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  The authors noted that possible mechanisms of action included a genetic predisposition in patients with familial cancer syndromes -- such as hereditary nonpolyposis colorectal cancer -- or misclassification of metastases as a new primary cancer. "Our data also support the hypothesis that the elevated risk of second primary small intestinal, stomach, bladder, and lung cancer reflects the shared origin of the endoderm-derived epithelia at these sites," they also noted.