At 23 years of follow-up in the SPCG-4 trial, mortality among men who underwent radical prostatectomy was 11.7 percentage points lower than that among men whose condition was managed by watchful ...waiting. Radical prostatectomy was associated with a mean of nearly 3 years of extra life.
This analysis of Norwegian registry data suggests that colonoscopic surveillance during the 8 years after removal of low-risk adenomas is not required for a reduction in colorectal-cancer mortality.
...Screening programs for colorectal cancer are currently implemented in many Western populations
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,
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because randomized trials have documented an association between screening and a sustained reduction in colorectal-cancer mortality.
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The benefit is most likely due to early detection of cancer, endoscopic removal of adenomas, and surveillance of patients who are considered to be at high risk for the development of new neoplastic lesions.
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However, precise quantification of the risk of death from cancer after adenoma removal has been hampered by the scarceness of large, population-based studies with long follow-up periods.
Previous studies were performed in populations undergoing intensive surveillance, . . .
The randomized Swedish trial of prostatectomy versus watchful waiting in disease detected mainly clinically (not by PSA screening) continues to show a benefit for early prostatectomy. The number of ...men younger than 65 needed to treat to prevent one death is now four.
The Scandinavian Prostate Cancer Group Study Number 4 (SPCG-4), a randomized trial of radical prostatectomy versus watchful waiting in men with localized prostate cancer diagnosed before the era of prostate-specific antigen (PSA) testing, showed a survival benefit of radical prostatectomy as compared with observation at 15 years of follow-up.
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By contrast, the Prostate Cancer Intervention versus Observation Trial (PIVOT), initiated in the early era of PSA testing, showed that radical prostatectomy did not significantly reduce prostate cancer–specific or overall mortality after 12 years.
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PSA screening profoundly changes the clinical domain of study. Among other considerations, the substantial additional lead time . . .
The epidemiology of nasopharyngeal carcinoma (NPC) has long been a source of fascination due to the malignancy's striking geographic distribution, the involvement of the oncogenic Epstein-Barr virus ...(EBV), the unique association with intake of Chinese-style salt-preserved fish, and etiologic heterogeneity by histologic subtype.
This review summarizes the current epidemiologic literature on NPC, highlighting recent results from our population-based case-control study in southern China.
Findings from our case-control study provide new insight into the epidemiology of NPC, including a diminished role of Chinese-style salt-preserved fish, a profound impact of EBV genetic sequence variation, modest positive associations with passive smoking and household air pollution, and possible effects of oral health and the oral microbiome. Recent findings from other studies include a protective association with infectious mononucleosis, suggesting a causal role of early EBV infection; familial risk conferred by shared genetic variation in the host antibody-mediated immune response to EBV infection; and an unclear association with occupational exposure to formaldehyde.
To shed further light on the interplay of environmental, genetic, and viral causes of NPC, large pooled studies must accumulate sufficient cases with detailed exposure data.
New epidemiologic findings have reshaped the causal model for NPC.
Summary
Previous studies have found a U‐shaped relationship between mortality and (weekday) sleep duration. We here address the association of both weekday and weekend sleep duration with overall ...mortality. A cohort of 43,880 subjects was followed for 13 years through record‐linkages. Cox proportional hazards regression models with attained age as time‐scale were fitted to estimate multivariable‐adjusted hazard ratios and 95% confidence intervals for mortality; stratified analyses on age (<65 years, ≥65 years) were conducted. Among individuals <65 years old, short sleep (≤5 hr) during weekends at baseline was associated with a 52% higher mortality rate (hazard ratios 1.52; 95% confidence intervals 1.15–2.02) compared with the reference group (7 hr), while no association was observed for long (≥9 hr) weekend sleep. When, instead, different combinations of weekday and weekend sleep durations were analysed, we observed a detrimental association with consistently sleeping ≤5 hr (hazard ratios 1.65; 95% confidence intervals 1.22–2.23) or ≥8 hr (hazard ratios 1.25; 95% confidence intervals 1.05–1.50), compared with consistently sleeping 6–7 hr per day (reference). The mortality rate among participants with short sleep during weekdays, but long sleep during weekends, did not differ from the rate of the reference group. Among individuals ≥65 years old, no association between weekend sleep or weekday/weekend sleep durations and mortality was observed. In conclusion, short, but not long, weekend sleep was associated with an increased mortality in subjects <65 years. In the same age group, short sleep (or long sleep) on both weekdays and weekend showed increased mortality. Possibly, long weekend sleep may compensate for short weekday sleep.
About 20 years ago, the scientific community was first alerted to an enigmatic increase of oesophageal adenocarcinomas in the UK and USA. Subsequently, a virtual epidemic-still unexplained-was ...confirmed in several western countries. Detailed descriptive data might provide clues to its causes.
We collected data on incident cases of oesophageal adenocarcinoma from population-based cancer registries in Australia, Europe, North America and Asia. We calculated age-standardised incidence rates and fitted log-linear Poisson models to assess annual rate of increase and to disentangle age-period-cohort effects, linear spine models to estimate rate of increase since 1985, and Joinpoint models to identify possible inflection points.
