article in journal (Refereed)
    Abstract [en]

    This report describes maternal and perinatal risk factors for Wilms' tumor analyzed in a case-control study nested in a nationwide cohort in Sweden. The Swedish National Cancer Registry ascertained 110 cases from among successive birth cohorts from 1973 through 1984, identified by the Swedish Medical Birth Registry, the latter based on medical records. From the Birth Registry, we matched 5 controls without cancer to each case by sex and date of birth. Wilms'-tumor children were more likely to have mothers who had been exposed to penthrane (methoxyflurane) anesthesia during delivery than mothers of controls (odds ratio (OR) = 2.4; 95% confidence interval (CI) 1.1 to 5.1); this excess risk was higher in females than males and increased with age at diagnosis. Wilms'-tumor cases were also more likely to have had physiologic jaundice (OR = 2.3; 95% CI 1.1 to 5.0). Higher parity of the mother decreased the risk of Wilms' tumor among females (OR = 0.7; 95% CI 0.5 to 1.0). We were unable to confirm the reported increased risks of Wilms' tumor for those with high birth weights or with a maternal history of hypertension or fluid retention during pregnancy, nor did we find any association with mother's age at delivery, previous stillbirth, previous live birth, gestational length or height of the child.

  • 28.
    Ma, X.
    et al.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Yang, K.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Egevad, L.
    Department of Pathology and Cytology, Karolinska Hospital, Stockholm, Sweden.
    Hemminki, K.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    VHL gene alterations in renal cell carcinoma patients: novel hotspot or founder mutations and linkage disequilibrium2001In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 20, no 38, p. 5393-5400Article in journal (Refereed)
    Abstract [en]

    Mutations in the von Hippel-Lindau (VHL) gene are frequently detected in human sporadic renal cell carcinoma (RCC). We analysed 102 Swedish RCCs for VHL mutations by PCR-SSCP and sequencing. In 47 patients (46.1%), 70 different mutations were found, and most of them represented novel variations of the VHL gene. Mutations in the VHL gene were found in 54% of clear cell renal cell carcinomas (CCRCC) and in 18% of chromophilic cancers but in no chromophobe cancers or oncocytomas (P=0.016). Three novel hotspot or founder mutations were detected in our study: four CCRCCs carried a missense mutation (glutamic acid to lysine) at codon 160 which is critical in the stabilization of the H1 helix of the alpha domain and the alpha-beta domain interface in the VHL protein. Five CCRCCs and one chromophilic RCC harbored a 15-nucleotide in-frame deletion (codons 41-45) at a duplex tandem repeat sequence site. Moreover, this deletion was in linkage disequilibrium with a C-->T transition in the promoter region. The frequency of linkage was 17 times more common than chance. Five patients with this linked mutation resided in the same hospital district and at least three of them showed the two sequence variants in the tumor-adjacent tissue. In 5/6 patients the wild-type allele was lost in the tumor samples, suggesting a causal role for the mutations in RCC. These linked mutations might be novel polymorphisms maintained in a relative isolated population. Multiple mutations in VHL were found in 17 tumors out of 47 tumors with the VHL mutation. A higher multiple mutation detected rate (33%) was observed in grade 3 CCRCCs than those in grade 1 (22%) and grade 2 (9%) (P=0.04). This is evidence on the association between VHL mutation and extent of nuclear atypia.

  • 29.
    Malmström, P U
    et al.
    Department of Urology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Boston MA, United States.
    Thörn, M
    Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden; Department of Epidemiology, Boston MA, United States.
    Lindblad, Per
    Department of Urology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Boston MA, United States.
    Bergström, R
    Department of Statistics, Uppsala University, Uppsala, Sweden.
    Adami, H O
    Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden; Department of Epidemiology, Boston MA, United States.
    Increasing survival of patients with urinary bladder cancer: A nationwide study in Sweden 1960-19861993In: European Journal of Cancer, ISSN 0959-8049, E-ISSN 1879-0852, Vol. 29A, no 13, p. 1868-1872Article in journal (Refereed)
    Abstract [en]

    Survival rates were analysed in 29,055 patients with urinary bladder cancer diagnosed in Sweden from 1960 to 1986 and followed up until 1987. The 2-, 5- and 10-year relative survival rates were 79, 70 and 64% for men and 75, 68 and 63% for women, respectively. Patients with a history of bladder cancer for at least 15 years ran a negligible risk of dying from their disease. Prognosis was consistently better in younger than in older patients; below 50 years of age the 5-year relative survival rate was 90%, as compared with 60% in patients aged 70-79 years. Patients diagnosed between 1960 and 1964 had a 60% 5-year relative survival, as compared to 71% in those diagnosed between 1980 and 1984. Multivariate analyses further confirmed that age but not sex is an important prognostic factor in bladder cancer and, further, that a substantial improvement in survival rates took place during the 1960-1986 period. Compared with 1960-1964 the risk of dying of bladder cancer within 5 years in patients diagnosed between 1980 and 1984 was 51% lower in men [relative risk (RR) = 0.49; 95% confidence interval (C.I.) 0.42-0.57] and 44% lower in women (RR = 0.56; 95% C.I. 0.45-0.70).

