2002
DOI: 10.1016/s0165-4608(01)00521-0
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Comparative genomic hybridization in ganglioneuroblastomas

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Cited by 11 publications
(9 citation statements)
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“…Moreover, these regions of gain have also been reported in other array studies on neuroblastoma. 23,24,[28][29][30]38 Thus, although our results suggest there may be a genetic profile characteristic of nodular ganglioneuroblastoma, it would not appear to distinguish this subtype of neuroblastoma from others. In our series, there was no correlation between the total number of copy number alterations or specific gains and losses and histologic prognostic categories (favorable vs unfavorable) or patient outcome.…”
Section: Discussioncontrasting
confidence: 66%
See 1 more Smart Citation
“…Moreover, these regions of gain have also been reported in other array studies on neuroblastoma. 23,24,[28][29][30]38 Thus, although our results suggest there may be a genetic profile characteristic of nodular ganglioneuroblastoma, it would not appear to distinguish this subtype of neuroblastoma from others. In our series, there was no correlation between the total number of copy number alterations or specific gains and losses and histologic prognostic categories (favorable vs unfavorable) or patient outcome.…”
Section: Discussioncontrasting
confidence: 66%
“…13,[17][18][19] Neuroblastoma is characterized by multiple chromosomal abnormalities (reviewed in refs 1,3), but whether these are shared by the nodular ganglioneuroblastoma subtype is not known. Genome-wide approaches such as array comparative genomic hybridization [20][21][22][23][24][25] and single-nucleotide polymorphism arrays 26,27 have been used to identify whole chromosome and segmental gains and losses in neuroblastoma; however, only two studies specifically mentioned the inclusion of ganglioneuroblastoma samples 28,29 and results were inconsistent. The neuroblastoma component is thought to have a clonal origin distinct from the ganglioneuromatous part of the tumor.…”
mentioning
confidence: 99%
“…For primary glioblastoma-specific MCRs, there are 23 gains/amplifications with a median size of 0.87 Mb and median number of 13 genes. Of these 23 loci, 6 represent loci that have been significantly narrowed and 11 loci have not been described in glioblastoma, yet their cancer relevance is reinforced by validated connections to other cancer types such 2p25 in ganglioneuroblastoma (29), 6p25 in uveal melanoma (30), and 17q21 in medulloblastoma (ref. 31; Table 2).…”
Section: Comparison Of Primary and Secondary Glioblastoma Genomic Promentioning
confidence: 99%
“…Interestingly, a recent research analysing of stage 4 and 4S NB, suggests that 11q loss might appear at early stages of metastatic tumorigenesis, preceding 3p loss [125]. CGH analysis of ganglioneuroblastoma (GNB) showed no 11q deletion, suggesting that this event might occur rarely in this less aggressive NB subgroup [126]. Similar results were obtained by Coco et al and Bourdeaut et al where CGH did not show any abnormalities at chromosome 11 in ganglioneuroma (GN) and GNB intermixed, while 11q loss was detected in NB [127, 128].…”
Section: Introductionmentioning
confidence: 99%