With considerable between-registry variation in magnitude and timing, we found a consistent dramatic increase in incidence with an observed or estimated start between 1960 and 1990. The average annual increase ranged from 3.5% in Scotland to 8.1% in Hawaii with similar proportional increase among men and women in most registries and a maintained three to sixfold higher incidence among men. Generally, calendar period was a more important determinant of incidence trends than birth cohort. Where possible to conduct, Joinpoint analyses indicated that the onset of the epidemic varied considerably even between neighbouring countries.
Given the preponderant period effect and the abrupt onset observed or inferred in most populations, the epidemic appears to be caused by some exposure that was first introduced around 1950. At least 30 years' variation in estimated time of onset opens prospects for hypothesis-generating ecological analyses.
The etiology of Parkinson's disease (PD) is not well understood but likely to involve both genetic and environmental factors. Incidence and prevalence estimates vary to a large extent—at least partly ...due to methodological differences between studies—but are consistently higher in men than in women. Several genes that cause familial as well as sporadic PD have been identified and familial aggregation studies support a genetic component. Despite a vast literature on lifestyle and environmental possible risk or protection factors, consistent findings are few. There is compelling evidence for protective effects of smoking and coffee, but the biologic mechanisms for these possibly causal relations are poorly understood. Uric acid also seems to be associated with lower PD risk. Evidence that one or several pesticides increase PD risk is suggestive but further research is needed to identify specific compounds that may play a causal role. Evidence is limited on the role of metals, other chemicals and magnetic fields. Important methodological limitations include crude classification of exposure, low frequency and intensity of exposure, inadequate sample size, potential for confounding, retrospective study designs and lack of consistent diagnostic criteria for PD. Studies that assessed possible shared etiological components between PD and other diseases show that REM sleep behavior disorder and mental illness increase PD risk and that PD patients have lower cancer risk, but methodological concerns exist. Future epidemiologie studies of PD should be large, include detailed quantifications of exposure, and collect information on environmental exposures as well as genetic polymorphisms.
Cancer survivorship has traditionally received little prioritisation and attention. For a long time, the treatment of cancer has been the main focus of healthcare providers’ efforts. It is time to ...increase the amount of attention given to patients’ long‐term well‐being and their ability to return to a productive and good life. This article describes the current state of knowledge and identifies research areas in need of development to enable interventions for improved survivorship for all cancer patients in Europe. The article is summed up with 11 points in need of further focus.
Cancer survivorship has traditionally received little attention. It is time to increase the amount of attention given to patients’ long‐term well‐being and their ability to return to a productive and good life. This article describes the current state of knowledge and identifies research areas in need of development to enable interventions for improved survivorship for all cancer patients in Europe.
Assessment of the effect of breast-cancer screening has been hampered by difficulty in measuring secular trends. In this study, data from a cancer registry were used to determine secular trends and ...to evaluate the effect of screening on breast-cancer mortality.
On the basis of several randomized clinical trials,
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the World Health Organization concluded in 2002 that screening mammography for women between the ages of 50 and 69 years reduced the rate of death from breast cancer by 25%.
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Nevertheless, the use of screening mammography is still debated, chiefly because of concern regarding methodologic limitations in some of the randomized trials.
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In addition, the benefit of mammography when implemented in a population-based service program remains poorly quantified. Therefore, continued evaluation of breast-cancer screening programs is warranted.
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The main challenge in quantifying the reduction in mortality from nonrandomized screening programs is . . .
Nasopharyngeal carcinoma (NPC) has a unique and complex etiology that is not completely understood. Although NPC is rare in
most populations, it is a leading form of cancer in a few well-defined ...populations, including natives of southern China, Southeast
Asia, the Arctic, and the Middle East/North Africa. The distinctive racial/ethnic and geographic distribution of NPC worldwide
suggests that both environmental factors and genetic traits contribute to its development. This review aims to summarize the
current knowledge regarding the epidemiology of NPC and to propose new avenues of research that could help illuminate the
causes and ultimately the prevention of this remarkable disease. Well-established risk factors for NPC include elevated antibody
titers against the Epstein-Barr virus, consumption of salt-preserved fish, a family history of NPC, and certain human leukocyte antigen class I genotypes. Consumption of other preserved foods, tobacco smoking, and a history of chronic respiratory tract conditions
may be associated with elevated NPC risk, whereas consumption of fresh fruits and vegetables and other human leukocyte antigen genotypes may be associated with decreased risk. Evidence for a causal role of various inhalants, herbal medicines, and occupational
exposures is inconsistent. Other than dietary modification, no concrete preventive measures for NPC exist. Given the unresolved
gaps in understanding of NPC, there is a clear need for large-scale, population-based molecular epidemiologic studies to elucidate
how environmental, viral, and genetic factors interact in both the development and the prevention of this disease. (Cancer
Epidemiol Biomarkers Prev 2006;15(10):1765–77)