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In a 81-years old man synchronous triple cancers (prostate, kidney and lung) were found at autopsy. The poorly differentiated prostatic adenocarcinoma metastasized to the clear cell carcinoma of the right kidney and to its solitary lung metastasis. The "neoplasm to neoplasm" metastasis and the "metastasis in metastasis" was confirmed by immunohistochemistry.
BACKGROUND: Familial risks in kidney cancer and association with second primary malignancies were studied using the nationwide Swedish Family Cancer Database. METHODS: Cancer data were retrieved from the Swedish Cancer Registry from years 1961 to 1998 and included 23,137 cases of kidney cancer. Standardized incidence ratios (SIRs) were used to measure the cancer risks. RESULTS: Seventy-one families were identified where both a parent and an offspring had kidney cancer, giving a familial risk for offspring of 1.56 (1.22 to 1.95) and population attributable proportion of 0.78%. A risk for kidney cancer from an affected sibling was considerably higher with a SIR of 4.72 (2.28 to 9.20), giving an attributable proportion of 0.77%. The discordant tumor site that was associated with kidney cancer between two generations was hemangioblastoma of central nervous system. Discordant cancer sites that were associated with kidney cancer in siblings were ovaries, endocrine glands and pancreas. There was an over threefold increase of second primary malignancies of the urinary bladder, nervous system and endocrine gland in kidney cancer patients. The risks for second primary hemangioblastoma following kidney cancer or familial kidney cancer was 21.19 (6.69 to 43.83) and 1206 (114 to 3456), respectively. CONCLUSIONS: The high ratio of sibling risk to offspring risk in kidney cancer may reflect a recessive susceptibility. The high risk for second primary cancers in the patients without family history is consistent with a polygenic model and variable degree of environmental modification.
BACKGROUND: The role of hypertension as a kidney cancer risk factor remains unclear. The objectives of this study were to prospectively examine the effects of hypertension on kidney cancer death, and to determine the synergistic effect of hypertension and smoking on kidney cancer risk. METHODS: The cohort was composed of 576,562 Korean men, aged 30 and older, who received health insurance from the National Health Insurance Corporation, and who underwent biennial medical evaluations in 1992 and 1994. At baseline, 343,132 men (59.5%) were identified as current cigarette smokers. Between 1995 and 2001, there were 92 deaths from kidney cancer (2.2/100,000 person years). Using deaths from kidney cancer as the main outcome variable, Cox proportional hazards models were tested while controlling for age and other covariates. RESULTS: An initial finding indicated that hypertension increased the mortality risk of kidney cancer [relative risk (RR) 2.43; 95% confidence interval (CI) 1.57-3.76]. After stratification of smoking status, RR for hypertension on kidney cancer was still increased for current smokers (RR 2.80; 95% CI 1.64-4.79). For current smokers, those with systolic blood pressure >/=160 mm Hg had a risk of kidney cancer that was 8.18 (95% CI, 3.13-21.36) times higher than those with a pressure less than 120 mm Hg. When the interaction term was included in the multivariate model, there was no significant synergistic effect of hypertension with current smoking on the risk of death from kidney cancer. CONCLUSION: This study supports the hypothesis that hypertension is an independent risk factor of kidney cancer mortality.
Renal-cell carcinoma usually affects those over 40 years old, and, in any age group, the disease occurs about twice as frequently among men as it does among women. The incidence of the disease has been steadily increasing over the years. In the United States, the probability of surviving after diagnosis of renal cancer has been improving since 1940 regardless of race, sex, and age at diagnosis. The relationship between SES and the chance of developing the disease is sporadic with an indication of a slightly higher risk in the upper socioeconomic classes. Urbanrural comparisons consistently suggest that a higher risk is associated with urban residence. Tobacco use is probably the only environmental factor that could be considered to be etiologically related to cancer of the kidney. A variety of studies point to a moderate but consistent association with tobacco use in the form of cigarette, cigar, or pipe smoking. The excess of the disease in males compared to females and the lower incidence in Mormons may partly be due to the confounding effect of smoking. Dietary vitamin A or vitamin A supplements may have an antipromoting effect in the development of kidney cancer. Hypotheses implicating fat and/or cholesterol intake in the etiology of cancer of the kidney appear to be too tenuous. The evidence of a relationship between concentrations of certain trace metals in drinking water and incidence of renal cancer is weak. Similarly, there is no strong indication of an increased risk among individuals exposed to radiation. In general, with the exception of the observation of an unusually high risk among coke-oven workers, occupational studies have not identified any high-risk groups. Familial aggregation, though rare, occurs with peculiar disease characteristics that may predict similar cancers in the proband's relatives with a high degree of accuracy. In conclusion, the etiology of cancer of the kidney is poorly understood. The descriptive epidemiology of the disease provides some interesting insights into the correlates of the distribution of the disease.(ABSTRACT TRUNCATED AT 400 WORDS)
The percent population attributable risk (AR) for kidney cancer was estimated in relation to smoking habits, beta-carotene intake, history of cystitis and family history of kidney cancer, using data from a case-control study conducted between 1985 and 1989 in Milan, northern Italy. The data comprised 133 histologically confirmed cases of incident kidney cancer and 392 controls, admitted to hospital for a wide range of acute, non-neoplastic, non-smoking-related diseases. On the basis of multivariate odds ratios (ORs), smoking habits accounted for about 26% of cases, a low beta-carotene intake for 18%, a history of cystitis for 7%, and a family history of kidney cancer in first-degree relatives for 3% of cases. Ever smoking and low beta-carotene intake combined explained 38% of all kidney cancers, and the combination of these two factors plus a history of cystitis and a family history of kidney cancer explained 45% of the incidence of the disease. Thus, even if available, dietary information was limited and the AR estimates were based on somewhat arbitrary assumptions. A considerable proportion of kidney cancers could be avoided simply by eliminating smoking and increasing consumption of fruit and vegetables in this Italian population. This would mean that about 1,500 kidney cancer deaths every year in the whole of Italy could be avoided.
