Mitochondrial calcium signaling regulates the response of NB cells to chemotherapeutic stress

Identification: Lange, Ingo


Description

Mitochondrial calcium signaling regulates the response of NB cells to chemotherapeutic stress
 
Ingo Lange1, Dana-Lynn Koomoa1
1University of Hawaii at Hilo, Daniel K. Inouye College of Pharmacy
 
Neuroblastoma (NB) is the most common extra-cranial pediatric solid tumor in children. High-risk NB (~40-50% of patients) signifies poor prognosis, and is difficult to treat due to the lack of response to current therapies and aggressive disease progression. Novel drugs and alternative treatments are being investigated for patients with high-risk NB. However, finding an effective treatment strategy for these patients continues to be a major challenge due to a myriad of complex mechanisms that promote NB progression (e.g. increased tumor growth and metastasis, and resistance to treatments). Current research investigating novel targets and potential drugs for high-risk and refractory NB has improved our understanding of NB and current treatment strategies. However, NB cell populations are heterogeneous in cell identity and treatment response, which often leads to NB drug resistance and relapse. There are currently no effective treatments available for refractory and relapsed NB.
To address this limitation, the proposed project will elucidate the mechanisms that promote NB drug resistance, and identify ion channels that may be novel targets for the development of more effective anticancer agents for drug resistant and relapsed NB. Current literature and our the preliminary data support the hypothesis that mitochondrial calcium signaling regulates the response of NB cells to therapeutic stress. The results showed that the mechanisms that promote drug resistance in NB involves the calcium signaling nexus of NB, specifically mitochondrial calcium signaling. Current investigations are focused on identifying potential targets within the NB calcium signaling nexus that may be targeted for refractory and relapsed NB.

Credits

Credits: None available.

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