The Wallis Report and Implications of Bank Mergers for Efficiencies

This paper examines the competitive consequences of bank mergers and acquisitions with particular reference to the Wallis Inquiry into the Australian Financial System in 1996. The Government responded by adopting a four pillars policy preventing mergers among the four major banks. Using the super-efficiency data envelopment analysis model, the technical efficiencies of banks operating in Australia over the period from 1983 to 2001 are estimated. Two separate methods are employed to evaluate the characteristics and determinants of merger and acquisition activities in the sector. The first method examines economic performance of banks involved in merger activities. A second method is also used to determine program efficiency differences between banks of different entry types after adjusting for differences in intra-group managerial inefficiency. The empirical results demonstrate the role of takeover in improving efficiency performance of individual banks, banks of different types and the entire Australian banking sector. Conclusions and policy implications are drawn.bank mergers, data envelopment analysis, technical efficiency, super efficiency

SREBP1-dependent de novo fatty acid synthesis gene expression is elevated in malignant melanoma and represents a cellular survival trait.

de novo fatty acid biosynthesis (DNFA) is a hallmark adaptation of many cancers that supports survival, proliferation, and metastasis. Here we elucidate previously unexplored aspects of transcription regulation and clinical relevance of DNFA in cancers. We show that elevated expression of DNFA genes is characteristic of many tumor types and correlates with poor prognosis, especially in melanomas. Elevated DNFA gene expression depends on the SREBP1 transcription factor in multiple melanoma cell lines. SREBP1 predominantly binds to the transcription start sites of DNFA genes, regulating their expression by recruiting RNA polymerase II to promoters for productive transcription elongation. We find that SREBP1-regulated DNFA represents a survival trait in melanoma cells, regardless of proliferative state and oncogenic mutation status. Indeed, malignant melanoma cells exhibit elevated DNFA gene expression after the BRAF/MEK signaling pathway is blocked (e.g. by BRAF inhibitors), and DNFA expression remains higher in melanoma cells resistant to vemurafenib treatment than in untreated cells. Accordingly, DNFA pathway inhibition, whether by direct targeting of SREBP1 with antisense oligonucleotides, or through combinatorial effects of multiple DNFA enzyme inhibitors, exerts potent cytotoxic effects on both BRAFi-sensitive and -resistant melanoma cells. Altogether, these results implicate SREBP1 and DNFA enzymes as enticing therapeutic targets in melanomas