  • 30.
    Mandel, J. S.
    et al.
    School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States.
    McLaughlin, J. K.
    National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland, United States.
    Schlehofer, B.
    German Cancer Research Center, Division of Epidemiology, Heidelberg, Germany.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark.
    Helmert, U.
    Bremer Institute for Prevention and Social Medicine, Bremen, Germany.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    McCredie, M.
    Cancer Epidemiology Research Unit, New South Wales Cancer Council, Sydney, Australia .
    Adami, H. O.
    Uppsala University, Uppsala, Sweden .
    International renal-cell cancer study. IV. Occupation1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 61, no 5, p. 601-605Article in journal (Refereed)
    Abstract [en]

    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.

  • 31.
    McCredie, M.
    et al.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia.
    Pommer, W.
    Humboldt Hospital, Berlin, Germany.
    McLaughlin, J. K.
    Biostatistics Branch, National Cancer Institute, Bethesda, Maryland, United States .
    Stewart, J. H.
    Western Clinical School, University of Sydney, Sydney, Australia.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Mandel, J. S.
    School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States .
    Mellemgaard, A.
    Copenhagen, Denmark.
    Schlehofer, B.
    Division of Epidemiology, German Cancer Research Centre, Heidelberg, Germany.
    Niwa, S.
    Westat Inc., Rockville, Maryland, United States.
    International renal-cell cancer study. II. Analgesics1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 60, no 3, p. 345-349Article in journal (Refereed)
    Abstract [en]

    There has been concern about the role of analgesics in the development of renal-cell cancer, although a few studies have reported moderately elevated risks with regular or long-term use. In a large international case-control study of renal-cell cancer we examined, among other hypotheses, the effect of phenacetin-containing and of other types of analgesics: paracetamol (acetaminophen), salicylates (mainly aspirin) and pyrazolones (e.g., antipyrine or phenazone). Relative risks, adjusted for the effects of age, sex, body-mass index, tobacco smoking and study centre, were not significantly increased with intake of phenacetin, either when lifetime consumption was categorized at the level of > or = 0.1 kg or when subjects were subdivided further by amount. Nor were paracetamol, salicylates or pyrazolones linked with renal-cell cancer. No consistently increasing risks with consumption level was found. The lack of association was not altered by restricting analgesic use to that which occurred 5 or 10 years before the defined "cut-off" date or when analysis was restricted to exclusive users of a particular type of analgesic. Neither was the risk influenced by the rate of consumption or whether the consumption had occurred at a young age. Our study provides clear evidence that aspirin is unrelated to renal-cell cancer risk, and our findings do not support the hypothesis that analgesics containing phenacetin or paracetamol increase the risk, although the number of "regular" users and the amount of these types of analgesic consumed were too small to confidently rule out a minor carcinogenic effect of phenacetin and paracetamol.

  • 32.
    McLaughlin, J. K.
    et al.
    National Cancer Institute, Bethesda, Maryland, United States; International Epidemiology Institute, Rockville, Maryland, United States.
    Chow, W. H.
    National Cancer Institute, Bethesda, Maryland, United States.
    Mandel, J. S.
    Division of Environmental Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark.
    McCredie, M.
    Cancer Epidemiology Research Unit, New South Wales Cancer Council, Kings Cross, Australia .
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Schlehofer, B.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    Pommer, W.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    Niwa, S.
    Westat Inc., Rockville, Maryland, United States .
    Adami, H. O.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany .
    International renal-cell cancer study. VIII. Role of diuretics, other anti-hypertensive medications and hypertension1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 63, no 2, p. 216-221Article in journal (Refereed)
    Abstract [en]

    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.

  • 33.
    McLaughlin, J. K.
    et al.
    National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland, United States; International Epidemiology Institute, Rockville, Maryland, United States .
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark.
    McCredie, M.
    Cancer Epidemiology Research Unit, New South Wales Cancer Council, Kings Cross, Australia.
    Mandel, J. S.
    Division of Environmental Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States.
    Schlehofer, B.
    Division of Epidemiology, German Cancer Research Center, Heidelberg, Germany .
    Pommer, W.
    Humboldt Hospital, Berlin, Germany .
    Adami, H. O.
    Danish Cancer Society, Copenhagen, Denmark.
    International renal-cell cancer study. I. Tobacco use1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 60, no 2, p. 194-198Article in journal (Refereed)
    Abstract [en]

    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.

