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A Protocol for Rapid Post-mortem Cell Culture of Diffuse Intrinsic Pontine Glioma DIPG
Published on: March 7, 2017
Advanced Pediatric Diffuse Pontine Glioma Murine Models Pave the Way towards Precision Medicine
Zirong Chen1, Peng Peng1, Xiaolin Zhang1
1Department of Neurological Surgery, Tongji Hospital, Tongji Medical College, Huazhong University Science and Technology, Wuhan 430030, China.
Abstract:
Diffuse intrinsic pontine gliomas (DIPGs) account for ~15% of pediatric brain tumors, which invariably present with poor survival regardless of treatment mode. Several seminal studies have revealed that 80% of DIPGs harbor H3K27M mutation coded by HIST1H3B, HIST1H3C and H3F3A genes. The H3K27M mutation has broad effects on gene expression and is considered a tumor driver. Determination of the effects of H3K27M on posttranslational histone modifications and gene regulations in DIPG is critical for identifying effective therapeutic targets. Advanced animal models play critical roles in translating these cutting-edge findings into clinical trial development. Here, we review current molecular research progress associated with DIPG. We also summarize DIPG animal models, highlighting novel genomic engineered mouse models (GEMMs) and innovative humanized DIPG mouse models. These models will pave the way towards personalized precision medicine for the treatment of DIPGs.
Insights
Diffuse intrinsic pontine gliomas (DIPG) are aggressive pediatric brain tumors. Understanding the H3K27M mutation and utilizing advanced animal models are key to developing effective treatments and personalized medicine for DIPG.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Diffuse intrinsic pontine gliomas (DIPG) represent 15% of pediatric brain tumors with poor prognoses.
- The H3K27M mutation, present in 80% of DIPGs and encoded by specific genes, is a critical tumor driver.
- Understanding H3K27M's impact on gene regulation and histone modifications is vital for therapeutic target identification.
Purpose of the Study:
- To review molecular research advancements in DIPG.
- To summarize current and novel animal models for DIPG research.
- To highlight the role of these models in advancing personalized medicine for DIPG.
Main Methods:
- Literature review of molecular mechanisms in DIPG.
- Analysis of genomic engineered mouse models (GEMMs) for DIPG.
- Evaluation of humanized DIPG mouse models.
Main Results:
- The H3K27M mutation significantly influences gene expression in DIPG.
- Various advanced animal models, including GEMMs and humanized models, are available for DIPG research.
- These models are crucial for translating research findings into clinical applications.
Conclusions:
- H3K27M mutation is a central factor in DIPG pathogenesis.
- Advanced animal models are essential tools for studying DIPG biology and testing therapies.
- The development of these models facilitates progress toward personalized precision medicine for DIPG patients.
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