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Genomic typing was performed by using PCR with sequence-specific primers specific for HLA class II molecules [ 43, 44].
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A segmental genomic type was more frequent in patients >18 months and in stage 4 disease (P<0.0001).
A segmental genomic type was observed more frequently in stage 4 disease and in children aged >18 months (Table 1).
In particular, a segmental genomic type was associated with a significantly poorer EFS in the 86 patients older than 18 months with non-stage 4 disease (P<0.02).
A genomic type was attributed to all analysed samples, taking into account all observed genomic alterations, as described previously, with slight modifications (Janoueix-Lerosey et al, 2009; Schleiermacher et al, 2010).
Among these 505 patients, 108 cases had no segmental chromosomal alterations, whereas in 397 other cases a segmental genomic type was observed, with the chromosome status known at all three chromosomal loci in 221 cases.
According to one hypothesis, the genomic type is thought to reflect an underlying genomic abnormality.
In univariate analysis, 11q deletion, 17q gain and a segmental genomic type were associated with a poorer event-free survival (EFS) (P<0.0001, P=0.0002 and P<0.0001, respectively).
In multivariate analysis modelling EFS, the parameters age, stage and a segmental genomic type were retained in the model, whereas the individual genetic markers were not (P<0.0001 and RR=2.56; P=0.0002 and RR=1.8; P=0.01 and RR=1.7, respectively).
Likewise, in a multivariate analysis modelling for OS, the same parameters age, stage and a segmental genomic type were retained in the model (P<0.0001 and RR=4.6; P<0.0001 and RR=3.1; P=0.05 and RR=1.8, respectively).
Four genomic types were subsequently defined taking into account the status of chromosomes 3 and 8: tumours with disomy 3 and normal dosage of chromosome 8 (named as 'D3/8nl'), monosomy 3 and normal dosage of chromosome 8 ('M3/8nl'), disomy 3 and any type of gain of chromosome 8 ('D3/8g') and monosomy 3 with any type of gain of chromosome 8 ('M3/8g').
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