Reply to Mohlin et al.: High levels of EPAS1 are closely associated with key features of low-risk neuroblastoma

Our principal aim was not to explore the role of EPAS1 /HIF2α in neuroblastoma (NB). Neither do we claim to present conclusive data showing that HIF2α is a bona fide NB tumor suppressor. We simply followed our analysis of the transcriptional response induced by 5-aza-deoxycytidine (AZA)+retinoic acid (RA) treatment to the analysis of large ( n = 498 + 649) sequenced/microarrayed NB cohorts. We show that EPAS1 /HIF2α expression strongly correlates with better outcome and low-risk NB, while being inversely correlated with key features of high-risk NB. Thus, our analysis indicates a possible tumor suppressor role and question whether HIF2α is a NB oncogene (1). The claim that we have not measured HIF2α protein levels in NB (2) is simply … [↵][1]1To whom correspondence should be addressed. Email: johan.holmberg{at}ki.se. [1]: #xref-corresp-1-1