Erratum BDNF splice variants from the second promoter cluster support cell survival of differentiated neuroblastoma upon cytotoxic stress

The author's names were wrongly given as Baj Gabriele and Tongiorgi Enrico. The correct names appear in the print and online versions of the article. We apologise for this mistake. Introduction The neurotrophin brain-derived neurotrophic factor (BDNF), is known to regulate a large spectrum of developmental processes of the nervous system, including cell survival, growth and differentiation (Casaccia-Bonnefil et al., 1999; Bibel and Barde, 2000; Huang and Reichardt, 2003). In transformed cells, BDNF can promote differentiation and cell survival even under conditions of cytotoxic stress as in the case of neuroblastoma, a tumour derived from the neural crest that is responsible for at least 15% of cancer-related deaths in children (Brodeur et al., 1992; Matthay, 1995). A large number of poor prognosis neuroblastoma tumours consistently express BDNF and differentially express the gene encoding its tyrosine kinase TrkB receptor (Brodeur et al. By contrast, neuroblastoma tumours with a good prognosis typically produce high levels of TrkA, the signal-transducing receptor for nerve growth factor (Nakagawara and Brodeur, 1997; Yamashiro et al., 1997). In addition, a subset of neuroblastoma tumours with extremely aggressive growth potential has been shown to be characterised by amplified levels of N-myc (reviewed by Schwab, 2004). N-myc belongs to the Myc/Max/Mad family of proto-oncogenes encoding transcription factors of the basic-helix-loop-helix-zipper (bHLHZ) class, which regulate the expression of several genes by binding to E-box sequences (Grandori et al., 2000). Early in embryogenesis, N-myc is present primarily in migrating neural crest cells where it promotes cell division and inhibits cellular differentiation; however, later in development, production of N-myc becomes limited to those cells that are undergoing neuronal