Folate is an essential water soluble B-vitamin required for the de novo synthesis of purines and dTMP and the synthesis of methionine. Disruption of any of the three folatedependent biosynthetic pathways has been shown to have serious implications in a cell's survival and an individual's disease risk. Folate, generally folate deficiency, has been associated with colorectal cancer (CRC) and acute lymphocytic leukemia (ALL) in epidemiological studies. However, CRC risk has also been associated with high FA intake. Previous studies have shown that FA deficiency induces higher mutant frequency (MF) in bone marrow in addition to increasing chromosomal instability in RBC. Here, we used the MutaMouse model to determine the mutagenic potential of dietary FA in the colon, and to determine if there is a tissue-and diet-specific effect induced by FA intake in colon and bone marrow. Male mice were fed experimental FA defined diets: deficient (0 mg/kg), control (2 mg/kg) and supplemented (8 mg/kg) for 20 weeks from weaning. To determine First and foremost, I would like to thank the amazing Dr. Amanda MacFarlane who besides being an incredible scientist and my supervisor, she has also become a mentor and a role model inside and outside the lab. Also thank you for being so understanding, supporting and for embracing my uniqueness and culture ;). Thank you, Dr. Alex Wong, for all your teachings and being my first formal introduction into programming. You and Dr. MacFarlane are not only two exemplary scientists but also individuals and parents. Also, a special thanks to my thesis supervisory committee, Dr.
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