scholarly journals Analysis of genes involved in response to doxorubicin and a GD2 ganglioside-specific 14G2a monoclonal antibody in IMR-32 human neuroblastoma cells

2015 ◽  
Vol 62 (3) ◽  
pp. 423-433 ◽  
Author(s):  
Irena Horwacik ◽  
Małgorzata Durbas ◽  
Elżbieta Boratyn ◽  
Anna Sawicka ◽  
Paulina Węgrzyn ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Gd2 Ganglioside

Internalization and degradation of monoclonal antibody chCE7 by human neuroblastoma cells

1994 ◽  
Vol 57 (3) ◽  
pp. 427-432 ◽  
Author(s):  
Ilse Novak-Hofer ◽  
Hans Peter Amstutz ◽  
Jean-Jacques Morgenthaler ◽  
P. August Schubiger
Keyword(s):  
Monoclonal Antibody ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Targeting GD2 ganglioside and aurora A kinase as a dual strategy leading to cell death in cultures of human neuroblastoma cells

2013 ◽  
Vol 341 (2) ◽  
pp. 248-264 ◽  
Author(s):  
Irena Horwacik ◽  
Małgorzata Durbas ◽  
Elżbieta Boratyn ◽  
Paulina Węgrzyn ◽  
Hanna Rokita
Keyword(s):  
Cell Death ◽  
Neuroblastoma Cells ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Dual Strategy ◽  
Gd2 Ganglioside

The GD2-specific 14G2a monoclonal antibody induces apoptosis and enhances cytotoxicity of chemotherapeutic drugs in IMR-32 human neuroblastoma cells

2009 ◽  
Vol 281 (2) ◽  
pp. 171-182 ◽  
Author(s):  
Aleksandra Kowalczyk ◽  
Małgorzata Gil ◽  
Irena Horwacik ◽  
Żaneta Odrowąż ◽  
Danuta Kozbor ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Neuroblastoma Cells ◽  
Chemotherapeutic Drugs ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Complement killing of human neuroblastoma cells: A cytotoxic monoclonal antibody and its F(ab)'2-cobra venom factor conjugate are equally cytotoxic

1990 ◽  
Vol 27 (10) ◽  
pp. 957-964 ◽  
Author(s):  
Hartmut Juhl ◽  
Eugene C. Petrella ◽  
Nai-Kong V. Cheung ◽  
Reinhard Bredehorst ◽  
Carl-Wilhelm vogel
Keyword(s):  
Monoclonal Antibody ◽  
Neuroblastoma Cells ◽  
Cobra Venom ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Cobra Venom Factor

Title>Additive cytotoxicity of different monoclonal antibody-cobra venom factor conjugates for human neuroblastoma cells

Immunobiology ◽  
1997 ◽  
Vol 197 (5) ◽  
pp. 444-459 ◽  
Author(s):  
Hartmut Juhl ◽  
Eugene C. Petrella ◽  
Nai-Kong V. Cheung ◽  
Reinhard Bredehorst ◽  
Carl-Wilhelm Vogel
Keyword(s):  
Monoclonal Antibody ◽  
Neuroblastoma Cells ◽  
Cobra Venom ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Cobra Venom Factor

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

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