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The profound influence that nutrients have on the development of colon cancer is reflected in diet induced acceleration and amplification of tumor formation, and modulation of tumor phenotype, in even the most penetrant of mouse genetic models of intestinal cancer. Moreover, a Western-style mouse diet that mimics the levels of major risk factors for colon cancer (higher fat, lower calcium and vitamin D) can initiate mouse colon tumor formation when fed over two-thirds of the lifespan. Tumor formation in this model of dietary induced sporadic cancer, as well as in mouse genetic models is highly sensitive to calcium and vitamin D levels in the diet. We used the interaction of dietary and genetic factors in the mouse to probe molecular changes in the mucosa that alter probability of tumor formation. Alterations in cell maturation as cells migrate from the progenitor cell compartment are fundamental to tumorigenesis, and shifts in metabolic pathways may also play a significant role in perturbing complex transcriptional and signaling networks that normally maintain homeostasis and proper functioning of the intestinal mucosa.
Leonard Augenlicht, Ph.D.
Albert Einstein Cancer Center
Montefiore Medical Center