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. 2021 Aug 31;20(11):2228–2239. doi: 10.1158/1535-7163.MCT-20-1034

Table 2.

Neuroblastoma cell line panel genomics and clinical covariates.

Cell line Clinical phenotypea Patient gendera Primary tumor site/cell origina Stagea TP53b ALKb MYCN b Other mutation/Ampb
NB-SD Relapse M Unk./BM 4 C176F F1174L Amp ARID1A S1985fs*13
NB-EbC1 Relapse M Adrenal/adrenal 4 WT WT NA KRAS G12D
SMS-SAN Diagnosis F Adrenal/BM 4 WT F1174L Amp
NB-1643 Diagnosis M RP/RP 4 WT R1275Q Amp
LA-N-5 Diagnosis M Unk./BM 4 WT R1275Q Amp
CHP-134 Post-mortem M Adrenal/adrenal 4 WT WT Amp
NB69 Diagnosis M Adrenal/adrenal 3 WT WT NA NTRK3 Q759K
NBL-S Diagnosis M Adrenal/adrenal 3 WT WT NA
NGP Post-treatment M Unk./lung 4 A159D C141W WT Amp CDK4 Amp, MDM2 Amp
IMR-5c Diagnosis M Abd./abd. Unk. WT WT Amp ATM R189K
SK-N-AS Relapse F Adrenal/BM 4 Nulld WT NA NRAS Q61K

Abbreviations: Abd., abdomen; Amp, MYCN or other indicated gene amplified cell line; BM, bone marrow; F, female; LN, lymph node; M, male; NA, MYCN non-amplified cell line; RP, retroperitoneal; Unk., unknown; WT, wild-type.

aAs previously described (58–61).

bAs previously described (25, 26).

cSubclone of IMR32, IMR32 clinical information shown.

dDeletion of one TP53 allele and expression of C-terminally truncated TP53 variants from remaining TP53 allele due to a deletion in the intron 9/exon 10 junction, although SK-N-AS cells may maintain some partial TP53 functionality (9).