scholarly journals P08.36 Radioresistance of glioblastoma stem-like cells is associated with DNA replication stress, which is a promising therapeutic target

2016 ◽  
Vol 18 (suppl_4) ◽  
pp. iv49-iv49
Author(s):  
S. U. Ahmed ◽  
R. Carruthers ◽  
D. Biasoli ◽  
N. Gomez-Roman ◽  
L. Gilmour ◽  
...  
Keyword(s):  
Dna Replication ◽  
Therapeutic Target ◽  
Replication Stress ◽  
Promising Therapeutic Target ◽  
Dna Replication Stress

scholarly journals Targeting DNA Replication Stress for Cancer Therapy

Genes ◽  
2016 ◽  
Vol 7 (8) ◽  
pp. 51 ◽  
Author(s):  
Jun Zhang ◽  
Qun Dai ◽  
Dongkyoo Park ◽  
Xingming Deng
Keyword(s):  
Dna Replication ◽  
Cancer Therapy ◽  
Replication Stress ◽  
Dna Replication Stress

scholarly journals Targeting the DNA replication stress phenotype of KRAS mutant cancer cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tara Al Zubaidi ◽  
O. H. Fiete Gehrisch ◽  
Marie-Michelle Genois ◽  
Qi Liu ◽  
Shan Lu ◽  
...  
Keyword(s):  
Dna Replication ◽  
Single Molecule ◽  
Replication Stress ◽  
Proton Radiation ◽  
Wild Type ◽  
Cellular Effects ◽  
Proton Treatment ◽  
Dna Replication Stress ◽  
Fork Stalling ◽  
Mutant Cells

AbstractMutant KRAS is a common tumor driver and frequently confers resistance to anti-cancer treatments such as radiation. DNA replication stress in these tumors may constitute a therapeutic liability but is poorly understood. Here, using single-molecule DNA fiber analysis, we first characterized baseline replication stress in a panel of unperturbed isogenic and non-isogenic cancer cell lines. Correlating with the observed enhanced replication stress we found increased levels of cytosolic double-stranded DNA in KRAS mutant compared to wild-type cells. Yet, despite this phenotype replication stress-inducing agents failed to selectively impact KRAS mutant cells, which were protected by CHK1. Similarly, most exogenous stressors studied did not differentially augment cytosolic DNA accumulation in KRAS mutant compared to wild-type cells. However, we found that proton radiation was able to slow fork progression and preferentially induce fork stalling in KRAS mutant cells. Proton treatment also partly reversed the radioresistance associated with mutant KRAS. The cellular effects of protons in the presence of KRAS mutation clearly contrasted that of other drugs affecting replication, highlighting the unique nature of the underlying DNA damage caused by protons. Taken together, our findings provide insight into the replication stress response associated with mutated KRAS, which may ultimately yield novel therapeutic opportunities.

scholarly journals MCM10 compensates for Myc‐induced DNA replication stress in breast cancer stem‐like cells

2020 ◽  
Author(s):  
Takahiko Murayama ◽  
Yasuto Takeuchi ◽  
Kaoru Yamawaki ◽  
Toyoaki Natsume ◽  
Li Mengjiao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Replication ◽  
Replication Stress ◽  
Dna Replication Stress

scholarly journals MTA2 sensitizes gastric cancer cells to PARP inhibition by induction of DNA replication stress

2021 ◽  
Vol 14 (10) ◽  
pp. 101167
Author(s):  
Jinwen Shi ◽  
Xiaofeng Zhang ◽  
Jin'e Li ◽  
Wenwen Huang ◽  
Yini Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Replication ◽  
Cancer Cells ◽  
Replication Stress ◽  
Parp Inhibition ◽  
Gastric Cancer Cells ◽  
Dna Replication Stress

scholarly journals Mrc1 phosphorylation in response to DNA replication stress is required for Mec1 accumulation at the stalled fork

2009 ◽  
Vol 106 (31) ◽  
pp. 12765-12770 ◽  
Author(s):  
M. L. Naylor ◽  
J.-m. Li ◽  
A. J. Osborn ◽  
S. J. Elledge
Keyword(s):  
Dna Replication ◽  
Replication Stress ◽  
Dna Replication Stress ◽  
Stalled Fork

scholarly journals RPA-Binding Protein ETAA1 Is an ATR Activator Involved in DNA Replication Stress Response

2016 ◽  
Vol 26 (24) ◽  
pp. 3257-3268 ◽  
Author(s):  
Yuan-Cho Lee ◽  
Qing Zhou ◽  
Junjie Chen ◽  
Jingsong Yuan
Keyword(s):  
Dna Replication ◽  
Stress Response ◽  
Binding Protein ◽  
Replication Stress ◽  
Dna Replication Stress
Sign in / Sign up

Export Citation Format

Share Document