Background: In neuroblastoma (NB), activating ALK receptor tyrosine kinase point mutations are detected in 8-10% of patients at diagnosis using conventional sequencing. To determine the occurrence and the prognostic impact of both high and low level clonal ALK mutations in high-risk NB patients we studied ALK variation frequencies using targeted deep sequencing in samples of patients enrolled in the HR-NBL1/SIOPEN trial.
Methods: Diagnostic NB samples from 524 high-risk NB patients were analyzed, focusing on the exons 23, 24 and 25 containing the F1174, F1245 and R1275 hotspots respectively. DNA was amplified via a two-step PCR approach, the second step consisting of addition of sample-specific barcodes for targeted resequencing in a single experiment. Amplicon sequencing (Illumina HiSeq2500) achieved an extremely high depth of coverage (80,000X). The background base variability (error rate) in 32 control samples was 0.017%+/-0.010; thus a base frequency >0.06% was significantly different from background noise (Fisher’s exact test). Mutated allele fractions (MAF) <20% were defined as low level clonal.
Results: At the F1174 hotspot, mutations were observed in 28/524 samples, 15 being high (MAF was >20%) and 13 low level clonal (MAF: 0.123%-11.688%). At the R1275 hotspot, mutations were observed in 31/524 samples, 18 high and 13 low level clonal. Finally, at the F1245 hotspot, mutations were observed in 3/524 samples, 2 high and 1 low level clonal. All clonal mutations were validated by Sanger sequencing. Validation of all other events and analysis of additional samples from collaborating groups is ongoing.
A correlation between ALK mutations and MYCN amplification was detected (chi-square, p=0.0124). No statistically significant difference in survival of patients with ALK wild-type versus ALK-mutated NB was observed.
Conclusion: Our study documents a high frequency of both high level (6.6%) and low level clonal ALK mutations (4.9%) in high-risk NB patients. These findings are of clinical importance given the potential role of ALK mutations in clonal evolution, and the possibility of ALK-targeted therapy.