  • 34.
    Mellemgaard, A.
    et al.
    Danish Cancer Society, Division of Cancer Epidemiology, Copenhagen, Denmark.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Schlehofer, B.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    Bergström, R.
    Dept. of Statistics, University of Uppsala, Uppsala, Sweden.
    Mandel, J. S.
    Division of Environmental Health, School of Public Health, University of Minnesota, Minnesota, United States.
    McCredie, M.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia .
    McLaughlin, J. K.
    National Cancer Institute, Division of Cancer Etiology, Rockville, Maryland, United States .
    Niwa, S.
    WESTAT Inc, Rockville, Maryland, United States.
    Odaka, N.
    WESTAT Inc, Rockville, Maryland, United States .
    Pommer, W.
    Humbolt Hospital, Berlin, Germany .
    International renal-cell cancer study. III. Role of weight, height, physical activity, and use of amphetamines1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 60, no 3, p. 350-354Article in journal (Refereed)
    Abstract [en]

    Although numerous studies have identified obesity or high relative weight as a risk factor for renal-cell cancer in women, the degree to which this effect is present in men remains unclear. A multicenter population-based case-control study concerning incident cases of histologically verified renal-cell cancer (n = 1,732) and age- and sex-matched controls (n = 2,309) was conducted in Australia, Denmark, Germany (2 centers), Sweden and the United States. Relative weight was estimated by the body mass index, and the association between this factor and other factors, such as height, physical activity and use of amphetamines, was measured by the relative risk estimated in logistic regression models. Body mass index was found to be a risk factor among women and, to a lesser extent, among men. A 3-fold increased risk (RR = 3.6, 95% CI = 2.3-5.7) was observed for women with a relative weight in the top 5% compared with those in the lowest quartile. Rate of weight change (estimated as weight change per annum in kilograms) appeared to be an independent risk factor among women but not among men. Physical activity and height were unrelated to risk of renal-cell cancer regardless of level of BMI, while use of amphetamines was associated with an increased risk among men, although no dose or duration effect was seen. Our findings verify the link between high relative weight and risk of renal-cell cancer, particularly among women. The mechanism that underlies this association is, however, still unclear, although the rate of weight change may play a role.

  • 35.
    Mucci, L. A.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Lindblad, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Steineck, G.
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Adami, H. O.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Dietary acrylamide and risk of renal cell cancer2004In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 109, no 5, p. 774-776Article in journal (Refereed)
    Abstract [en]

    The detection of acrylamide, classified as a probable human carcinogen, in commonly consumed foods created public health alarm. Thus far, only 2 epidemiologic studies have examined the effect of dietary acrylamide on cancer risk. Presently, we reanalyzed data from a large population-based Swedish case-control study of renal cell cancer. Food frequency data were linked with national food databases on acrylamide content, and daily acrylamide intake was estimated for participants. The risk of renal cell cancer was evaluated for intake of food items with elevated acrylamide levels and for total daily acrylamide dose. Adjusting for potential confounders, there was no evidence that food items with elevated acrylamide, including coffee (OR(highest vs. lowest quartile) = 0.7; 95% CI = 0.4-1.1), crisp breads (OR(highest vs. lowest quartile) = 1.0; 95% CI = 0.6-1.6) and fried potatoes (OR(highest vs. lowest quartile) = 1.1; 95% CI = 0.7-1.7), were associated with a higher risk of renal cell cancer risk. Furthermore, there was no association between estimated daily acrylamide intake through diet and cancer risk (OR(highest vs. lowest quartile) = 1.1; 95% CI = 0.7-1.8; p for trend = 0.8). The results of this study are in line with the 2 previous studies examining dietary acrylamide and suggest there is no association between dietary acrylamide and risk of renal cell cancer.

  • 36.
    Rashidkhani, B.
    et al.
    Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fruits, vegetables and risk of renal cell carcinoma: a prospective study of Swedish women2005In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 113, no 3, p. 451-455Article in journal (Refereed)
    Abstract [en]

