This SuperSeries is composed of the SubSeries listed below.
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Age, Specimen part, Cell line, Treatment
View SamplesWe were interested in studying the role of DOT1L-mediated H3K79 methylation on N-Myc target gene transcription in MYCN-induced neuroblastoma.
No associated publication
Specimen part, Treatment
View SamplesBET bromodomain inhibitors are emerging as very promising novel anticancer agents. Combination of BET bromodomain inhibitor JQ1 and quinone-containing compound nanaomycin exerts synergistic anticancer effect in neuroblastoma
No associated publication
Specimen part, Treatment
View SamplesWe analyed the gene expression profiles after knocking down MYCN or TFAP4. Results showed that transcription factor MYCN and TFAP4 commonly regulats a subset of genes that may contribute to neuroblastoma cells proliferation and migration.
MYCN promotes neuroblastoma malignancy by establishing a regulatory circuit with transcription factor AP4.
Specimen part
View SamplesAmplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Cell line, Treatment
View SamplesN-Myc oncoprotein induces neuroblastoma and exerts its biological effects through modulation of its target genes.
No associated publication
Specimen part, Cell line
View SamplesAmplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Cell line, Treatment
View SamplesThe bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects
No associated publication
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part, Cell line
View SamplesN-Myc oncoprotein induces neuroblastoma by modulating gene transcription, and long noncoding RNAs exert biological effects by regulating gene expression.
No associated publication
Specimen part
View Samples