Cancer surveillance series: interpreting trends in prostate cancer--part I: Evidence of the effects of screening in recent prostate cancer incidence, mortality, and survival rates.
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BACKGROUND: The prostate-specific antigen test was approved by the U.S. Food and Drug Administration in 1986 to monitor the disease status in patients with prostate cancer and, in 1994, to aid in prostate cancer detection. However, after 1986, the test was performed on many men who had not been previously diagnosed with prostate cancer, apparently resulting in the diagnosis of a substantial number of early tumors. Our purpose is to provide insight into the effect of screening on prostate cancer rates. Detailed data are presented for whites because the size of the population allows for calculating statistically reliable rates; however, similar overall trends are seen for African-Americans and other races. METHODS: Prostate cancer incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program and mortality data from the National Center for Health Statistics were analyzed. RESULTS/CONCLUSIONS: The following findings are consistent with a screening effect: 1) the recent decrease since 1991 in the incidence of distant stage disease, after not having been perturbed by screening; 2) the decline in the incidence of earlier stage disease beginning the following year (i.e., 1992); 3) the recent increases and decreases in prostate cancer incidence and mortality by age that appear to indicate a calendar period effect; and 4) trends in the incidence of distant stage disease by tumor grade and trends in the survival of patients with distant stage disease by calendar year that provide suggestive evidence of the tendency of screening to detect slower growing tumors. IMPLICATIONS: The decline in the incidence of distant stage disease holds the promise that testing for prostate-specific antigen may lead to a sustained decline in prostate cancer mortality. However, population data are complex, and it is difficult to confidently attribute relatively small changes in mortality to any one cause. (+info)
Cancer surveillance series: interpreting trends in prostate cancer--part II: Cause of death misclassification and the recent rise and fall in prostate cancer mortality.
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BACKGROUND: The rise and fall of prostate cancer mortality correspond closely to the rise and fall of newly diagnosed cases. To understand this phenomenon, we explored the role that screening, treatment, iatrogenic (i.e., treatment-induced) deaths, and attribution bias (incorrect labeling of death from other causes as death from prostate cancer) have played in recent mortality trends. METHODS: Join point regression is utilized to assess the recent rise and fall in mortality and the relationship of total U.S. trends to those areas served by the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Cancer Registry Program. Incidence-based mortality (IBM) is estimated with the use of prostate cancer data from the SEER Program to partition (from overall prostate cancer mortality trends) the contribution of cases diagnosed since the widespread use of prostate-specific antigen (PSA) testing starting in 1987. IBM is also used to examine the contribution of stage at diagnosis to the recent prostate cancer mortality trends. RESULTS: IBM for cases diagnosed since 1987 rose above the pre-1987 secular (i.e., background) trend, peaked in the early 1990s, and almost returned to the secular trend by 1994. This rise and fall of IBM track with the pool of prevalent cases diagnosed within the prior 2 years. IBM for cases diagnosed with metastatic disease fell starting in 1991, while IBM for those diagnosed with localized/regional disease was relatively flat. CONCLUSIONS: The rise and fall in prostate cancer mortality observed since the introduction of PSA testing in the general population are consistent with a hypothesis that a fixed percent of the rising and falling pool of recently diagnosed patients who die of other causes may be mislabeled as dying of prostate cancer. The decline in IBM for distant stage disease and flat IBM trends for localized/regional disease provide some evidence of improved prognosis for screen-detected cases, although alternative interpretations are possible. (+info)
Cancer surveillance series: interpreting trends in prostate cancer--part III: Quantifying the link between population prostate-specific antigen testing and recent declines in prostate cancer mortality.
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BACKGROUND: The objective of this study was to investigate the circumstances under which dissemination of prostate-specific antigen (PSA) testing, beginning in 1988, could plausibly explain the declines in prostate cancer mortality observed from 1992 through 1994. METHODS: We developed a computer simulation model by use of information on population-based PSA testing patterns, cancer detection rates, average lead time (the time by which diagnosis is advanced by screening), and projected decreased risk of death associated with early diagnosis of prostate cancer through PSA testing. The model provides estimates of the number of deaths prevented by PSA testing for the 7-year period from 1988 through 1994 and projects what prostate cancer mortality for these years would have been in the absence of PSA testing. RESULTS: Results were generated by assuming a level of screening efficacy similar to that hypothesized for the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Under this assumption, the projected mortality in the absence of PSA testing continued the increasing trend observed before 1991 only when it was assumed that the mean lead time was 3 years or less. Projected mortality trends in the absence of PSA screening were not consistent with pre-1991 increasing trends for lead times of 5 years and 7 years. CONCLUSIONS: When screening is assumed to be at least as efficacious as hypothesized in the PLCO trial, it is unlikely that the entire decline in prostate cancer mortality can be explained by PSA testing based on current beliefs concerning lead time. Only very short lead times would produce a decline in mortality of the magnitude that has been observed. (+info)
Cancer surveillance series: changing geographic patterns of lung cancer mortality in the United States, 1950 through 1994.
