However, the Aspirin/Folate Polyp

Prevention Trial demonstrated that about 67% increased risk of advanced lesions with high malignant potential, and an increased risk of having multiple adenomas among the folic acid supplementation group by providing folic acid for 6 years at 1 mg/d [14]. While other researches have reported that there is no relation or positive association between folic acid supplementation selleck chemical and the risk of colon adenoma [15]. Therefore, a systematic description from RCTs investigating the relation between folic acid supplementation and the risk of colorectal cancer was conducted by many groups. One recent Meta-analysis data revealed that folic acid supplementary for 3 years had no effect on the adenoma recurrence while had an increased risk of adenoma lesion for those who received folic Navitoclax research buy acid over 3 years [16]. Another Meta-analysis divided the RCTs into different groups including

populations with a history of adenoma and with an-average risk populations. They concluded that the evidence that folic acid was effective in the chemoprevention of colorectal cancer was not enough in both populations [17]. Further, many researchers consider that the role of folic acid might be two-sided, that is to prevent in early phage of adenoma formation and to promote in late stage depending on the time of folic acid administration. Preclinical studies have suggested that folic acid

may only protect against the development of CRC in normal colon-rectum rather in mucosa with an Aberrant Crypt Foci (ACF) status [18], which is the earliest pre-neoplastic lesion that can be recognized based on the morphology and pathology features [19, 20], and the results were consistent with an AOM induced rat model of CRC [21]. These experiments demonstrated that folic acid had dual effects on the development of CRC depending on the timing and dose of the intervention of folic acid next [11] However, the function that folic acid may perform to the exiting adenomas in chemicals induced mouse model and the possible mechanism is still un-established now. In this study, we use ICR mice with 1, 2-Dimethylhydrazine (DMH) interfered models to analyze the impact of folic acid on different timing courses during the processes of CRC. We have previously demonstrated that 4 weeks old ICR mice given high dosage (8 mg/ml) folic acid for 20 weeks have much more apparent effects to prevent CRC incidence than low folic acid dosage (4 mg/kg bodyweight) group using DMH-induced mice model [9]. Therefore, to investigate the role of folic acid in the process of adenoma formation, we use the dose of 8 mg/kg bodyweight.