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. Author manuscript; available in PMC: 2013 Mar 20.
Published in final edited form as: Cancer Cell. 2012 Mar 20;21(3):362–373. doi: 10.1016/j.ccr.2012.02.010

Figure 3. Activated ALK accelerates disease onset and increases the penetrance of MYCN-induced neuroblastoma.

Figure 3

(A) Cumulative frequency of neuroblastoma in stable transgenic zebrafish by Kaplan-Meier analysis. ALKmut represents stable transgenic fish expressing the ALK (F1174L) transgene. WT, wild-type.

(B) Onset of neuroblastoma in MYCN transgenic fish or wild-type (WT) fish as mosaics coinjected with the following DNA constructs: i) dβh-ALKF1174L and dβh-mCherry (mosaic ALKmut), ii) dβh-ALKWT and dβh-mCherry (mosaic ALKWT), or iii) dβh-mCherry alone. The difference between tumor onset by 9 wpf in the MYCN fish coinjected with dβh-ALKF1174L and dβh-mCherry (MYCN; mosaic ALKmut) and that in the MYCN line coinjected with dβh-ALKWT and dβh-mCherry (MYCN; mosaic ALKWT) or dβh-mCherry alone (MYCN) is significant at p=0.002 and p=0.007, respectively, with two-tailed Fisher exact test.

See also Figure S3.