Esophageal Cancer Other Achievements: Highlights
- Do trends in obesity and other lifestyle-associated risk factors match trends in Esophageal Adenocarcinoma (EAC) in three western countries?
- How do the rate-limiting steps involved in tumor initiation, malignant transformation, and progression influence the shape of the cancer incidence curve?
Do trends in obesity and other lifestyle-associated risk factors match trends in Esophageal Adenocarcinoma (EAC) in three western countries?
As obesity is a well-established factor in EAC risk, the obesity epidemic is believed to be an important driver of the rise of EAC in western countries. We aimed to test this hypothesis by comparing changes in lifestyle-associated factors with changes in EAC incidence over time between the US, Spain, and the Netherlands.
We used population-based data bases from the three countries to extract cancer incidence (US Surveillance, Epidemiology, and End Results (SEER) data base; Spain 13 cancer registries; the Netherlands Eindhoven Cancer Registry). Obesity, smoking rates, and alcohol use were gathered from national US and European health surveys or the World Health Organization (WHO) data repository).
We found that the US, Spain, and the Netherlands showed large differences in both absolute rates and time trends in EAC incidence. Time trends for obesity, smoking, and alcohol in these countries do not correlate with EAC incidence trends. Therefore, other important drivers of this increase in EAC incidence in these countries must be present. While reversing the trend in obesity is important for overall population health, reduction in EAC must rely on the identification of other causative factors. (Kroep S et al., 2014)
How do the rate-limiting steps involved in tumor initiation, malignant transformation, and progression influence the shape of the cancer incidence curve?
Cancer incidence curves harbor information about hidden processes of tumor initiation, premalignant clonal expansion, malignant transformation, and even some limited information on tumor growth before clinical detection. Our analyses of the incidences of four digestive tract cancers show that the age-specific incidence curvesupon adjustments for secular trends and, in the case of esophageal adenocarcinoma (EAC), inclusion of an event describing the conversion of normal squamous to metaplastic Barrett's epitheliumare well approximated by a model that explicitly incorporates the stochastic growth kinetics of premalignant clones, the sporadic appearance of malignant cells within these clones, and a constant time delay corresponding to the mean sojourn time of a malignant clone. While this sojourn seems very short for pancreatic cancer (3 years), intermediate for colorectal cancer (5-7 years), it is much longer for gastric cancer and esophageal adenocarcinoma (10-12 years). Furthermore, with the exception of pancreatic cancer, our results are consistent with the assumption of a high (>95%) probability of tumor stem cell extinction or terminal differentiation. We conclude that malignant clone extinction and tumor sojourn times play important roles in reducing and delaying cancer incidence and influencing the shape of incidence curves for colorectal, gastric, pancreatic, and esophageal cancers. (Luebeck EG et al., 2013)