Brain tumor stem cells

2010 ◽  
Vol 391 (6) ◽  
Author(s):  
Thomas Palm ◽  
Jens C. Schwamborn
Keyword(s):  
Stem Cells ◽  
Brain Tumor ◽  
Neural Stem Cells ◽  
Molecular Mechanisms ◽  
Adult Brain ◽  
Tumor Stem Cells ◽  
Cellular Mechanisms ◽  
Cell Pool ◽  
Brain Tumor Stem Cells ◽  
Stem Cell Pool

Abstract Since the end of the ‘no-new-neuron’ theory, emerging evidence from multiple studies has supported the existence of stem cells in neurogenic areas of the adult brain. Along with this discovery, neural stem cells became candidate cells being at the origin of brain tumors. In fact, it has been demonstrated that molecular mechanisms controlling self-renewal and differentiation are shared between brain tumor stem cells and neural stem cells and that corruption of genes implicated in these pathways can direct tumor growth. In this regard, future anticancer approaches could be inspired by uncovering such redundancies and setting up treatments leading to exhaustion of the cancer stem cell pool. However, deleterious effects on (normal) neural stem cells should be minimized. Such therapeutic models underline the importance to study the cellular mechanisms implicated in fate decisions of neural stem cells and the oncogenic derivation of adult brain cells. In this review, we discuss the putative origins of brain tumor stem cells and their possible implications on future therapies.

scholarly journals TMIC-56. ROLE OF HUMAN BRAIN TUMOR STEM CELLS-DERIVED EXTRACELLULAR VESICLES ON THE PHENOTYPIC TRANSDIFFERENTIATION OF HUMAN NEURAL PROGENITOR CELLS

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi260-vi260
Author(s):  
Natanael Zarco ◽  
Emily Norton ◽  
Montserrat Lara-Velazquez ◽  
Anna Carrano ◽  
Alfredo Quinones-Hinojosa ◽  
...  
Keyword(s):  
Stem Cells ◽  
Brain Tumor ◽  
Tumor Microenvironment ◽  
Extracellular Vesicles ◽  
Primary Cultures ◽  
Adult Brain ◽  
Cell Subpopulation ◽  
Tumor Stem Cells ◽  
Brain Tumor Stem Cells

Abstract Glioblastoma (GBM) is the most aggressive of all the brain tumors with a median patient survival less than 15 months. Despite of surgical resection, radiotherapy, and chemotherapy, recurrence rate is almost 100%. A great percentage of GBM tumors (~60%) infiltrate and contact the ventricular-subventricular zone (V-SVZ). Interestingly, these tumors are the most aggressive, and invariably lead to higher distal recurrence rates, shorter time to tumor progression, and lower overall survival of the patient. The reason for this role of V-SVZ-proximity on the outcome of GBM patients is unknown. We suggest that a potential explanation is the interaction of GBM with the V-SVZ. This region is the largest neurogenic niche in the adult brain where neural stem cells (NSCs) give rise to newborn neuroblasts that migrate toward the olfactory bulb. In GBM there is a cell subpopulation called brain tumor stem cells (BTSCs) with NSCs-like characteristics, but with added potential for tumor initiation, recurrence and invasiveness. Tumor microenvironment plays an important role in migration and invasion process. In the present work, we used the total exosome isolation kit to purify Extracellular Vesicles (EVs) from human primary cultures of BTSCs. We determined that BTSCs-derived EVs contain specific information that is transfer to primary cultures of human Neural Progenitors Cells (NPCs) modulating their proliferation rate, cell viability, and migration. In addition, we identify that NPCs taken up BTSCs-derived EVs and significantly increase the expression levels of stemness-related genes such as Nestin, Nanog, and Sox2, suggesting that a phenotypic transdifferentiation is being carry out. These results support our hypothesis that GBM modulate the tumor microenvironment close to the V-SVZ by releasing EVs that target cellular components in this region and promote their phenotypic transformation, highlighting that NPCs biology changes in the context of tumor environment.

