Showing papers by "Olof Nyrén published in 2013"
TL;DR: The epidemic appears to be caused by some exposure that was first introduced around 1950, and at least 30 years' variation in estimated time of onset opens prospects for hypothesis-generating ecological analyses.
Abstract: Objective 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. Design 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. Results 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. Conclusions 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 years9 variation in estimated time of onset opens prospects for hypothesis-generating ecological analyses.
300 citations
University of Washington1, QIMR Berghofer Medical Research Institute2, University of Cambridge3, Fred Hutchinson Cancer Research Center4, University of North Carolina at Chapel Hill5, University of California, San Francisco6, Kaiser Permanente7, University of Sheffield8, University of Leeds9, Queen's University Belfast10, University of Texas MD Anderson Cancer Center11, Yale University12, Karolinska Institutet13, University of Toronto14, Mayo Clinic15, City of Hope National Medical Center16, University of Southern California17, University of Saskatchewan18, National Institutes of Health19
TL;DR: A previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 is refined and extended to now include esophageal adenocarcinoma.
Abstract: Esophageal adenocarcinoma is a cancer with rising incidence and poor survival. Most such cancers arise in a specialized intestinal metaplastic epithelium, which is diagnostic of Barrett's esophagus. In a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individuals with precancerous Barrett's esophagus (n = 3,175) with 10,120 controls in 2 phases. For the combined case group, we identified three new associations. The first is at 19p13 (rs10419226: P = 3.6 × 10(-10)) in CRTC1 (encoding CREB-regulated transcription coactivator), whose aberrant activation has been associated with oncogenic activity. A second is at 9q22 (rs11789015: P = 1.0 × 10(-9)) in BARX1, which encodes a transcription factor important in esophageal specification. A third is at 3p14 (rs2687201: P = 5.5 × 10(-9)) near the transcription factor FOXP1, which regulates esophageal development. We also refine a previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 and extend our findings to now include esophageal adenocarcinoma.
177 citations
TL;DR: A history of tobacco use, even exclusive use of the seemingly benign snus, is associated with moderately increased cancer‐specific mortality, and although nicotine might play a role, the mechanisms warrant further investigation.
Abstract: On theoretical grounds, nicotine has been implicated as a modifier of cancer progression. We investigated possible associations of smoking or use of Scandinavian moist snuff (snus) with survival after cancer among Swedish male construction workers. Snus use is associated with substantial exposure to nicotine but not to the combustion products in smoke. Among 336,381 workers with detailed information on tobacco use in 1971–1992, we observed 40,230 incident cancers. Complete follow-up through 2007 was accomplished through linkage to population and health registers. Hazard ratios (HRs) and 95% confidence intervals (CIs) for death from any cause, cancer-specific death and death from other causes were derived from Cox proportional hazards regression models adjusted for age at diagnosis, body mass index at study entry and period of diagnosis. Never users of any tobacco served as reference. Increased risks of cancer-specific death were observed both among exclusive smokers (HRall cancer 1.15, 95% CI: 1.10–1.21) and never-smoking snus users (1.15, 95% CI: 1.05–1.26). As regards deaths due to other causes, exclusive smokers had higher relative risks than exclusive snus users (p = 0.03). A history of tobacco use, even exclusive use of the seemingly benign snus, is associated with moderately increased cancer-specific mortality. Although nicotine might play a role, the mechanisms warrant further investigation.
22 citations
TL;DR: In this article, a passive long-term surveillance through self-initiated, event-driven outcome reporting underestimates incidence rates of common upper respiratory tract infections in Sweden during two 8 week periods in 2008 and 2009.
Abstract: BACKGROUND The 2009/2010 pandemic influenza highlighted the need for valid and timely incidence data. In 2007 we started the development of a passive surveillance scheme based on passive follow-up of representative general population cohorts. Cohort members are asked to spontaneously report all instances of colds and fevers as soon as they occur for up to 9 months. Suspecting that compliance might be poor, we aimed to assess the validity of self-initiated, event-driven outcome reporting over long periods. METHODS During two 8 week periods in 2008 and 2009, 2376 and 2514 cohort members in Stockholm County were sent one-week recall questionnaires, which served as reference method. RESULTS The questionnaires were completed by 88% and 86% of the cohort members. Whilst the false positive proportion (1-specificity) in the reporting was low (upper bound of the 95% confidence interval [CI] ≤ 2% in each season), the false negative proportion (failure to report, 1-sensitivity) was considerable (60% [95% CI 52%-67%] in each season). Still, the resulting epidemic curves for influenza-like illness compared well with those from existing General Practitioner-based sentinel surveillance in terms of shape, timing of peak, and year-to-year variation. This suggested that the error was fairly constant. CONCLUSIONS Passive long-term surveillance through self-initiated, event-driven outcome reporting underestimates incidence rates of common upper respiratory tract infections. However, because underreporting appears predictable, simple corrections could potentially restore validity.
17 citations