scholarly journals Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

1989 ◽  
Vol 80 ◽  
pp. 3-15 ◽  
Author(s):  
E Abemayor ◽  
N Sidell
Keyword(s):  
Cell Differentiation ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Neuronal Cell ◽  
In Vitro Study ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Neuronal Cell Differentiation ◽  
Neuroblastoma Cell Lines

In vitro cytotoxicity of fenthion and related metabolites in human neuroblastoma cell lines

Chemosphere ◽  
1995 ◽  
Vol 30 (9) ◽  
pp. 1709-1715 ◽  
Author(s):  
D. Cova ◽  
R. Perego ◽  
C. Nebuloni ◽  
G. Fontana ◽  
G.P. Molinari
Keyword(s):  
Cell Lines ◽  
Neuroblastoma Cell ◽  
In Vitro Cytotoxicity ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Neuroblastoma Cell Lines

scholarly journals Combined ALK and MDM2 inhibition increases antitumor activity and overcomes resistance in human ALK mutant neuroblastoma cell lines and xenograft models

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Hui Qin Wang ◽  
Ensar Halilovic ◽  
Xiaoyan Li ◽  
Jinsheng Liang ◽  
Yichen Cao ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Human Neuroblastoma Cell ◽  
Wild Type ◽  
Combination Strategy ◽  
Human Neuroblastoma ◽  
Xenograft Models ◽  
Neuroblastoma Cell Lines

The efficacy of ALK inhibitors in patients with ALK-mutant neuroblastoma is limited, highlighting the need to improve their effectiveness in these patients. To this end, we sought to develop a combination strategy to enhance the antitumor activity of ALK inhibitor monotherapy in human neuroblastoma cell lines and xenograft models expressing activated ALK. Herein, we report that combined inhibition of ALK and MDM2 induced a complementary set of anti-proliferative and pro-apoptotic proteins. Consequently, this combination treatment synergistically inhibited proliferation of TP53 wild-type neuroblastoma cells harboring ALK amplification or mutations in vitro, and resulted in complete and durable responses in neuroblastoma xenografts derived from these cells. We further demonstrate that concurrent inhibition of MDM2 and ALK was able to overcome ceritinib resistance conferred by MYCN upregulation in vitro and in vivo. Together, combined inhibition of ALK and MDM2 may provide an effective treatment for TP53 wild-type neuroblastoma with ALK aberrations.

In vitro toxicity of bisphosphonates on human neuroblastoma cell lines

2004 ◽  
Vol 15 (8) ◽  
pp. 795-802 ◽  
Author(s):  
Marta Vorotnjak ◽  
Joachim Boos ◽  
Claudia Lanvers-Kaminsky
Keyword(s):  
Cell Lines ◽  
Neuroblastoma Cell ◽  
In Vitro Toxicity ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Neuroblastoma Cell Lines

scholarly journals Cell Line-Dependent Variability of Coordinate Expression of p75NTR and CRABP1 and Modulation of Effects of Fenretinide on Neuroblastoma Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Yaoli Pu Yang ◽  
Simeng Wang ◽  
Xingguo Li ◽  
Nina F. Schor
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Neurotrophin Receptor ◽  
Human Neuroblastoma Cell ◽  
P75 Neurotrophin Receptor ◽  
Human Neuroblastoma ◽  
Neuroblastoma Cell Lines

Neuroblastoma is a childhood neural crest tumor. Fenretinide, a retinoic acid analogue, induces accumulation of mitochondrial reactive oxygen species and consequent apoptosis in neuroblastoma cells. The p75 neurotrophin receptor (p75NTR) enhances the antineuroblastoma cell efficacy of fenretinidein vitro. We examined the role of the retinoid binding protein, CRABP1, in p75NTR-mediated potentiation of the efficacy of fenretinide. Knockdown and overexpression, respectively, of either p75NTR or CRABP1 were effected in neuroblastoma cell lines using standard techniques. Expression was determined by qRT-PCR and confirmed at the protein level by Western blot. Metabolic viability was determined by Alamar blue assay. While protein content of CRABP1 correlated roughly with that of p75NTR in the three neuroblastoid or epithelioid human neuroblastoma cell lines studied, manipulation of p75NTR expression resulted in cell line-dependent, variable change in CRABP1 expression. Furthermore, in some cell lines, induced expression of CRABP1 in the absence of p75NTR did not alter cell sensitivity to fenretinide treatment. The effects of manipulation of p75NTR expression on CRABP1 expression and the effects of CRABP1 expression on fenretinide efficacy are therefore neuroblastoma cell line-dependent. Potentiation of the antineuroblastoma cell effects of fenretinide by p75NTR is not mediated solely through CRABP1.

Delta opioid receptor in human neuroblastoma cell lines

1986 ◽  
Vol 382 (2) ◽  
pp. 327-331 ◽  
Author(s):  
Günther Hochhaus ◽  
Victor C. Yu ◽  
Wolfgang Sadée
Keyword(s):  
Opioid Receptor ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Delta Opioid Receptor ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Neuroblastoma Cell Lines
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