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Background  The relevance of recurrent molecular abnormalities in cytogenetically normal (CN) acute myeloid leukemia (AML) was recently acknowledged by the inclusion of molecular markers such as  NPM1 ,  FLT3 , and  CEBPA  as a complement to cytogenetic information within both the World Health Organization and the European Leukemia Net classifications. Mitochondrial metabolism is different in cancer and normal cells. A novel cytosolic type 2-hydroxybutyrate dehydrogenase, BDH2, originally named DHRS6, plays a physiological role in the cytosolic utilization of ketone bodies, which can subsequently enter mitochondria and the tricarboxylic acid cycle. Moreover, BDH2 catalyzes the production of 2, 3-DHBA during enterobactin biosynthesis and participates in 24p3 (LCN2)-mediated iron transport and apoptosis.    Results  We observed that  BDH2  expression is an independent poor prognostic factor for CN-AML, with an anti-apoptotic role. Patients with high  BDH2  expression have relatively shorter overall survival ( P  = 0.007) and a low complete response rate ( P  = 0.032).  BDH2 -knockdown ( BDH2 -KD) in THP1 and HL60 cells increased the apoptosis rate under reactive oxygen species stimulation. Decrease inducible survivin, a member of the inhibitors of apoptosis family, but not members of the Bcl-2 family, induced apoptosis via a caspase-3-independent pathway upon  BDH2 -KD.    Conclusions   BDH2  is a novel independent poor prognostic marker for CN-AML, with the role of anti-apoptosis, through surviving.

Human BDH2, an anti-apoptosis factor, is a novel poor prognostic factor for de novo cytogenetically normal acute myeloid leukemia