Status of the 68 genes from Sjöblom et al. list (23) in the subjects of this study.

<p>The most frequently deleted genes in our samples were <i>EPHB6, EXOC4 (SEC8L1), GNAS, MLL3 and TBX22</i>. The most frequently amplified genes were <i>HAPLN1, ADAM29, SMAD2 and SMAD4</i>. Gene names are according to the official HUGO Gene Nomenclature Committee and the old names in parentheses are from Sjöblom et al.</p

Number and frequency of aberrations per chromosome.

<p>*3(3) means 3 amplification in 3 cases; 8 (5) means 8 deletions in 5 cases from total of 15 for the calculated frequency.</p

Clinical and demographic characteristics of the 15 patients enrolled in this study.

<p>Clinical and demographic characteristics of the 15 patients enrolled in this study.</p

Effects of exogenous miR-211 on the migration ability of colorectal cancer cell lines.

<p>(A) The scratched open areas were observed at hours 0, 5, 8, and 24 for HCT-116^vec and HCT-116^miR-211 cell lines under a light microscope at ×400 magnification. (B) The cells were counted from the various time period in the same size of scratch area as referenced at time 0 hr. The results of the scratch assay were from two independent experiments with triplicates and * indicated as P<0.05.</p

Effects of exogenous miR-211 on cell growth-associated proteins and p53-related pathway proteins in colorectal cancer cell lines.

<p>(A) The levels of cell growth-associated proteins in HCT-116^vec and HCT-116^miR-211 cell lines were analyzed by Western blot and (B) semi-quantified based on targeted protein/β-actin relative intensities. The levels of p53-related pathway proteins in HCT-116^vec and HCT-116^miR-211 cell lines were analyzed by Western blot (C) and semi-quantified based on targeted protein/β-actin relative intensities (D).</p

Exogenous miR-211 potentiates proliferation and growth of colorectal cancer cells <i>in vivo</i>.

<p>(A) Tumor xenograft growth of HCT-116 and HCT-116^miR-211 are shown under a light and fluorescence imaging system. The tumor mass (g) was measured on the final experimental day immediately after the tumor tissue was removed from the mouse by surgical excision. Tumor xenograft growth for HCT-116 and HCT-116^miR-211 groups was compared. (B) The day of cell inoculation was the experimental start day and all mice were sacrificed on day 43. The growth of solid tumor xenografts was monitored once a week and measured using vernier calipers.</p

Comparison of CHD5 and miR-211 expression in various colorectal cancer cell lines.

<p>(A) RNA sequence map of the 3′-UTR of CHD5 (Gene ID 26038) mRNA with the complementary site (3′-UTR 130–136) for the seed region of miRNA-211. (B) miR-211 levels in RKO, HCT-116, RKO-S, and RKO-AS cell lines by quantitative RT-PCR based on miR-211/U6 expression fold values. (C) CHD5 protein levels in two colon cancer cell lines (RKO and HCT-116) and two established cell lines (RKO-S and RKO-AS) with enforced CHD5-S expression were analyzed by Western blot and semi-quantified based on CHD5/β-actin relative intensities. Bio-Rad Quantity One software was used for densitometric analysis of the Western blots. (D) Comparison of CHD5 and miR-211 expression levels in HCT-116 and RKO cell lines. * indicated as P<0.05.</p

Exogenous miR-211 potentiates proliferation and growth of colorectal cancer cells <i>in vitro</i>.

<p>Cell proliferation and cell viability of cultured HCT-116^vec and HCT-116^miR-211 cell lines were compared using (A) colony formation assay, (B) MTT assay,and (C and D) cell cycle profiles and the distribution of cells in G1, S, and G2-M phases for each group were analyzed by flow cytometry. The results represent the mean ± SD of two independent experiments with triplicates and * indicated as P<0.05.</p

miR-211 inhibits CHD5 expression in colorectal cancer cells stably expressing exogenous miR-211.

<p>(A) Schematic representation of the miR-211 vector, which contains an expression cassette of the P_CMV promoter, EGFP, and miR-211 precursor and a selective cassette of the P_PGK promoter and Puro^r. (B) CHD5 protein levels in cell lines HCT-116^vec and HCT-116^miR-211 were evaluated by Western blot and (C) semi-quantified based on CHD5/β-actin relative intensities. (D) Luciferase reporter assay using HEK 293T cells that were transfected with either the luciferase/3′-UTR miR-211 reporter vector, the miR-211 vector, or both. Schematic representation of the luciferase-CHD5 reporter vector and luciferase reporter control vector were also inserted. * indicated as P<0.05.</p

Atrial Fibrillation and Colonic Neoplasia in African Americans

<div><p>Background</p><p>Colorectal cancer (CRC) and atrial fibrillation/flutter (AF) share several risk factors including increasing age and obesity. However, the association between CRC and AF has not been thoroughly examined, especially in African Americans. In this study we aimed to assess the prevalence of AF and its risk factors in colorectal neoplasia in an African American.</p><p>Methods</p><p>We reviewed records of 527 African American patients diagnosed with CRC and 1008 patients diagnosed with benign colonic lesions at Howard University Hospital from January 2000 to December 2012. A control group of 731 hospitalized patients without any cancer or colonic lesion were randomly selected from the same time and age range, excluding patients who had diagnosis of both CRC and/or adenoma. The presence or absence of AF was based upon ICD-9 code documentation. The prevalence of AF in these three groups was compared by multivariate logistic regression.</p><p>Results</p><p>The prevalence of AF was highest among CRC patients (10%) followed by adenoma patients (7.2%) then the control group (5.4%, P for trend = 0.002). In the three groups of participants, older age (P<0.008) and heart failure (P<0.001) were significantly associated with higher risk of AF. After adjusting for these risk factors, CRC (OR: 1.4(95%CI):0.9–2.2, P = 0.2) and adenoma (OR: 1.1(95%CI):0.7–1.6, P = 0.7) were not significantly associated AF compared to control group.</p><p>Conclusions</p><p>AF is highly prevalent among CRC patients; 1 in 10 patients had AF in our study. The predictors of AF in CRC was similar to that in adenoma and other patients after adjustment for potential confounders suggesting that the increased AF risk in CRC is explained by higher prevalence of AF risk factors.</p></div