In this paper, results from current randomized and other relevant studies on cytokine and vaccine therapy of kidney cancer in the adjuvant setting and in metastatic disease are reviewed. Improvement of medical therapy of kidney cancer is required since the relative 5-year survival of kidney cancer is only 62%. In the adjuvant setting, cytokine monotherapy (interferon [IFN]-alpha or interleukin [IL]-2) is not effective in improving progression-free or overall survival. Recently, an autologous kidney cancer cell vaccine has been shown to reduce the risk of tumor progression following radical nephrectomy for organ-confined or locally advanced kidney cancer in a randomized Phase III study. There were only a few vaccine-related side effects. Presently, this is the only promising approach for the adjuvant treatment of kidney cancer following nephrectomy. In metastatic kidney cancer patients with the tumor-bearing kidney in situ, a combination of radical nephrectomy plus IFN-alpha is more effective than IFN-alpha alone. In metastatic kidney cancer without the option of operative removal of the primary tumor and/or metastases, cytokines such as IFN-alpha, IL-2 and IL-12 and their combinations result in response rates of 10-30%, but the 5-year overall survival is less than 10%. Furthermore, the ideal dose, administration and combination of different agents are yet to be defined. Vaccine therapy of metastatic kidney cancer has been investigated only in Phase I and II studies with limited clinical benefit. Based on the current literature there is a clear need for new approaches in metastatic kidney cancer.
BACKGROUND: The incidence of kidney cancer is high in Western and Northern Europe and North America, and low in Asia. Although the incidence of kidney cancer in Japan is lower than the rates in the other industrialized countries, there is no doubt that it is increasing. METHODS: We evaluated the risk factors for kidney cancer death using the database of the Japan Collaborative Cohort (JACC) Study (i.e., medical history, anthropometry, and lifestyle including dietary habits). The analytic cohort included 47,997 males and 66,520 females aged 40 years and older. The Cox proportional hazards model was used to determine adjusted relative risks. RESULTS: A total of 36 males and 12 females died from kidney cancer during the follow-up of 9.6+/-2.6 years and 9.9+/-2.2 years, respectively. A medical history of hypertension, a fondness for fatty food, and consumption of black tea were associated with an increased risk of kidney cancer death while an intake of taro, sweet potato and potato was associated with a decreased risk. CONCLUSIONS: The present study showed four factors to be related to kidney cancer death. However, further studies may be needed to evaluate risk factors for kidney cancer death in Japan because the number of kidney cancer death in the present study was small.
Reports of increasing rates for kidney cancers in several count prompted this analysis of global incidence trends for total kidney cancers and by subsite. International incidence data for 5-year periods 1973-1977, 1978-1982, 1983-1987 and 1988-1992 were obtained from volumes IV to VII of Cancer Incidence in Five Continents published by the International Agency for Research on Cancer. The USA data for the same 5-year periods were obtained from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute. Percentage changes in incidence rates were computed using the relative difference between the time periods 1973-1977 and 1988-1992, and annual percentage changes in incidence rates were computed using log linear regression. In 1988-1992, kidney cancer incidence rates (age-adjusted to the world-standard population) were highest in France (16.1/100,000 man-years and 7.3/100,000 woman-years) and lowest in India (2.0 and 0.9, respectively). Between 1973-1977 and 1988-1992, incidence rates rose among men and women in all regions and ethnic groups, with a few exceptions, mostly in Scandinavian countries. The largest percentage increase for men was in Japan (171%) and for women in Italy (107%). Rates for renal pelvis cancer were less than 1/100,000 person-years in almost all regions in both sexes, and the temporal trends were inconsistent. Incidence trends for renal parenchyma cancer tracked those for total kidney cancers, and appeared to result from increases in the prevalence of risk factors and in use of diagnostic imaging procedures.
