Corporate governance and management earnings forecast behaviour:Evidence from a low private litigation environment

Purpose The purpose of our study is to examine the influence of three external corporate governance mechanisms (continuous disclosure regulatory reform, analyst following and ownership concentration) and one internal corporate governance mechanism (board structure) on the likelihood, frequency, horizon, precision and accuracy of management earnings forecasts in the low private litigation environment of New Zealand. Design/methodology/approach The authors use a sample of 1,082 management earnings forecasts issued by 125 firms listed on the New Zealand Exchange during the 1998-2007 financial reporting periods. The authors effectively control the self-selection bias problem inherent in management earnings forecasts. Findings The findings provide strong evidence that corporate governance significantly influences management earnings forecast behaviour. Firms with effective corporate governance tend to forecast earnings and provide these earnings forecasts more frequently and precisely. Earnings forecasts issued by firms with more non-executive directors on the board are less optimistically biased. A possible interpretation of the findings is that effective corporate governance mechanisms are able to substitute for a private enforcement alternative. Originality/value The findings have value in informing governance choices in the absence of external disciplinary mechanisms such as private litigation

Low levels of nuclear ß-catenin coincide with high levels of E-cadherin in BCC.

<p><b>A.</b> Microphotographs of selected sample of ß-catenin, showing nuclear staining only at the periphery or the tumor. Bar = 200 µm. <b>B.</b> Microphotographs of selected sample of E-cadherin showing lowered expression of the tumor compared with the normal epidermis.</p

Sample characteristics.

*<p>FFPE =  Formalin-fixed, paraffin-embedded, FF =  Fresh- frozen.</p

Expression of SHH, APC, SFRP5 and RASSF1A is reduced in BCC versus healthy skin control tissue.

<p><b>A.</b> Relative expression levels of <i>APC</i> and <i>SFRP5 i</i>n BCC tissues as compared to the expression level in normal skin (n = 6) (2−^ΔΔCt). All reactions were done in triplicates, standard error of the mean (SEM) is shown as error bars. Expression levels were normalized to Cyclophilin A. U, unmethylated sample; M, methylated sample. *p≤0.05, **p≤0.001. <b>B.</b> Relative mRNA expression in unmethylated versus methylated BCC samples for either <i>APC</i> or <i>SFRP5. </i><b>C.</b> Microphotographs of selected samples of SHH, APC and RASSF1A. Bar = 200 µm.</p

N-Myc Downstream-Regulated Gene 4 (NDRG4): A Candidate Tumor Suppressor Gene and Potential Biomarker for Colorectal Cancer

BACKGROUND: Identification of hypermethylated tumor suppressor genes in body fluids is an appealing strategy for the noninvasive detection of colorectal cancer. Here we examined the role of N-Myc downstream-regulated gene 4 (NDRG4) as a novel tumor suppressor and biomarker in colorectal cancer. METHODS: NDRG4 promoter methylation was analyzed in human colorectal cancer cell lines, colorectal tissue, and noncancerous colon mucosa by using methylation-specific polymerase chain reaction (PCR) and bisulfite sequencing. NDRG4 mRNA and protein expression were studied using real-time-PCR and immunohistochemistry, respectively. Tumor suppressor functions of NDRG4 were examined by colony formation, cell proliferation, and migration and invasion assays in colorectal cancer cell lines that were stably transfected with an NDRG4 expression construct. Quantitative methylation-specific PCR was used to examine the utility of NDRG4 promoter methylation as a biomarker in fecal DNA from 75 colorectal cancer patients and 75 control subjects. All P values are two-sided. RESULTS: The prevalence of NDRG4 promoter methylation in two independent series of colorectal cancers was 86% (71/83) and 70% (128/184) compared with 4% (2/48) in noncancerous colon mucosa (P < .001). NDRG4 mRNA and protein expression were decreased in colorectal cancer tissue compared with noncancerous colon mucosa. NDRG4 overexpression in colorectal cancer cell lines suppressed colony formation (P = .014), cell proliferation (P < .001), and invasion (P < .001). NDRG4 promoter methylation analysis in fecal DNA from a training set of colorectal cancer patients and control subjects yielded a sensitivity of 61% (95% confidence interval [CI] = 43% to 79%) and a specificity of 93% (95% CI = 90% to 97%). An independent test set of colorectal cancer patients and control subjects yielded a sensitivity of 53% (95% CI = 39% to 67%) and a specificity of 100% (95% CI = 86% to 100%). CONCLUSIONS: NDRG4 is a candidate tumor suppressor gene in colorectal cancer whose expression is frequently inactivated by promoter methylation. NDRG4 promoter methylation is a potential biomarker for the noninvasive detection of colorectal cancer in stool samples