Cash contributions to defined benefit pension (DB) plans reduce cash flows from operations without directly affecting the current year's net income. We utilize this unique setting to investigate how managerial incentives to report higher cash flows from operations, executive compensation in particular, affect contributions. Using a comprehensive dataset of DB plan contributions, we find that firms with higher chief executive officer (CEO) compensation contribute less to DB plans, consistent with managers benefiting from lower pension contributions. Results are stronger when CEO compensation is directly linked to cash flows from operations or when CEO compensation is more sensitive to cash flows from operations. We also find enhanced disclosure and more transparent reporting under the recent pension accounting regime mitigates the negative association between executive compensation and cash contributions.
Background
To assess the feasibility of a novel DNA‐based probe panel to detect copy number alterations (CNAs) in prostate tumor DNA and its performance for predicting clinical progression.
Methods
A probe panel was developed and optimized to measure CNAs in trace amounts of tumor DNA (2 ng) isolated from formalin‐fixed paraffin‐embedded tissues. Ten genes previously associated with aggressive disease were targeted. The panel's feasibility and performance were assessed in 175 prostate cancer (PCa) patients who underwent radical prostatectomy with a median 10‐year follow‐up, including 42 men who developed disease progression (either metastasis and/or PCa‐specific death). Association with disease progression was tested using univariable and multivariable analyses.
Results
The probe panel detected CNAs in all 10 genes in tumor DNA isolated from either diagnostic biopsies or surgical specimens. A four‐gene model (PTEN/MYC/BRCA2/CDKN1B) had the strongest association with disease progression; 64.3% of progressors and 22.5% of non‐progressors had at least one CNA in these four genes, odds ratio (OR) (95% confidence interval) = 6.21 (2.77‐13.87), P = 8.48E−06. The association with disease progression remained significant after adjusting for known clinicopathological variables. Among the seven progressors of the 65 patients with clinically low‐risk disease, three (42.9%) had at least one CNA in these four genes.
Conclusions
The probe panel can detect CNAs in trace amounts of tumor DNA from biopsies or surgical tissues at the time of diagnosis or surgery. CNAs independently predict metastatic/lethal cancer, particularly among men with clinically low‐risk disease at diagnosis. If validated, this may improve current abilities to assess tumor aggressiveness.
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