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BACKGROUND: Geographic surveys revealing variations in lung cancer mortality rates across the United States have prompted epidemiologic studies in high-risk communities. We have updated these maps to track the changing patterns and to provide further clues to the determinants of lung cancer. METHODS: Age-adjusted race- and sex-specific lung cancer mortality rates from 1950 through 1994 were calculated for nine Census Divisions and 508 State Economic Areas of the United States. RESULTS: Pronounced geographic variation in lung cancer rates was evident, with the patterns changing substantially over time. Among white males in the 1950s and 1960s, high rates were observed in urban areas of the northeast and north central states and in areas along the southeast and Gulf coasts. By the 1970s, the northern excess began to fade, with high rates starting to cover wider areas of the south. By the 1980s to the mid-1990s, clustering of elevated rates was prominent across the southeast and south central areas, with relatively low rates throughout much of the northeast. Among white females, little geographic variation was evident in the 1950s, but thereafter relatively high rates began to appear in clusters along the Atlantic and Pacific coasts. For both sexes, consistently low rates were seen in the mountain and the plains states. Rates among blacks were consistently elevated in northern areas and low across the south. CONCLUSIONS: The changing mortality patterns for lung cancer generally coincide with regional trends in cigarette smoking, indicating that public health measures aimed at smoking prevention and cessation should have a dramatic effect in reducing lung cancer rates. (+info)
Cancer surveillance series: recent trends in childhood cancer incidence and mortality in the United States.
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BACKGROUND: Public concern about possible increases in childhood cancer incidence in the United States led us to examine recent incidence and mortality patterns. METHODS: Cancers diagnosed in 14540 children under age 15 years from 1975 through 1995 and reported to nine population-based registries in the National Cancer Institute's Surveillance, Epidemiology, and End Results Program were investigated. Age-adjusted incidence was analyzed according to anatomic site and histologic categories of the International Classification of Childhood Cancer. Age-adjusted U.S. mortality rates were calculated. Trends in rates were evaluated by use of standard regression methods. RESULTS: A modest rise in the incidence of leukemia, the most common childhood cancer, was largely due to an abrupt increase from 1983 to 1984; rates have decreased slightly since 1989. For brain and other central nervous system (CNS) cancers, incidence rose modestly, although statistically significantly (two-sided P = .020), largely from 1983 through 1986. A few rare childhood cancers demonstrated upward trends (e.g., the 40% of skin cancers designated as dermatofibrosarcomas, adrenal neuroblastomas, and retinoblastomas, the latter two in infants only). In contrast, incidence decreased modestly but statistically significantly for Hodgkin's disease (two-sided P = .037). Mortality rates declined steadily for all major childhood cancer categories, although less rapidly for brain/CNS cancers. CONCLUSIONS: There was no substantial change in incidence for the major pediatric cancers, and rates have remained relatively stable since the mid-1980s. The modest increases that were observed for brain/CNS cancers, leukemia, and infant neuroblastoma were confined to the mid-1980s. The patterns suggest that the increases likely reflected diagnostic improvements or reporting changes. Dramatic declines in childhood cancer mortality represent treatment-related improvements in survival. (+info)
Long-term survival and late deaths after allogeneic bone marrow transplantation. Late Effects Working Committee of the International Bone Marrow Transplant Registry.
