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Additional copies of a 25 Mb chromosomal region originating from 17q23.1‐17qter are present in 90% of high‐grade neuroblastomas
Author(s) -
Meddeb Mounira,
Danglot Gisèle,
Chudoba Iise,
Vénuat AnneMarie,
Bénard Jean,
AvetLoiseau Hervé,
Vasseur Béatrice,
Le Paslier Denis,
TerrierLacombe MarieJose,
Hartmann Olivier,
Bernheim Alain
Publication year - 1996
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199611)17:3<156::aid-gcc3>3.0.co;2-3
Subject(s) - neuroblastoma , chromosomal translocation , biology , chromosomal abnormality , chromosome , cancer research , genetics , karyotype , gene , cell culture
Neuroblastoma shows remarkable heterogeneity, ranging from spontaneous regression to progression toward highly malignant tumors. In search of genetic abnormalities that could explain this variability, we have characterized neuroblastoma tumors by using multiple fluorescent hybridizations. Our results indicate that chromosome 17 is rearranged very frequently in the form of unbalanced translocations with numerous chromosomal partners, all leading to the presence of supernumerary copies of a 25 Mb chromosomal region originating from 17q23.1‐qter. Additional 17q material was detected in more than 90% of untreated high‐grade neuroblastomas and, along with 1p36 deletion, should represent the most frequent genetic abnormality of neuroblastoma observed until now. Genes Chromosom Cancer 17:156–165 (1996). © 1996 Wiley‐Liss, Inc.