Purpose The purpose of this paper is to apply the self-concept theory and conservation of resources theory to develop a model that explains how both corporate social responsibility (CSR) and ethical leadership influence turnover intention through work engagement and burnout. Design/methodology/approach A survey of employees from banking industry in Taiwan and the research hypotheses were empirically tested by two-step structural equation modeling (SEM) and regression analysis. Findings The empirical findings indicate that CSR and ethical leadership are both related to work engagement positively and burnout negatively. Turnover intention is affected by work engagement negatively and burnout positively. While the relationship between CSR and work engagement is positively moderated by ethical leadership, the relationship between burnout and turnover intention is negatively moderated by self-efficacy. Research limitations/implications This study confirms that both CSR and ethical leadership play critical roles for influencing turnover intention through the mediation of work engagement and burnout. The moderating effects of ethical leadership and self-efficacy are also presented in this study. Practical implications The authors’ findings bring some suggestions for managers who want to prevent high turnover intention from spreading all over their organization. Specifically, CSR and ethical leadership should be taken into account when managers develop their strategies to reduce turnover intention. Originality/value This study analyzes how turnover intention takes shape from ethical perspectives and through which work-related state of mind (such as burnout, work engagement) can turnover intention be eventually affected.

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Male breast cancer comprises less than 1% of breast cancer diagnoses. Although estrogen exposure has been causally linked to the development of female breast cancers, the etiology of male breast cancer is unclear. Here, we show via fluorescence in situ hybridization (FISH) and droplet digital PCR (ddPCR) that the Y chromosome was clonally lost at a frequency of ~16% (5/31) in two independent cohorts of male breast cancer patients. We also show somatic loss of the Y chromosome gene TMSB4Y in a male breast tumor, confirming prior reports of loss at this locus in male breast cancers. To further understand the function of TMSB4Y, we created inducible cell lines of TMSB4Y in the female human breast epithelial cell line MCF-10A. Expression of TMSB4Y resulted in aberrant cellular morphology and reduced cell proliferation, with a corresponding reduction in the fraction of metaphase cells. We further show that TMSB4Y interacts directly with β-actin, the main component of the actin cytoskeleton and a cell cycle modulator. Taken together, our results suggest that clonal loss of the Y chromosome may contribute to male breast carcinogenesis, and that the TMSB4Y gene has tumor suppressor properties.