Neural crest development and neuroblastoma: the genetic and biological link

GATA factors in human neuroblastoma: distinctive expression patterns in clinical subtypes

“…Thus, GATA factors have been associated with favourable or unfavourable tumours, depending on the type of cancer. In neuroblastoma, favourable tumour subtypes have been described to be more differentiated on the molecular level (Ohira et al, 2003;Nakagawara, 2004;Fischer et al, 2006). Accordingly, GATA-2 overexpression has been shown to cause differentiation of human neuroblastoma SK-N-BE2 cells (Kaneko et al, 2006).…”

“…Although younger patients with localised tumours and those with stage 4S disease have an excellent prognosis and often follow spontaneous regression, the outcome of older patients with disseminated disease (stage 4) is still very poor despite intensive multimodal treatment (Maris et al, 2007). Although the exact mechanisms leading to the divergent neuroblastoma phenotypes have yet not been characterised, it has been noticed that markers of neuronal differentiation are downregulated in unfavourable tumours (Ohira et al, 2003;Nakagawara, 2004;Fischer et al, 2006). From these data it has been suggested that de-regulation of normal developmental pathways may contribute to the pathogenesis of the biologically distinct neuroblastoma subtypes.…”

Novel risk stratification of patients with neuroblastoma by genomic signature, which is independent of molecular signature

“…The GGP group is characterized by the presence of 17q gain with other chromosomal abnormalities including MYCN amplification, 1p loss and 11q loss. Since this group of tumors shows multiple chromosomal aberrations with partial gains and/or losses, unknown causes to induce genomic instability might have triggered genesis of neuroblastoma in progenitor or stem cells of sympathetic cell lineage (Maris and Matthay, 1999;Nakagawara, 2004). The frequently observed GGP tumors are as follows: GGP1a tumors with both 1p loss and MYCN amplification and GGP3s tumors with 11q loss but without MYCN amplification.…”

“…Since the pattern of chromosomal aberrations is represented by whole chromosomal gains and/or losses, mitotic dysfunction during the cell division cycle in progenitor or stem cells might have generated neuroblastoma (Maris and Matthay, 1999;Nakagawara, 2004). Interestingly, 1p loss or 11q loss in a minor population of GGWs tumors (GGW1s and GGW3s) seems not to affect the prognosis.…”

Unravelling the Mechanism of TrkA-Induced Cell Death by Macropinocytosis in Medulloblastoma Daoy Cells

“…MEDs arise from progenitor cells in the cerebellum (3) while NBs arise from undifferentiated sympathoadrenal cells of neural crest origin (2,4). In general, the age of onset for both MEDs and NBs is an important determinate of the final prognosis, with complete regression often being reported in children under 1 year of age.…”