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Comparative genomic hybridization (CGH) analysis of stage 4 neuroblastoma reveals high frequency of 11q deletion in tumors lacking MYCN amplification
Author(s) -
Plantaz D.,
Vandesompele J.,
Van Roy N.,
Łastowska M.,
Bown N.,
Combaret V.,
Favrot M.C.,
Delattre O.,
Michon J.,
Bénard J.,
Hartmann O.,
Nicholson J.C.,
Ross F.M.,
Brinkschmidt C.,
Laureys G.,
Caron H.,
Matthay K.K.,
Feuerstein B.G.,
Speleman F.
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(200002)9999:9999<::aid-ijc1114>3.0.co;2-r
Subject(s) - comparative genomic hybridization , neuroblastoma , biology , gene duplication , genetics , cancer research , genome , gene , cell culture
We have studied the occurrence and association of 11q deletions with other chromosomal imbalances in Stage 4 neuroblastomas. To this purpose we have performed comparative genomic hybridization (CGH) analysis on 50 Stage 4 neuroblastomas and these data were analyzed together with those from 33 previously published cases. We observed a high incidence of 11q deletion in Stage 4 neuroblastoma without MYCN amplification (59%) whereas 11q loss was only observed in 15% of neuroblastomas with MYCN ‐amplification ( p = 0.0002) or 11% of cases with 1p deletion detected by CGH ( p = 0.0001). In addition, 11q loss showed significant positive correlation with 3p loss ( p = 0.0002). Event‐free survival was poor and not significantly different for patients with or without 11q deletion. Our study provides further evidence that Stage 4 neuroblastomas with 11q deletions represent a distinct genetic subgroup that typically shows no MYCN ‐amplification nor 1p deletion. Moreover, it shows that neuroblastomas with 11q deletion also often present 3p deletion. This genetic subgroup shows a similar poor prognosis as MYCN amplified 4 neuroblastomas. © 2001 Wiley‐Liss, Inc.