Most patients who develop kidney cancer are effectively treated with a radical nephrectomy; however, for those patients who present with or develop metastatic disease, the therapeutic options are limited. Interferon and interleukin-2 remain the standard therapies. Several studies have identified the optimal doses and schedules of these cytokines and groups of patients most likely to benefit from immunotherapy. Although cytotoxic chemotherapy continues to have a minor role in patients with clear cell renal carcinoma, it may become the treatment of choice for some patients with variant renal cancers. Novel agents targeting the vascular endothelial growth factor, its receptor, and other hypoxia-induced proteins are showing great promise and soon may expand the therapeutic options for patients with advanced kidney cancer.
Twenty patients with either melanoma ( 7) or kidney cancer ( 13) were treated with outpatient bolus interleukin (IL)-2 18-22 MIU/m2 IVPB for 3 consecutive days for 6 consecutive weeks followed by a 2-week rest break (on an 8-week cycle). Patient characteristics included 16 males/4 females, eleven patients had received no prior systemic therapy, median ECOG performance status = 1, and most common disease sites being lung, lymph node, subcutaneous, bone, and liver. Two patients with melanoma (29% response rate) (95% CI: 8-64%) and two with kidney cancer (15%) (95% CI: 3-43%) have achieved partial responses. Two minor responses in kidney cancer were also seen. The most common toxicities were nausea, fatigue, rigors, fever, and myalgias/arthralgias. No cardiac events occurred, and no patients required hospitalization due to toxicity. IL-2 at this outpatient dose and schedule is well tolerated and displays some evidence of activity in melanoma and kidney cancer. Larger patient numbers are required to corroborate these response rates and to determine whether complete responses are possible.
Kidney cancer, although relatively rare when compared to other malignancies, occurs not uncommonly in patients with renal disease and is often discovered incidentally during the initial nephrologic work-up, or by the savvy clinician who is familiar with the paraneoplastic signs. While surgical approaches are generally curative when the disease is confined to the kidney, one-third of the cases that present in the metastatic form and require conventional medical therapy are associated with a truly dismal patient survival rate. In light of the emerging knowledge of the molecular mechanisms of kidney cancer oncogenesis, several novel and promising therapeutic approaches are emerging. In this review, we summarize the current state of kidney cancer diagnosis and therapy, as well as some of the novel treatments that capitalize on those newly elucidated molecular pathways that are deranged in this disease.
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BACKGROUND: The incorporation of diagnostic and therapeutic improvements, as well as the different smoking patterns, may have had an influence on the observed variability in renal cancer mortality across Europe. This study examined time trends in kidney cancer mortality in fourteen European countries during the last two decades of the 20th century. METHODS: Kidney cancer deaths and population estimates for each country during the period 1981-2000 were drawn from the World Health Organization Mortality Database. Age- and period-adjusted mortality rates, as well as annual percentage changes in age-adjusted mortality rates, were calculated for each country and geographical region. Log-linear Poisson models were also fitted to study the effect of age, death period, and birth cohort on kidney cancer mortality rates within each country. RESULTS: For men, the overall standardized kidney cancer mortality rates in the eastern, western, and northern European countries were 20, 25, and 53% higher than those for the southern European countries, respectively. However, age-adjusted mortality rates showed a significant annual decrease of -0.7% in the north of Europe, a moderate rise of 0.7% in the west, and substantial increases of 1.4% in the south and 2.0% in the east. This trend was similar among women, but with lower mortality rates. Age-period-cohort models showed three different birth-cohort patterns for both men and women: a decrease in mortality trend for those generations born after 1920 in the Nordic countries, a similar but lagged decline for cohorts born after 1930 in western and southern European countries, and a continuous increase throughout all birth cohorts in eastern Europe. Similar but more heterogeneous regional patterns were observed for period effects. CONCLUSION: Kidney cancer mortality trends in Europe showed a clear north-south pattern, with high rates on a downward trend in the north, intermediate rates on a more marked rising trend in the east than in the west, and low rates on an upward trend in the south. The downward pattern observed for cohorts born after 1920-1930 in northern, western, and southern regions suggests more favourable trends in coming years, in contrast to the eastern countries where birth-cohort pattern remains upward.
