Open AccessAmplification of the MYCN oncogene and deletion of putative tumour suppressor gene in human neuroblastomas
Author(s) -
Schwab Manfred
Publication year - 1990
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.1990.tb00637.x
Subject(s) - suppressor , neuroblastoma , cancer research , oncogene , gene , n myc , oncogene proteins , biology , tumor suppressor gene , gene duplication , genetics , carcinogenesis , regulation of gene expression , ganglioneuroma , cell culture , cell cycle
Human neuroblastoma cells often carry non‐random chromosomal abnormalities signalling genetic alterations. Quite frequent are ‘double minutes’ (DMs) and homogeneously staining regions (HSRs), both cytogenetic manifestations of amplified DNA, and chromosome Ip‐deletions indicating loss of genetic information. With the identification of amplified MYCN and the demonstration of a consensus deletion spanning the chromosome 1p36.1–2 region it appears now likely that both amplification of a cellular oncogene and loss of a tumour‐suppressor gene play an important role in neuroblastoma. Amplification of MYCN is an indicator for poor prognosis, even when classical morphological criteria would suggest a better outcome. Consequently, patients with amplification are subjected to more intensive therapeutic regimens. Amplification of MYCN is a paradigm for the clinical use of an oncogene alteration.