Format

Send to

Choose Destination
Cell Mol Life Sci. 2018 Mar;75(6):1057-1070. doi: 10.1007/s00018-017-2685-8. Epub 2017 Oct 22.

WNT signaling, the development of the sympathoadrenal-paraganglionic system and neuroblastoma.

Author information

1
Institute of Anatomy and Cell Biology, University Medical School Göttingen, 37075, Göttingen, Germany. juergen.becker@med.uni-goettingen.de.
2
Institute of Anatomy and Cell Biology, University Medical School Göttingen, 37075, Göttingen, Germany.

Abstract

Neuroblastoma (NB) is a tumor of the sympathoadrenal system arising in children under 15 years of age. In Germany, NB accounts for 7% of childhood cancer cases, but 11% of cancer deaths. It originates from highly migratory progenitor cells that leave the dorsal neural tube and contribute neurons and glial cells to sympathetic ganglia, and chromaffin and supportive cells to the adrenal medulla and paraganglia. Clinically, histologically and molecularly, NBs present as extremely heterogeneous, ranging from very good to very poor prognosis. The etiology of NB still remains unclear and needs to be elucidated, however, aberrant auto- and paracrine embryonic cell communications seem to be likely candidates to initiate or facilitate the emergence, progression and regression of NB. The wingless-type MMTV integration site (WNT) family of proteins represents an evolutionary highly conserved signaling system that orchestrates embryogenesis. At least 19 ligands in the human, numerous receptors and co-receptors are known, which control not only proliferation, but also cell polarity, migration and differentiation. Here we seek to interconnect aspects of WNT signaling with sympathoadrenal and paraganglionic development to define new WNT signaling cues in the etiology and progression of NB.

KEYWORDS:

Neural crest; Neuroblastoma; Paraganglion; Sympathoadrenal system

PMID:
29058015
PMCID:
PMC5814469
DOI:
10.1007/s00018-017-2685-8
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center