논문 (학술지)
The origin-of-cell harboring cancer-driving mutations in human glioblastoma
| 등록번호 | RPMS-2019-0090738637 | SCI 구분
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※구분 : SCI(SCIE포함), 비SCI |
SCI |
|---|---|---|---|
| 저자명 (주·공동저자) | Lee Joo Ho; Lee Jeong Ho | ||
| 논문구분 | 국내전문학술지 | 학술지명 | BMB REPORTS |
| ISSN | 1976-6696 | 학술지 출판일자 | 2018-10-31 |
| 학술지 볼륨번호 | 51 | 논문페이지 | 481 ~ 483 |
| 학술지 임팩트팩터 | 3.08 | 기여율 | 0 % |
| DOI | 10.5483/BMBRep.2018.51.10.233 | ||
| 초록 | Glioblastoma (GBM) is the most common and aggressive form of human adult brain malignancy. The identification of the cell of origin harboring cancer-driver mutations is the fundamental issue for understanding the nature of GBM and developing the effective therapeutic target. It has been a long-term hypothesis that neural stem cells in the subventricular zone (SVZ) might be the origin-of-cells in human glioblastoma since they are known to have life-long proliferative activity and acquire somatic mutations. However, the cell of origin for GBM remains controversial due to lack of direct evidence thereof in human GBM. Our recent study using various sequencing techniques in triple matched samples such as tumor-free SVZ, tumor, and normal tissues from human patients identified the clonal relationship of driver mutations between GBM and tumor-free SVZ harboring neural stem cells (NSCs). Tumor-free SVZ tissue away from the tumor contained low-level GBM driver mutations (as low as 1% allelic frequency) that were found in the dominant clones in its matching tumors. Moreover, via single-cell sequencing and microdissection, it was discovered that astrocyte-like NSCs accumulating driver mutations evolved into GBM with clonal expansion. Furthermore, mutagenesis of cancer-driving genes of NSCs in mice leads to migration of mutant cells from SVZ to distant brain and development of high-grade glioma through the aberrant growth of oligodendrocyte precursor lineage. Altogether, the present study provides the first direct evidence that NSCs in human SVZ is the cell of origin that develops the driver mutations of GBM. | ||
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