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BACKGROUND AND METHODS: It is uncertain whether mortality rates among patients who have undergone bone marrow transplantation return to the level of the mortality rates of the general population. We analyzed the characteristics of 6691 patients listed in the International Bone Marrow Transplant Registry. All the patients were free of their original disease two years after allogeneic bone marrow transplantation. Mortality rates in this cohort were compared with those of an age-, sex-, and nationality-matched general population. Cox proportional-hazards regression was used to identify risk factors for death more than two years after transplantation (late death). RESULTS: Among patients who were free of disease two years after transplantation, the probability of living for five more years was 89 percent (95 percent confidence interval, 88 to 90 percent). Among patients who underwent transplantation for aplastic anemia, the risk of death by the sixth year after transplantation did not differ significantly from that of a normal population. Mortality remained significantly higher than normal throughout the study among patients who underwent transplantation for acute lymphoblastic leukemia or chronic myelogenous leukemia and through the ninth year among those who underwent transplantation for acute myelogenous leukemia. Recurrent leukemia was the chief cause of death among patients who received a transplant for leukemia, whereas chronic graft-versus-host disease was the chief cause among those who received a transplant for aplastic anemia. Advanced, long-standing disease before transplantation and active chronic graft-versus-host disease were important risk factors for late death. CONCLUSIONS: In patients who receive an allogeneic bone marrow transplant as treatment for acute myelogenous or lymphoblastic leukemia, chronic myelogenous leukemia, or aplastic anemia and who are free of their original disease two years later, the disease is probably cured. However, for many years after transplantation, the mortality among these patients is higher than that in a normal population. (+info)
Effect of hypertension on mortality in Pima Indians.
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BACKGROUND: The effect of hypertension on mortality was examined in 5284 Pima Indians, 1698 of whom had type 2 diabetes at baseline or developed it during follow-up. METHODS AND RESULTS: During a median follow-up of 12.2 years (range, 0.01 to 24.8 years), 470 nondiabetic subjects and 488 diabetic subjects died. In the nondiabetic subjects, 45 of the deaths were due to cardiovascular disease, 208 to other natural causes, and 217 to external causes; in the diabetic subjects, 106 of the deaths were due to cardiovascular disease, 85 to diabetic nephropathy, 226 to other natural causes, and 71 to external causes. In the nondiabetic subjects, after adjusting for age, sex, body mass index, and serum cholesterol concentration in a proportional hazards model, hypertension predicted death from cardiovascular disease (death rate ratio [DRR]=2.8; 95% CI, 1.4 to 5. 6; P=0.003). In the diabetic subjects, after additional adjustment for duration of diabetes, plasma glucose concentration, and proteinuria, hypertension strongly predicted deaths from diabetic nephropathy (DRR=3.5; 95% CI, 1.7 to 7.2; P<0.001), but it had little effect on deaths from cardiovascular disease (DRR=1.4; 95% CI, 0.88 to 2.3; P=0.15). CONCLUSIONS: We propose that the weak relationship between hypertension and cardiovascular disease in diabetic Pima Indians is not because of a diminished effect of hypertension on cardiovascular disease in diabetes, but because of a relatively greater effect of hypertension on the progression of diabetic nephropathy. Factors that may account for this finding in Pima Indians include a younger age at onset of type 2 diabetes, a low frequency of heavy smoking, favorable lipoprotein profiles and, possibly, enhanced susceptibility to renal disease. (+info)
An increase in the number of deaths in the United States in the first week of the month--an association with substance abuse and other causes of death.
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BACKGROUND AND METHODS: There are regular changes in mortality rates, such as increased rates of death from influenza in the winter and from motor vehicle accidents on long holiday weekends. Previous research has shown that among persons with schizophrenia, the rates of cocaine use and hospital admissions increase at the beginning of the month, after the receipt of disability payments. Using computerized data from all death certificates in the United States between 1973 and 1988, we compared the number of deaths in the first week of the month with the number of deaths in the last week of the preceding month. RESULTS: The average number of deaths was about 5500 per day, or about 165,000 in a 30-day month. There were 100.9 deaths (95 percent confidence interval, 100.8 to 101.0) in the first week of the month for every 100 deaths in the last week of the preceding month. This was equivalent to about 4320 more deaths in the first week of each month than in the last week of the preceding month in an average year. Between 1983 and 1988, for deaths involving substance abuse and an external cause (such as suicides, accidents, and homicides), there were 114.2 deaths (95 percent confidence interval, 110.5 to 117.9) in the first week of the month for every 100 in the last week of the preceding month. There were significant increases in the number of deaths in the first week of the month for many causes of death, including substance abuse, natural causes, homicides, suicides, and motor vehicle accidents. CONCLUSIONS: In the United States, the number of deaths is higher in the first week of the month than in the last week of the preceding month. The increase at the beginning of the month is associated with substance abuse and other causes of death. (+info)