In the aggressive SDHB-PHEOs/PGLs into the related energy metabolism pathways, we evaluated the 4-(Benzyloxy)phenol expression of several glycolysis and OXPHOS genes in the human tumors, and in some cases in normal adrenal medulla. We confirmed an elevated GLUT1 and HK2 mRNA expression in VHL- relative to SDHB-PHEOs/PGLs and put it into perspective to normal adrenal 
medulla. Elevated HK2 expression is considered a driving force towards a glycolytic phenotype. Increased HK2 expression reportedly leads to enhanced proliferation and resistance to cell death in culture and correlates with poor prognosis in human glioblastoma multiforme. Since VHL-PHEOs/PGLs have a better prognosis than SDHB-PHEOs/PGLs, the difference in HK2 does not seem to contribute to their distinct tumor aggressiveness in these particular tumors. Previously, decreased OXPHOS activity and expression of selected OXPHOS complex subunits have been reported for VHL-derived PHEOs/PGLs. When comparing VHLand SDHB-derived tumor tissues, in the latter we observed the expected decrease in complex II activity, but also an increase in complex III activity. In addition, we found the activity of CS, the first enzyme of the Krebs’ cycle, to be elevated in SDHB-derived tumors. Similar to the data presented by Goffrini et al., our data indicates a selective decrease of complex II activity in SDHBderived PGLs; however there is no evidence for complete disruption of OXPHOS. While we assume that the subunits we evaluated are crucial for the function of the respective complexes, we cannot exclude that they may not reflect the expression levels of other subunits of the same complexes and complex activity. In the present study, findings from the differential expression analysis of the aggressive MTT cells compared to MPC guided our choice for the evaluation of key players in glycolysis and OXPHOS in human SDHB- and VHL-derived PHEOs/PGLs, as a first step in uncovering potential causes for increased tumor aggressiveness in SDHB-related tumors. Our data confirm that both SDHB- and VHL-related PHEOs/PGLs show features of a glycolytic phenotype, while presenting further support for the presence of distinct mechanisms of manifestation of the Warburg effect. In-depth analysis of the roles of elevated LDHA as well as elevated H2O2 production as a possible result of increased SOD2 expression may lead to a better understanding of these tumors and discovery of potential new therapeutic targets for the aggressive phenotype related to SDHB-mutations. Ovarian cancer represents the most Orbifloxacin lethal gynecological malignant disease in the United States. According to the American Cancer Society, if diagnosed at the localized stage, the 5-year survival rate is 94%; however, only 15% of all cases are detected at this stage. The majority of cases of ovarian cancer are diagnosed with distant metastases. For these women the 5-year survival rate is 28%, therefore determining the unique genetic programming that drives ovarian cancer progression is key in diagnosing and treating this disease. We previously identified ARID3B as a target of miR-125a, a microRNA that is under expressed in ovarian cancer. However, the function of ARID3B is relatively unknown. ARID3B belongs to the ARID family of proteins. The ARID family of transcriptional regulators is a conserved group of DNA binding proteins that regulates gene expression. ARID proteins harbor a distinctive DNA-binding domain, the AT-rich interactive domain. Proteins of this family have been implicated in regulation of cell cycle, gene expression, differentiation, embryonic development, chromatin remodeling and transcriptional regulation. Thus, ARID3B could be key regulator in ARID3A function by regulating cellular localization in B cells. Since ARID3B is expressed more broadly than ARID3A it likely has other functions than its regulation of ARID3A.