Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Autores: Shideng Bao, Qing Shi, Yueling Hao, Roger E. McLendon, Darell D. Bigner, Qiulian Wu, Anita B. Hjelmeland, Jeremy N. Rich, Mark W. Dewhirst

Cancer stem cells contribute to glioma radioresistance by an increase of DNA repair capacity through preferential activation of the DNA damage response checkpoints. Potential therapies that modulate or target cancer stem cells are also reviewed.

In response to DNA damage, normal cells activate the DNA damage response (DDR), utilizing a variety of DNA damage sensing and repair pathways (e.g., base excision repair, nucleotide excision repair, homologous recombination, nonhomologous end-joining, mismatch repair, direct reversal) to maintain genomic integrity, whereas the inability to repair DNA damage leads to apoptosis . 2017-10-09 · Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature 2006; 444 : 756–760. CAS Article Google Scholar In response to DNA damage, normal cells activate the DNA damage response (DDR), utilizing a variety of DNA damage sensing and repair pathways (e.g., base excision repair, nucleotide excision repair, homologous recombination, nonhomologous end-joining, mis-match repair, direct reversal) to maintain genomic integrity, whereas the inability to View 0 peer reviews of Glioma stem cells promote radioresistance by preferential activation of the DNA damage response on Publons Download Web of Science™ My Research Assistant : Bring the power of the Web of Science to your mobile device, wherever inspiration strikes.

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Nature. 2006;444:756–60. Google Scholar | Crossref |  Bao, S., et al. Glioma stem cells promote radioresistance by preferential activation of the DNA damage response.

Glioma stem cells promote radioresistance by preferential activation of the DNA damage response.

2019-08-27 · Glioma stem cells promote radioresistance by preferential activation of the DNA damage response Nature , 444 ( 2006 ) , pp. 756 - 760 CrossRef View Record in Scopus Google Scholar

The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas. Here we show that short-term cultures of glioma xenografts subjected to three serial cancer stem cells contribute to glioma radioresistance through cycles of IR also contained greater percentages of CD1331 cells than preferential activation of the DNA damage checkpoint response parental populations (Supplementary Fig. S2). The mechanisms underlying tumour radioresistance have remained elusive. Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity.

Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas.

The sign of radioresistance was the accumulation of The mechanisms underlying tumour radioresistance have remained elusive. Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas. In both cell culture and the brains of immunocompromised mice, CD133-expressing glioma cells survive ionizing radiation in increased proportions Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas.

The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas. Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity.
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Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature.

Nature 2006; 444 : 756–760.
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Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature 2006; 444 : 756–760. CAS Article Google Scholar

The fraction of tumour Notch inhibition with GSIs did not alter the DNA damage response of glioma stem cells following radiation, but rather impaired radiation-induced Akt activation and upregulated levels of the truncated apoptotic isoform of Mcl-1 (Mcl-1s). Taken together, our results suggest a critical role of Notch to promote radioresistance of glioma stem cells.

HuR represses Wnt/β-catenin-mediated transcriptional activity by promoting β-Catenin accumulates in the nucleus of cancer cells where it activates oncogenic Different modes of interaction by TIAR and HuR with target RNA and DNA. HuR distribution and leads to a preferential binding to U-rich bearing target mRNA.

It has been reported that cancer stem cells may contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. We have examined DNA repair in five stem and nonstem glioma cell lines. The population doubling time was … 2018-05-21 · Previous studies showed that, preferential activation of the DNA damage checkpoint and enhanced DNA repair capacity in gliomas lead to radioresistance [9, 14, 15]. Strategies depending on targeting DNA damage response network in gliomas were applied to sensitize tumors and reverse radioresistance [16, 17]. In this article, Singh and colleagues undertook a comparative evaluation of pre-clinical efficacy and safety of three immunotherapeutic modalities directed against CD133 braintumor-initiating cells. While all three modalities were efficacious in orthotopic GBM xenografts, CD133-specific CAR-T cells represented the most therapeutically tractable strategy against functionally important CD133 Bao S, Wu Q, McLendon RE, et al.

The emerging role of cancer stem cells in tumor Glioblastoma is an aggressive and heterogeneous tumor in which glioblastoma stem cells (GSCs) are at the apex of an entropic hierarchy and impart devastating therapy resistance. The high entropy of GSCs is driven by a permissive epigenetic landscape and a mutational landscape that revokes crucial cellular checkpoints. In response to DNA damage, normal cells activate the DNA damage response (DDR), utilizing a variety of DNA damage sensing and repair pathways (e.g., base excision repair, nucleotide excision repair, homologous recombination, nonhomologous end-joining, mismatch repair, direct reversal) to maintain genomic integrity, whereas the inability to repair DNA damage leads to apoptosis .