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Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
p53 family: Therapeutic targets in neuroblastoma
Jennifer Wolter1, Paola Angelini, Meredith Irwin
1Department of Medical Biophysics, University of Toronto, Hospital for Sick Children, ON, Canada.
Abstract:
Survival rates for metastatic neuroblastoma remain poor, despite significant increase in the intensity of therapy. Although it represents approximately 7% of pediatric cancer, neuroblastoma accounts for approximately 15% of childhood cancer deaths. Thus, novel approaches to enhance neuroblastoma chemotherapy sensitivity and prevent or bypass chemoresistance are required. Disruption of the p53 pathway is a common mechanism leading to defects in apoptosis in cancer cells. Increasing evidence suggests that the p53 pathway may be inactivated in neuroblastoma. Inactivation of the p53 pathway occurs most commonly at the time of relapse, and probably contributes to chemoresistance. The p53 family proteins, p73 and p63, can also induce apoptosis, and early studies suggest that p73 may be important in neuroblastoma pathogenesis and response to treatment. This article focuses on current therapies and novel drugs targeting p53 and p73 signaling pathways in neuroblastoma. Understanding the balance between the p53 family proteins in neuroblastoma and how their expression and activity are regulated will hopefully lead to the discovery of agents that target these pathways to induce neuroblastoma cell death, alone or in combination with chemotherapies.
Insights
Targeting the p53 and p73 signaling pathways offers a novel approach to improve chemotherapy sensitivity in neuroblastoma. Understanding these pathways may lead to new treatments for this aggressive childhood cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pediatric Cancer Research
Background:
- Metastatic neuroblastoma has poor survival rates despite intensive therapies.
- Neuroblastoma, a significant cause of childhood cancer deaths, often develops chemoresistance.
- Disruption of the p53 pathway is implicated in cancer apoptosis defects and may be inactivated in neuroblastoma, particularly at relapse.
Purpose of the Study:
- To review current therapies for neuroblastoma.
- To explore novel drugs targeting the p53 and p73 signaling pathways in neuroblastoma.
- To understand the role of p53 family proteins in neuroblastoma pathogenesis and treatment response.
Main Methods:
- Literature review of current neuroblastoma therapies.
- Analysis of research on p53 and p73 signaling pathways in neuroblastoma.
- Exploration of potential therapeutic targets within these pathways.
Main Results:
- The p53 pathway is frequently inactivated in neuroblastoma, contributing to chemoresistance.
- p53 family proteins, including p73 and p63, can induce apoptosis and may be crucial in neuroblastoma.
- Targeting p53 and p73 signaling presents a promising strategy for enhancing chemotherapy sensitivity.
Conclusions:
- Novel therapeutic strategies targeting p53 and p73 pathways are needed to improve neuroblastoma outcomes.
- Understanding the regulation of p53 family proteins is key to developing new treatments.
- Targeting these pathways may induce neuroblastoma cell death, alone or with chemotherapy.
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