    Findings of epidemiologic studies on the relationship between fruit and vegetable consumption and renal cell carcinoma (RCC) risk have been inconclusive. To study the association between fruits and vegetables and risk of RCC in a population-based prospective cohort study of Swedish women, we collected dietary information from 61,000 women age 40-76 years by a food-frequency questionnaire. During 13.4 years of follow-up 122 women developed RCC. Cox proportional hazards models were used to estimate relative risks (RR) with 95% confidence interval (CI). Women consuming 5 or more servings of fruit and vegetables daily had a relative risk of 0.59 (95% CI = 0.26-1.34) in comparison to them consuming less than once daily. When fruits and vegetables were examined separately, those who consumed more than 75 servings per month of fruits or vegetables had multivariate relative risk of 0.59 (95% CI = 0.27-1.25) and 0.60 (95% CI = 0.31-1.17) respectively, compared to those consuming 11 or less servings per month. Within the group of fruits, the strongest inverse association was observed for banana (p = 0.07 by Wald test). The risk of RCC increased monotonically with increasing intake frequencies of fruit juice (p-value for trend = 0.10). Within the group of vegetables, the strongest inverse association was observed for root vegetables (p = 0.03 by Wald test). The risk of RCC decreased with increasing consumption frequencies of white cabbage (p for trend = 0.07). Frequent consumption of salad vegetables (once or more per day) decreased the risk by 40% (RR = 0.60; 95% CI = 0.30-1.22), in comparison to no consumption. Our results suggested that high consumption of fruits and vegetables might be associated with reduced risk of RCC.

  • 37.
    Rashidkhani, B.
    et al.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Åkesson, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Alcohol consumption and risk of renal cell carcinoma: a prospective study of Swedish women2005In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 117, no 5, p. 848-853Article in journal (Refereed)
    Abstract [en]

    Previous literature, although not consistent, suggests that moderate alcohol consumption might be associated with decreased risk of renal cell carcinoma (RCC) in women. Thus, we examined the association between alcohol intake and the incidence of RCC by analyzing data from the Swedish Mammography Cohort, a population-based prospective cohort of 59,237 women, aged 40-76 years, who, at baseline in 1987-1990, were cancer free and had completed a food-frequency questionnaire including questions about alcohol consumption. Through June 30, 2004, 132 incident cases of RCC were diagnosed. We used the Cox proportional hazards model to estimate age and body mass index (BMI) adjusted rate ratios (RRs) and their 95% confidence intervals (CIs). Women who consumed >4.3 grams per day of alcohol (ethanol) had nonsignificantly lower risk of RCC than did women who consumed <2.5 g/d (RR = 0.71, 95% CI 0.42-1.19); among women > or = 55 years of age at entry into the cohort, corresponding risk estimates were RR = 0.33, 95% CI 0.10-1.05, p for trend = 0.04 and among women with BMI >25 kg/m2, RR = 0.30, 95% CI 0.09-0.97, p for trend = 0.04. Consistent with these findings, women who drank 1 or more servings of total alcoholic beverages per week had lower RCC risk than did women who drank less (RR = 0.62, 95% CI 0.41-0.94); the corresponding estimate for women > or = 55 years of age was RR = 0.44, 95% CI 0.22-0.88. Results from our prospective cohort study of middle-aged and elderly women indicate that moderate alcohol consumption may be associated with decreased risk of RCC.

  • 38.
    Rashidkhani, B.
    et al.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Åkesson, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Major dietary patterns and risk of renal cell carcinoma in a prospective cohort of Swedish women2005In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 135, no 7, p. 1757-1762Article in journal (Refereed)
    Abstract [en]

    Links between specific foods and the risk of renal cell carcinoma (RCC) are not well established. Dietary patterns may be a better predictor of RCC risk. Our aim was to identify and examine major dietary patterns and their relation to the risk of RCC in a large prospective cohort study of Swedish women. Complete dietary information was available from a FFQ from 46,572 women aged 40-76 y at baseline. We conducted factor analysis to identify dietary patterns. Cox proportional hazard models were used to estimate rate ratios (RRs) and 95% CIs. During a mean of 14.3 y of follow-up, we identified 93 cases of RCC. We observed 3 major dietary patterns in the cohort: Healthy (vegetables, tomato, fish, fruits, poultry, whole grains), Western (sweets, processed meat, refined grains, margarine/butter, high-fat dairy products, fried potato, soft drinks, meat) and Drinker (wine, hard liquor, beer, snacks) pattern. Higher Healthy pattern scores were not significantly associated with decreased risk of RCC (highest vs. lowest tertile RR = 0.81; 95% CI 0.45-1.48 and RR = 0.54; 95% CI 0.27-1.10 among women < or = 65 y). There was a suggestion of an inverse association between the Drinker pattern and RCC risk (RR comparing the 2nd and 3rd with the first tertile, 0.56; 95% CI, 0.34-0.95; and 0.72; 95% CI, 0.42-1.22, respectively, P = 0.08 by Wald test); the association was clearer among women < or = 65 y (P = 0.02 by Wald test). Our data suggest an inverse association between Drinker pattern and the risk of RCC.

