Diffuse intrinsic pontine glioma(DIPG) is the main cause of brain tumor-related death among children.Until now, there is still a lack of effective therapy with prolonged overall survival for this disease. A typical st...Diffuse intrinsic pontine glioma(DIPG) is the main cause of brain tumor-related death among children.Until now, there is still a lack of effective therapy with prolonged overall survival for this disease. A typical strategy for preclinical cancer research is to find out the molecular differences between tumor tissue and para-tumor normal tissue, in order to identify potential therapeutic targets. Unfortunately, it is impossible to obtain normal tissue for DIPG because of the vital functions of the pons.Here we report the human fetal hindbrain-derived neural progenitor cells(pontine progenitor cells, PPCs) as normal control cells for DIPG. The PPCs not only harbored similar cell biological and molecular signatures as DIPG glioma stem cells, but also had the potential to be immortalized by the DIPG-specific mutation H3 K27 M in vitro. These findings provide researchers with a candidate normal control and a potential medicine carrier for preclinical research on DIPG.展开更多
基金supported by Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support (ZYLX201608)the Beijing Municipal Natural Science Foundation (7161004)
文摘Diffuse intrinsic pontine glioma(DIPG) is the main cause of brain tumor-related death among children.Until now, there is still a lack of effective therapy with prolonged overall survival for this disease. A typical strategy for preclinical cancer research is to find out the molecular differences between tumor tissue and para-tumor normal tissue, in order to identify potential therapeutic targets. Unfortunately, it is impossible to obtain normal tissue for DIPG because of the vital functions of the pons.Here we report the human fetal hindbrain-derived neural progenitor cells(pontine progenitor cells, PPCs) as normal control cells for DIPG. The PPCs not only harbored similar cell biological and molecular signatures as DIPG glioma stem cells, but also had the potential to be immortalized by the DIPG-specific mutation H3 K27 M in vitro. These findings provide researchers with a candidate normal control and a potential medicine carrier for preclinical research on DIPG.
