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Sökning: WFRF:(Lindblad Per 1953 ) > Forskningsöversikt

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1.
  • Bergström, A., et al. (författare)
  • Obesity and renal cell cancer : a quantitative review
  • 2001
  • Ingår i: British Journal of Cancer. - London, United Kingdom : Nature Publishing Group. - 0007-0920 .- 1532-1827. ; 85:7, s. 984-990
  • Forskningsöversikt (refereegranskat)abstract
    • 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.
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2.
  • Cho, Eunyoung, et al. (författare)
  • Epidemiology of renal cell cancer
  • 2011
  • Ingår i: Hematology/Oncology Clinics of North America. - Maryland Heights, USA : Saunders Elsevier. - 0889-8588 .- 1558-1977. ; 25:4, s. 651-665
  • Forskningsöversikt (refereegranskat)abstract
    • 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.
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3.
  • Lindblad, Per, 1953- (författare)
  • Epidemiology of renal cell carcinoma
  • 2004
  • Ingår i: Scandinavian Journal of Surgery. - London, United Kingdom : Sage Publications. - 1457-4969 .- 1799-7267. ; 93:2, s. 88-96
  • Forskningsöversikt (refereegranskat)abstract
    • 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.
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4.
  • Van Poppel, H., et al. (författare)
  • Precancerous lesions in the kidney
  • 2000
  • Ingår i: Scandinavian Journal of Urology and Nephrology, Supplementum. - Oslo, Norway : Taylor & Francis. - 0300-8886 .- 1651-2537 .- 0000-0000 .- 0036-5599. ; :205, s. 136-165
  • Forskningsöversikt (refereegranskat)abstract
    • 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.
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5.
  • Wolk, A., et al. (författare)
  • Nutrition and renal cell cancer
  • 1996
  • Ingår i: Cancer Causes and Control. - London, United Kingdom : Rapid Science Publisher. - 0957-5243 .- 1573-7225. ; 7:1, s. 5-18
  • Forskningsöversikt (refereegranskat)abstract
    • 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.
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