  • 39.
    Rentzhog, L.
    et al.
    Urologiska kliniken, Sundsvalls sjukhus, Sundsvall, Sweden.
    Kullenberg, K
    Urologiska kliniken, Sundsvalls sjukhus, Sundsvall, Sweden.
    Lindblad, Per
    Urologiska kliniken, Sundsvalls sjukhus, Sundsvall, Sweden.
    Quality of care and use of the resources in prostatic surgery: a follow-up study1991In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 88, no 18, p. 1688-1689Article in journal (Refereed)
  • 40.
    Schlehofer, B.
    et al.
    Division of Epidemiology, German Cancer Research Centre, Heidelberg, Germany; .
    Pommer, W.
    Humboldt Hospital, Berlin, Germany.
    Mellemgaard, A.
    Danish Cancer Registly, Danish Cancer Society, Copenhagen, Denmark.
    Stewart, J. H.
    Western Clinical School, University of Sydney, sydney, Australia.
    McCredie, M.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia.
    Niwa, S.
    Westat Inc., Rockville, MD, USA.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Mandel, J. S.
    School of Public Health, University of Minnesota, Minneapolis, MN, USA.
    McLaughlin, J. K.
    BiostatisticsB ranch, National Cancer Institute, Bethesda, MD, USA.
    Wahrendorf, J.
    Division of Epidemiology, German Cancer Research Centre, Heidelberg, Germany.
    International renal-cell-cancer study. VI. the role of medical and family history1996In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 66, no 6, p. 723-726Article in journal (Refereed)
    Abstract [en]

    A number of medical conditions have been linked with renal-cell cancer, although the evidence is not consistent in every case. In a large international case-control study of renal-cell cancer, we examined, among other hypotheses, associations with a personal history of certain medical conditions and a family history of cancer of the kidney or thyroid. Relative risks (RR), adjusted for the effects of age, gender, body-mass index, tobacco smoking and study centre, were significantly increased by a history of kidney stones or thyroid or kidney disease. The RR were not altered by additional adjustment for hypertension, or when diagnoses were restricted to those made at least 5 or 10 years before 1987 (the usual "cut-off" date). The link with kidney injury is particularly likely to be affected by recall bias. Increased RR of borderline significance were found for kidney infection (RR, 1.2) and diabetes (RR, 1.4). Having one first-degree relative with kidney cancer was associated with a significantly increased risk of renal-cell cancer (RR, 1.6; 95% Cl, 1.1-2.4). Seven cases reported 2 first-degree relatives with kidney cancer. No controls had first-degree relatives with kidney cancer. None of our participants reported having von Hippel-Lindau disease. The data suggests that a few conditions of the kidney are strongly associated with renal-cell cancer and that heredity plays a role in a small proportion of cases.

  • 41. Shiao, Y. H.
    et al.
    Forsti, A.
    Egevad, L.
    Anderson, L. M.
    Lindblad, Per
    Hemminki, K.
    VHL down-regulation and differential localization as mechanisms in tumorigenesis2003In: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, Vol. 64, no 5, p. 1671-1674Article in journal (Refereed)
    Abstract [en]

    Background: The von Hippel-Lindau (VHL) gene has been widely analyzed in many tumors. Early studies in animal tumors suggest that changes in VHL protein level and localization may be also important in tumorigenesis. In this study, we determined the role of VHL protein in human renal cell carcinomas. METHODS: Seventy-five human renal cell carcinomas, predominantly of clear cell type (60 of 75), were examined for VHL protein by immunohistochemistry. The level and pattern of protein expression were then compared to VHL mutations and tumor characteristics.

    Results: An apparent decline of VHL level (positive in <50% of tumor cells) was observed in 49 (65%) tumors, a change more frequent than VHL mutations (28 of 75) (37%). In tumors, VHL was localized to the cytoplasm and/or the cell membrane. The occurrence of a predominantly membranous signal was significantly associated with missense mutations (9 of 14 tumors with missense mutations versus 14 of 61 tumors with no or nonmissense mutations, P = 0.0025) and tumor stage (23 of 60 tumors with stage TI versus 0 of 15 tumors with TII and TIII, P = 0.0034).

    Conclusion: This study provides the first evidence of the role of VHL protein level and intracellular localization in tumorigenesis in humans.

  • 42.
    Thorstenson, Andreas
    et al.
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden; Department of Molecular Medicine and Surgery, Section of Urology, Karolinska Institute, Stockholm, Sweden; Surgical Intervention Trials Unit, Nuffield Department of Surgical Sciences, University of Oxford, Oxford, United Kingdom.
    Harmenberg, Ulrika
    Department of Oncology, Karolinska University Hospital, Solna, Stockholm, Sweden.
    Lindblad, Per
    Örebro University, School of Medicine, Örebro University, Sweden. Dept Urol, Örebro University Hospital, Örebro, Sweden.
    Holmström, Benny
    Department of Urology, Akademiska University Hospital, Uppsala, Sweden.
    Lundstam, Sven
    Department of Urology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Ljungberg, Börje
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Cancer Characteristics and Current Treatments of Patients with Renal Cell Carcinoma in Sweden2015In: BioMed Research International, ISSN 2314-6133, E-ISSN 2314-6141, article id 456040Article in journal (Refereed)
    Abstract [en]

    Methodology: Since the start in 2005 virtually all patients with newly diagnosed renal cell carcinoma (RCC) in Sweden are reported to the National Swedish Kidney Cancer Register (NSKCR). The register contains information on histopathology, nuclear grade, clinical stage, preoperative work-up, treatment, recurrence, and survival.