scholarly journals Differentiation profile of brain tumor stem cells: a comparative study with neural stem cells

Cell Research ◽  
2006 ◽  
Vol 16 (12) ◽  
pp. 909-915 ◽  
Author(s):  
Quan Bin Zhang ◽  
Xiao Yan Ji ◽  
Qiang Huang ◽  
Jun Dong ◽  
Yu De Zhu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Brain Tumor ◽  
Neural Stem Cells ◽  
Comparative Study ◽  
Tumor Stem Cells ◽  
Brain Tumor Stem Cells

scholarly journals STEM-21. INVESTIGATING DOT1L AS AN EPIGENETIC VULNERABILITY IN BRAIN TUMOR STEM CELLS

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi238-vi238
Author(s):  
Danielle Bozek ◽  
Graham MacLeod ◽  
Xiaoguang Hao ◽  
Nishani Rajakulendran ◽  
Moloud Ahmadi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Brain Tumor ◽  
Neural Stem Cells ◽  
Tumor Growth ◽  
Cell Lines ◽  
Histone Methyltransferase ◽  
Tumor Stem Cells ◽  
Self Renewal ◽  
Brain Tumor Stem Cells

Abstract Glioblastoma (GBM), the most common and aggressive primary adult brain cancer, is thought to be driven by a small subpopulation of brain tumor stem cells (BTSCs). BTSCs exhibit shared properties with normal stem cells such as self-renewal and multilineage differentiation. These stem cell properties have been proposed to underlie GBM tumorigenicity, treatment evasion and contribute to tumor heterogeneity. To investigate the biology underlying the stem cell properties of GBM, we compared gene essentiality profiles for a panel of BTSCs, fetal neural stem cells and non-GBM cell lines using a CRISPR Cas9 knockout library. Interestingly, from these screens, we identified the histone methyltransferase disrupter of telomeric silencing-1-like (DOT1L) as an essential gene for the growth of BTSCs and fetal neural stem cells but not for non-GBM cell lines. DOT1L is the only known histone methyltransferase responsible for histone 3 lysine 79 methylation, an epigenetic mark associated with active gene transcription. The role of this epigenetic regulator in BTSCs was investigated in depth using EPZ-5676, a clinically relevant small molecule inhibitor. Short-term treatment with EPZ-5676 in BTSCs showed minimal effects on cell viability but led to striking morphological changes, increased neuronal and astrocytic differentiation and a reduction in self-renewal. Longer treatment periods with EPZ-5676 led to a decrease in BTSC proliferation and an increase in apoptosis. Furthermore, BTSCs pretreated with EPZ-5676 led to slowed orthotopic tumor growth and improved overall survival in a SCID mouse model. Overall, these findings suggest DOT1L epigenetically regulates GBM stem cell properties and tumor growth. We are further investigating the mechanisms underlying DOT1L regulation of gene expression in BTSCs with the goal of improving the field’s understanding of epigenetics and the therapeutic implications of targeting epigenetic processes in GBM.

Flow Cytometric Analysis of Brain Tumor Stem Cells

2018 ◽  
pp. 69-77
Author(s):  
Minomi K. Subapanditha ◽  
Ashley A. Adile ◽  
Chitra Venugopal ◽  
Sheila K. Singh
Keyword(s):  
Stem Cells ◽  
Brain Tumor ◽  
Flow Cytometric Analysis ◽  
Tumor Stem Cells ◽  
Flow Cytometric ◽  
Brain Tumor Stem Cells

Brain Tumor Stem Cells

2014 ◽  
pp. 23-34
Author(s):  
N. Sumru Bayin ◽  
Aram S. Modrek ◽  
Dimitris G. Placantonakis
Keyword(s):  
Stem Cells ◽  
Brain Tumor ◽  
Tumor Stem Cells ◽  
Brain Tumor Stem Cells
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