**Conflict of interest**

The authors declare no potential conflicts of interest.

*Molecular Target Therapy against Neuroblastoma DOI: http://dx.doi.org/10.5772/intechopen.81706*

*Biophysical Chemistry - Advance Applications*

status and susceptibility to AZD8055 was not found.

**9. ALK as a therapeutic target in NB**

concomitant MYCN amplification.

**10. Conclusions**

**Conflict of interest**

status of NB cell lines affects susceptibility to AZD8055. Using fluorescence in situ hybridization (FISH), we observed MYCN amplification in all investigated nuclei of NB19, IMR32, TGW, OZAWA, LAN-1, SMS-KAN, and SCMC-N4 cell lines (**Figure 1A**). As shown in **Figure 1A**, MYCN amplification was not observed in INDEN (loss/ imbalance), SK-N-SH (gain), KP-N-SI (loss/imbalance), KP-N-SIFA (gain), and SJ-N-KP (loss/imbalance). As shown in **Figure 1B**, the relationship between MYCN

Constitutive activation of the ALK receptor tyrosine kinase by mutation or translocation appears to contribute to the malignant phenotype of several cancers, including NB, making it a potentially therapeutic target [49]. Both wild type ALK and the F1174L-mutated ALK upregulate MYCN expression [50], and these two genes lead to constitutive phosphorylation of ALK and of downstream signaling molecules, PI3K/AKT/mTOR, that are critical for cell proliferation and survival [51]. ALKF1174L cosegregates with MYCN amplification in patients, and this combination is associated with a particularly poor prognosis, as shown by the fatal outcome of 9 of 10 children with ALKF1174L/MYCN-amplified tumors [52]. Targeting ALK with PI3K/Akt/mTOR inhibitors may inhibit cell growth in tumor lines with

NB cell lines can be categorized into three groups by the patterns of IGF-1R/ Akt pathway response. PPP, MK2206, and AZD8055 showed significant antitumor effect in NB cells. Our current results highlight the potential of IGF-1R/PI3K/ Akt/mTOR pathway as a promising target for NB treatment. PPP, MK2206, and AZD8055 should be further investigated for NB treatment in clinical trials.

The authors declare no potential conflicts of interest.

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