    Results: A total of 8556 patients with newly diagnosed RCC were registered in the NSKCR from 2005 to 2013 resulting in a coverage of 99% as compared to the Swedish Cancer Registry. The mean tumor size at detection decreased from 70 mm in 2005 to 64 mm in 2010. The proportion of patients who were incidentally detected increased. The proportion of patients with tumor stage T1a who underwent partial nephrectomy increased from 22% in 2005 to 56% in 2012. Similarly, the proportion of laparoscopically performed radical nephrectomies increased from 6% in 2005 to 17% in 2010. During the five years of follow-up 20% of the patients had a recurrence.

    Conclusion: Over the last decade there has been a trend of earlier detection and less advanced tumors at detection in patients with RCC. An increasing proportion of the patients undergo laparoscopic and nephron-sparing procedures.

  • 43.
    Thorstenson, Andreas
    et al.
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden; Department of Molecular Medicine and Surgery, Section of Urology, Karolinska Institute, Stockholm, Sweden; Surgical Intervention Trials Unit, Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK.
    Harmenberg, Ulrika
    Department of Oncology, Karolinska University Hospital Solna, Stockholm, Sweden.
    Lindblad, Per
    Örebro University, School of Medicine, Örebro University, Sweden. Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Urology.
    Ljungberg, Börje
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Lundstam, Sven
    Department of Urology, Sahlgrenska University, Hospital, Göteborg, Sweden.
    Impact of quality indicators on adherence to National and European guidelines for renal cell carcinoma2016In: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 50, no 1, p. 2-8Article in journal (Refereed)
    Abstract [en]

    Objective: The aim of this population-based study was to evaluate the impact of quality indicators on the adherence to guidelines for renal cell carcinoma (RCC).

    Material and methods: Since 2005, virtually all patients with newly diagnosed RCC in Sweden have been registered in the National Swedish Kidney Cancer Register (NSKCR). The register contains information on histopathology, nuclear grade, clinical stage, preoperative work-up, treatment, recurrence and survival. In addition, a number of quality indicators have been measured in the register aiming to increase the quality of care. The quality indicators are: the coverage of the register, histology reports, preoperative chest computed tomography (CT), partial nephrectomy, laparoscopic surgery, centralization to high-volume hospitals and waiting times.

    Results: A total of 8556 patients with diagnosed RCC were registered from 2005 to 2013 (99% coverage). In 2013, 99% of the histopathology reports were standardized. The number of patients with preoperatively chest CT increased from 59% in 2005 to 89% in 2013. The proportion of patients with RCC T1aN0M0 who underwent partial nephrectomy increased from 22% in 2005 to 56% in 2013. Similarly, laparoscopic radical nephrectomies increased from 6% in 2005 to 24% in 2013. The median tumour size at detection decreased from 60 mm in 2005 to 55 mm in 2013. The proportion of patients who were incidentally detected increased from 43% in 2005 to 55% in 2013.

    Conclusions: The data show an improved adherence to the guidelines for RCC as measured by quality indicators and a steady process of earlier detection of patients with RCC.

  • 44. Van Poppel, H.
    et al.
    Nilsson, S.
    Algaba, F.
    Bergerheim, U.
    Department of Urology, University Hospital K.U. Leuven, Belgium.
    Dal Cin, P.
    Fleming, S.
    Hellsten, S.
    Kirkali, Z.
    Klotz, L.
    Lindblad, Per
    Ljungberg, B.
    Mulders, P.
    Roskams, T.
    Ross, R. K.
    Walker, C.
    Wersall, P.
    Precancerous lesions in the kidney2000In: Scandinavian Journal of Urology and Nephrology, Supplementum, ISSN 0300-8886, E-ISSN 1651-2537, no 205, p. 136-165Article in journal (Refereed)
    Abstract [en]

