We have no indicators to find other adverse PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28381880 effects but to observe the

We have no indicators to find other adverse PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28381880 effects but to observe the injury of organs in this study. Even though there are no abnormalities discovered in other organs except colon and rectum, the function of folic acid is needed to be further studied in terms of being effective to therapy. Finally, although some similarities do exist between chemical rodent models of colon cancer and human natural CRCs, several respects of differs may also exist indeed. For example, the dose and duration of folic acid supplementation used in our study may be different from human studies. So, considering the safety of chemoprevention in clinical application, the optimal researches should be established in humans based on these findings with an initial colonoscopy before incorporated. In summary, for the first time, our data suggest that folic acid supplementary in pre-cancerous era is much more protective than that in post-cancerous stage in a DMH induced mouse model and identify differentialLin et al. Journal of Experimental Clinical Cancer Research 2011, 30:116 http://www.jeccr.com/content/30/1/Page 10 ofgenes that folic acid can reversed and that between groups of pre or post-adenoma induced by folic acid using microarray gene order BLU-554 expression profile. Not only to the reason that floate supplementation facilitates the progression of (pre)neoplastic lesions PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 though providing nucleotide precursors to the rapidly replicating transformed cells, thus accelerating proliferation [11]. We also clarified that in gene expression profile, certain oncogenes that promote tumor growth, cell cycle, cell invasion such as TNFRSF12A, fibronectin 1, Cdca7 are high expressed in FA2 group compared to FA3 group while tumor suppressors are down-regulated such as VDR, CDX2, which may partly explain the result. However, the mechanism why folic acid provided in different phages can change these genes’ expression remains to be studied.Received: 17 November 2011 Accepted: 29 December 2011 Published: 29 December 2011 References 1. Centers for Disease Control and Prevention (CDC): Vital signs: Colorectal cancer screening, incidence, and mortality nited States, 2002-2010. MMWR Morb Mortal Wkly Rep 2011, 60:884-9. 2. Holt K: Common side effects and interactions of colorectal cancer therapeutic agents. J Pract Nurs 2011, 61:7-20. 3. Kohne CH, Bruce C, Folprecht GA, udisio R: Role of new agents in the treatment of colorectal cancer. Surg Oncol 2004, 13:75-81. 4. Buchanan DD, Sweet K, Drini M, Jenkins MA, Win AK, English DR, Walsh MD, Clendenning M, McKeone DM, Walters RJ, Roberts A, Pearson SA, Pavluk E, Hopper JL, Gattas MR, Goldblatt J, George J, Suthers GK, Phillips KD, Woodall S, Arnold J, Tucker K, Muir A, Field M, Greening S, Gallinger S, Perrier R, Baron JA, Potter JD, Haile R, Frankel W, de la Chapelle A, Macrae F, Rosty C, Walker NI, Parry S, Young JP: Risk factors for colorectal cancer in patients with multiple serrated polyps: a cross-sectional case series from genetics clinics. PLoS One 2010, 5:e11636. 5. Femia AP, Luceri C, Toti S, Giannini A, Dolara P, Caderni G: Gene expression profile and genomic alterations in colonic tumours induced by 1,2-dimethylhydrazine (DMH) in rats. BMC Cancer 2010, 10:194. 6. Perse M, Cerar A: Morphological and molecular alterations in 1,2 dimethylhydrazine and azoxymethane induced colon carcinogenesis in rats. J Biomed Biotechnol 2011, 2011:473964. 7. Slattery ML, Wolff RK, Herrick JS, Curtin K, Caan BJ, Samowitz W: Alcohol consumption and rect.