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A global assessment of the oesophageal adenocarcinoma epidemic
  1. Gustaf Edgren1,2,
  2. Hans-Olov Adami1,2,
  3. Elisabete Weiderpass2,3,4,5,
  4. Olof Nyrén2,6
  1. 1Department of Epidemiology, Harvard School of Public Health, Harvard University, Boston, Massachusetts, USA
  2. 2Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
  3. 3Cancer Registry of Norway, Oslo, Norway
  4. 4Department of Community Medicine, University of Tromsø, Tromsø, Norway
  5. 5Samfundet Folkhälsan, Helsinki, Finland
  6. 6Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
  1. Correspondence to Dr Gustaf Edgren, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm SE-171 77, Sweden; gustaf.edgren{at}


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 years' variation in estimated time of onset opens prospects for hypothesis-generating ecological analyses.

  • Oesophageal cancer
  • adenocarcinoma
  • cancer epidemiology
  • epidemiology
  • cancer
  • screening
  • biostatistics
  • cancer prevention
  • cancer vaccines
  • gastric adenocarcinoma
  • gastric cancer
  • Helicobacter pylori

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  • Some of the data in this article are from the Cancer Registry of Norway. The Cancer Registry of Norway is not responsible for the analysis or interpretation of the data presented.

  • Funding This work was supported by Karolinska Institutet, Distinguished Professor Award to H-OA (grant number: 2368/10-221). GE is supported by a postdoctoral grant from Svenska Sällskapet för Medicinsk Forskning (SSMF).

  • Competing interests None.

  • Ethics approval The analyses were solely based on publicly available data of population sizes and aggregate number of cancer cases and as such, Institutional Review Board approval was not deemed to be necessary.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement Almost all of the data is publicly available from IARC.

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