    Renal cell carcinoma (RCC), although occurring less frequently than prostate and bladder cancer, is actually the most malignant urologic disease, killing >35% of affected patients. Therefore, investigation of the nature of premalignant lesions of the kidney is a relevant issue. Following the most recent histological classification RCC can be subdivided into four categories: conventional RCC; papillary RCC; chromophobe RCC; and collecting duct carcinoma. In contrast to many genitourinary malignancies, premalignant alterations in the kidney are scarcely described. Intratubular epithelial dysplasia has been recognized as the most common precursor of RCC. In analogy to prostatic intraepithelial neoplasia (PIN), the premalignant lesions of the kidney are described as high or low-grade renal intratubular neoplasia. In contrast, precancerous lesions have been described as part of the von Hippel-Lindau syndrome (VHL) where the evolution from a simple cyst to an atypical cyst with epithelial hyperplasia to cystic or solid conventional-type RCC is well documented. Finally, in the genesis of papillary RCC an adenoma-carcinoma sequence has been recognized with specific genetic changes. There are no data on the epidemiology of premalignant lesions of the kidney, but research into the etiology of RCC has been extended substantially. Familial and genetic factors are well documented in VHL disease, in hereditary papillary RCC, in the tuberous sclerosis complex and in familial RCC. Cigarette smoking and obesity are established risk factors for RCC. Hypertension or its medication has also been associated with an increased risk. Among dietary factors an inverse relation between risk and consumption of vegetables and fruit has been found. Occupational exposure to substances such as asbestos and solvents has been linked to an increased risk of RCC. Specific RCC variants have distinctive chromosome alterations and several genes have been implicated in the development of RCC. Loss of material from the 3p chromosome characterizes conventional RCC and the deletion of the VHL suppressor gene plays an important role in the genesis of this RCC variant. In contrast, numerical changes with trisomy of chromosomes 7 and 17 and loss of the sex chromosome are typical changes in papillary tumors, whereas papillary RCC have additional trisomies. Chromophobe RCC is characterized by loss of chromosomes with a combination of monosomies. Less consistent genetic alterations are associated with collecting duct carcinoma. The traditional treatment of RCC is surgery by radical or partial nephrectomy. The latter approach carries a risk of tumor recurrence as a result of unrecognized satellite lesions or premalignant lesions that might have been present at the time of surgery. However, the reported recurrence rates after partial nephrectomy are <1% and therefore the possible presence of premalignant disease does not alter the actual treatment strategy advocated. Although multifocality and bilateral occurrence of RCC are much more likely in cases of papillary RCC, biopsy of the renal remnant or contralateral kidney is not justified even in patients with this tumor type. Conversely, patients with RIN in a partial or radical nephrectomy specimen or in a renal biopsy taken for whatever reason should be subjected to closer follow-up with regularly repeated ultrasound. When an effective chemopreventive regimen becomes available it might be useful for patients with an inherited risk of RCC as well as in those who are at risk of tumor recurrence after intervention. Mass screening with the purpose of detecting RCC at its earliest stage is not recommended at the present time, but screening focused on certain risk groups can be advocated. Further research is needed to identify avoidable risks, develop effective chemoprevention and recognize patients at risk.

  • 45.
    Wolk, A.
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Gridley, G.
    National Cancer Institute, Epidemiology and Biostatistics Program, Rochville, MD USA.
    Niwa, S.
    WESTAT Inc, Rockville, MD, USA.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    McCredie, M.
    Tamer Epidemiology Research Unit, NS W Cancer Council, Sydney, Australia.
    Mellemgaard, A.
    6Danish Cancer Society, Division of Cancer Epidemiology, Copenhagen, Denmark.
    Mandel, J. S.
    School of Public Health, University of Minnesota, Minneapolis MN USA.
    Wahrendorf, J.
    Division of Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    McLaughlin, J. K.
    1ntemational Epidemiology Institute, Rockville, MD, USA.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; ODepartment of Epidemiology, Harvard School of Public Health, Boston, M, USA.
    International renal cell cancer study. VII. Role of diet1996In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 65, no 1, p. 67-73Article in journal (Refereed)
    Abstract [en]

    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.

  • 46.
    Wolk, A.
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States.
    Nutrition and renal cell cancer1996In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 7, no 1, p. 5-18Article in journal (Refereed)
    Abstract [en]

    Epidemiologic evidence on the relation between nutrition and renal cell cancer is reviewed. Kidney cancer, comprising 1.7 percent of all malignant diseases diagnosed worldwide, shows about a 20-fold international variation in the incidence in men and 10-fold in women. This substantial variation indicates an important causal role of environmental factors. Renal cell (parenchymal) cancer (RCC) accounts for about 80 percent of all kidney cancers. While the etiology of RCC is incompletely understood, analytic epidemiologic studies provide consistent support for a positive association of obesity with risk of RCC; the dose-response observed supports a causal relationship. Only a few prospective studies, all of them limited in size, have been published, while ecologic and case-control studies suggest that diet may be important in the etiology of RCC. However, contradictory results and methodologic limitations in some case-control studies prevent definite conclusions concerning diet and RCC. A positive association of protein and fat intake, as well as their main food sources (meat, milk, fats), with risk of RCC-as suggested by ecologic studies-has no clear support in analytic epidemiologic studies. A protective effect of vegetables and fruits has been observed in most case-control studies, while the majority do not show an association between alcohol, coffee, and risk of RCC. Recent reports indicated an increased risk of RCC associated with consumption of fried/sauteed meat and low intakes of magnesium or vitamin E. An apparent positive association with total energy intake, perhaps due to bias, needs further investigation.

