Mutations or lack of expression of these genes have been implicated in many disorders

Colon cancer is the third most common form of cancer and the second leading cause of cancer-related deaths in American adults. The incidence of this disease in African Americans is higher than in the general population. African Americans are also more likely to die from colon cancer than others. There are different participating factors in colon carcinogenesis. Genetic factors impact gene or genome structures and integrity while epigenetic parameters have an effect on DNA structure and expression while environmental factors such as diet and its interaction with the gut flora impacts the colon mucosa through the metabolic products’ effects on colon tissue homeostasis. The metabolic byproducts are channeled through the colon mucosa by a set of genes of which the primary function is molecules’ transport. The SLC gene family encodes a group of proteins that are involved in such transport through cell membranes. Mutations or lack of expression of these genes have been implicated in many disorders. SLC5A8, also called SMCT for sodium-coupled monocarboxylate transporter, is a member of the SLC gene family and have been extensively studied. This gene is expressed in the retina, brain, kidney, thyroid and in the gastrointestinal system. It has been shown that the SLC5A8 protein sit within the apical membrane of the intestinal tract where it is involved in the absorption of short chain fatty acids into the colon. Butyrate, a byproduct of bacterial fermentation, has been proven to have anti-proliferative characteristics. As such,Carfilzomib SLC5A8 gene product that is involved in its transport through the colon mucosa have been labeled as a tumor suppressor gene. It has also been shown that butyrate impacts cell proliferation through its effect on histones acetylation status. Histone modifi- cation is very instrumental in the expression level of genes within the cell. Consequently, butyrate transport by SLC5A8 gene product impacts the expression level of many genes that are likely involved in the negative control, anti-proliferative, of the cell cycle within the colon mucosa. This gene’s involvement in cancer has already been highlighted in many studies. Indeed, Park et al have already shown that both pancreatic and prostate cancers display an SLC5A8 methylation level of 70% unlike in the adjacent non-tumor tissues. A similar situation was reported by Bennett et al. in head and neck squamous cell carcinoma patients. Using a Restriction Landmark Genomic Scanning technique, they found five methylation markers among which SLC5A8 gene. The other genes were SEPT9, FUSSEL18, EBF3 and IRX1. While studying posttranslational histones modifications in mixed lineage leukemia, Whitman et al., found that such modifications are generally associated with a hypermethylation profile in which SLC5A8 gene plays a central role. A recent study by Thangaraju et al have shown that SLC5A8 is silenced in humans, in cell lines and CHIR-99021 in a mouse model of colon cancer. Their findings strengthen earlier results by Li et al. They also proved that the re-expression of SLC5A8 in colon cancer cell lines in the presence of butyrate leads to apoptosis through the up-regulation of pro-apoptotic genes and down-regulation of proliferative genes. Most of the studies on SLC5A8 were done on cancer samples and none has checked in adenomas. As such, we here propose to analyze the methylation status of SLC5A8 gene in African American colon adenomas with the goal of finding early colon cancer markers in this group of patients to mitigate the high incidence of the disease in this group. Histones expression profiles was assessed using a proteomic analysis.