A new gastric cancer among us
From: Blaser und Chen, 2018
In 1900 gastric cancer was the leading cause of cancer death in the USA and other countries. This cancer has been decreased with the disappearance of the commensal stomach bacterium Helicobacter pylori, which has been blamed to be the cause for gastric cancer. This is actually good news, but here comes the bad news right away: with the disappearance of H. pylori and the decrease of gastric cancer, a new cancer arose: adenocarcinoma of the esophagus (mostly appearing at the gastro-esophageal junction, called GEJ). The incidence of GEJ cancers on non-Hispanic whites in the United States is now higher than the traditional noncardia (cardia is the entrance of the stomach) gastric cancers and GEJ is increasing drastically across many developed countries.
This phenomenon goes along with an inverse relationship of the presence of the bacterium H. pylori with GEJ, and their precursor lesions. Hence H. pylori seems to contribute to causing distal cancer, but protects from GEJ-cancers. With the disappearance of H. pylori, the gastric cancer rate decreased, however the GEJ rate increased!
The gastric cancer hands over to the esophageal cancer!
But not only the rise of esophageal cancer, but also the increase of a “new” class of stomach cancer has been observed by William Anderson and his colleagues at NIH: it is new because it is strongly age-specific and even more gender-specific. Although overall gastric cancers decreased, this is only true for a population over 50 years of age. In the population aged below 50 years, the incidence to gastric cancers increases, at 1.3% annually.
This new kind of gastric cancer is more pronounced in women
This new kind of gastric cancer is more pronounced in women than in men, in the population younger than 50 years, although gastric cancer has always been more common in men. This new type of cancer is called the CYF-dominant cancers for corpus-dominant, since it is centered in the gastric corpus, young age-dominant and female-dominant.
The important question is, what is causing this new disease?
Blaser and colleagues have different hypotheses which all end up in a changed microbiome. First of all, the disappearance of the dominant gastric inhabitant H. pylori made space for other bacteria to colonize the stomach. These new inhabitants might be especially injurious to the gastric mucosa. Next, the CYF cancer increase parallels the antibiotic era in timing.
The rise of antibiotic exposure altered the microbiome of the western civilization which in turn may have been fueling the development of CYF cancers. Last but not least, auto-immune diseases also lead to changes in the microbial composition and are more prevalent in women. This might be the third explanation for the development of this specific cancer due to a changed microbiome.
“Combined studies of antibiotic exposure, microbiota, cancer subtypes and premalignant states together will allow hypothesis testing” Martin Blaser states in his publication.
We are lucky that Blaser, Anderson and colleagues made these very important observations, now we have to wait for further understanding of the cause of these shifts in cancer development.