  • 47.
    Yang, K.
    et al.
    CNT, Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Egevad, L.
    Department of Pathology, Academic Hospital, Uppsala, Sweden.
    Hemminki, K.
    CNT, Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Novel somatic mutations in the VHL gene in Swedish archived sporadic renal cell carcinomas1999In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 141, no 1-2, p. 1-8Article in journal (Refereed)
    Abstract [en]

    Frequent loss-of-function somatic mutations of the VHL gene have been detected in sporadic renal cell carcinoma (RCC), indicating that inactivation of the VHL gene plays a critical role in RCC. In this study, we collected 35 archived Swedish sporadic RCCs identified from an epidemiological study on occupational exposure and kidney cancer to test how well stored pathological specimens could be retrieved and analyzed for VHL mutations. Thirty specimens were successfully analyzed with PCR-SSCP and sequencing. Aberrant SSCP bands were detected in 16 out of the 30 samples (53%). Sequencing analysis of the aberrant bands revealed seven deletions, one insertion, one base substitution on a splicing site, six missense mutations, one silent mutation and several base substitutions in the 5' non-coding region and intron 1. Most were novel somatic mutations that have not been reported in sporadic RCC. The mutations were found in three types of non-papillary RCC cases, i.e. 14 clear cells, one granular chromophilic and one sarcomatoid RCC. Interesting multiple mutations were found in three cases (5, 3, 2 mutations, respectively).

  • 48.
    Åström, Maria
    et al.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Division of Hematology, Department of Medicine, Örebro University Hospital, Örebro, Sweden; Department of Laboratory Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; iRiSC – Inflammatory Response and Infection Susceptibility Centre, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Tajeddinn, Walid
    iRiSC – Inflammatory Response and Infection Susceptibility Centre, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Karlsson, Mats G.
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine.
    Linder, Olle
    Division of Hematology, Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Palmblad, Jan
    Division of Hematology, Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Örebro University, School of Medical Sciences. Department of Urology.
    Cytokine Measurements for Diagnosing and Characterizing Leukemoid Reactions and Immunohistochemical Validation of a Granulocyte Colony-Stimulating Factor and CXCL8-Producing Renal Cell Carcinoma2018In: Biomarker Insights, ISSN 1177-2719, E-ISSN 1177-2719, Vol. 13, article id UNSP 1177271918792246Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Various paraneoplastic syndromes are encountered in renal cell carcinomas. This case report illustrates that a paraneoplastic leukemoid reaction may precede the diagnosis of renal cell carcinoma and be explained by cytokine production from the cancer cells.

    CASE PRESENTATIONS: A 64-year-old man was referred for hematology workup due to pronounced leukocytosis. While being evaluated for a possible hematologic malignancy as the cause, he was found to have a metastasized renal cell carcinoma, and hyperleukocytosis was classified as a leukemoid reaction. A multiplex panel for measurement of 25 serum cytokines/chemokines showed highly elevated levels of granulocyte colony-stimulating factor (G-CSF) and CXCL8 (C-X-C-motif chemokine ligand 8, previously known as interleukin [IL]-8). By immunohistochemistry it was shown that the renal carcinoma cells expressed both these cytokines. Two additional, consecutive patients with renal cell carcinoma with paraneoplastic leukocytosis also showed elevated serum levels of CXCL8, but not of G-CSF. Nonparametric statistical evaluation showed significantly higher serum concentrations of CXCL8, IL-6, IL-10, monocyte chemoattractant protein 1 (MCP-1), and tumor necrosis factor, but lower interferon gamma (IFN-gamma) and IL-1 alpha, for the 3 renal cell carcinoma cases compared with healthy blood donors.

    CONCLUSIONS: In suspected paraneoplastic leukocytosis, multiplex serum cytokine analyses may facilitate diagnosis and provide an understanding of the mechanisms for the reaction. In the index patient, combined G-CSF and CXCL8 protein expression by renal carcinoma cells was uniquely documented. A rapidly fatal course was detected in all 3 cases, congruent with the concept that autocrine/paracrine growth signaling in renal carcinoma cells may induce an aggressive tumor phenotype. Immune profiling studies could improve our understanding for possible targets when choosing therapies for patients with metastatic renal cell carcinoma.

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