Recent epidemiologic studies have suggested that tea may be protective against cancers of the urinary tract. The authors examined the association between usual adult tea consumption and risk of bladder and kidney cancers in a population-based case-control study that included 1,452 bladder cancer cases, 406 kidney cancer cases, and 2,434 controls. For bladder cancer, the age- and sex-adjusted odds ratios (OR) (95% confidence intervals (CI)) referent to nonusers of tea were 0.9 (0.7, 1.1) for <1.0 cup/day, 1.0 (0.8, 1.2) for 1.0-2.6 cups/day, and 0.9 (0.7, 1.1) for >2.6 cups/day (cutpoints for users based on the tertile distribution among controls). When more extreme cutpoints were used, persons who consumed >5 cups/day (>90th percentile) had a suggestive decreased risk (OR = 0.7; 95% CI 0.5, 1.0), but there was no evidence of a dose-response relation. In analyses stratified by median total beverage intake (2.6 liters/day), there was an inverse association with tea use among persons who consumed less than the median (OR = 0.5; 95% CI 0.3, 0.8) but no association for persons who consumed at or above the median. In contrast, for kidney cancer, there was no association with tea use. Adjustment for site-specific risk factors did not alter these results. This study offers only minimal support for an inverse association between tea consumption and bladder or kidney cancer risk.
OBJECTIVE: To study the risk of kidney cancer following asbestos exposure. METHODS: We carried out a meta-analysis of the results of cohort studies of workers predominantly exposed to asbestos. We contacted the authors of 70 cohort studies; published results were available from the reports of 10 cohorts; we obtained the relevant information for an additional 27 cohorts. RESULTS: The studies included in the analysis comprised a total of 169 kidney cancer deaths and 69 incident cases. The overall pooled standardized mortality ratio (SMR) of kidney cancer was 1.1, with a 95% confidence interval (95% CI) of 0.9-1.3. The pooled SMR was higher for workers with undefined asbestos exposure (SMR 1.2, 95% CI 0.9-1.6) than for workers with either predominant chrysotile (SMR 0.9, 95% CI 0.7-1.3) or some amphibole (SMR 0.96, 95% CI 0.6-1.5) exposure. Studies with published results had higher SMRs than studies for which information was obtained from the authors. Studies with high asbestos exposure and an elevated SMR of lung cancer tended to show an increased risk of kidney cancer. CONCLUSIONS: It is unlikely that asbestos exposure is responsible for an important increase in kidney cancer risk; however, high asbestos exposure might entail a small increase in risk.
To evaluate the hypothesis of increased kidney cancer risk after exposure to hydrocarbons, especially those present in gasoline, we conducted a case-control study in a cohort of approximately 100,000 male refinery workers from five petroleum companies. A review of 18,323 death certificates identified 102 kidney cancer cases, to each of whom four controls were matched by refinery location and decade of birth. Work histories, containing an average of 15.7 job assignments per subject, were found for 98% of the cases and 94% of the controls. To each job, industrial hygienists assigned semiquantitative ratings for the intensity and frequency of exposures to three hydrocarbon categories: nonaromatic liquid gasoline distillates, aromatic hydrocarbons, and the more volatile hydrocarbons. Ratings of "present" or "absent" were assigned for seven additional exposures: higher boiling hydrocarbons, polynuclear aromatic hydrocarbons, asbestos, chlorinated solvents, ionizing radiation, and lead. Each exposure had either no association or a weak association with kidney cancer. For the hydrocarbon category of principal a priori interest, the nonaromatic liquid gasoline distillates, the estimated relative risk (RR) for any exposure above refinery background was 1.0 (95% confidence interval [CI] 0.5-1.9). Analyses of cumulative exposures and of exposures in varying time periods before kidney cancer occurrence also produced null or near-null results. In an analysis of the longest job held by each subject (average duration 9.2 years or 40% of the refinery work history), three groups appeared to be at increased risk: laborers (RR = 1.9, 95% CI 1.0-3.9); workers in receipt, storage, and movements (RR = 2.5, 95% CI 0.9-6.6); and unit cleaners (RR = 2.3, 95% CI 0.5-9.9).
A recent animal experiment suggests that gasoline exposure may be a cause of human kidney cancer. This is a literature review to see whether there is any epidemiologic support for these animal findings. Trends and geographic patterns in gasoline consumption and kidney cancer mortality are moderately supportive of a relationship, although this cannot be considered important evidence for a causal relationship. Most other ecological correlations are not supportive of a relationship. Eleven oil refinery populations and one population of petroleum products distribution workers have been studied. These studies taken as a group do not appear to support the notion of a relationship between gasoline exposure and kidney cancer. However, most were not designed or analyzed with this hypothesis in mind. An examination of these data which attempts to consider the ages of the populations studied provides some evidence of a small kidney cancer excess among older workers or among workers exposed for long periods. Because of the importance of gasoline and the potential for exposure by the public further study of exposed populations is needed.