scholarly journals Using Drosophila Larval Imaginal Discs to Study Low-Dose Radiation-Induced Cell Cycle Arrest

Author(s):  
Shian-Jang Yan ◽  
Willis X. Li
2004 ◽  
Vol 37 (4) ◽  
pp. 871-880 ◽  
Author(s):  
Hyo-Soo Kim ◽  
Hyun-Jai Cho ◽  
Hyun-Ju Cho ◽  
Sun-Jung Park ◽  
Kyung-Woo Park ◽  
...  

2013 ◽  
Vol 18 ◽  
pp. S179-S180 ◽  
Author(s):  
I. Alastuey ◽  
A. Noé ◽  
C. Chiaramello ◽  
S. Montemuiño ◽  
J. Pardo

2009 ◽  
Vol 172 (3) ◽  
pp. 306-313 ◽  
Author(s):  
Kelvin K. C. Tsai ◽  
Jeremy Stuart ◽  
Yao-Yu Eric Chuang ◽  
John B. Little ◽  
Zhi-Min Yuan

2008 ◽  
Vol 2 ◽  
pp. CMO.S463
Author(s):  
Elizabeth K. Balcer-Kubiczek ◽  
Mona Attarpour ◽  
Jian Z. Wang ◽  
William F. Regine

Low-dose radiation hypersensitivity (HRS) describes a phenomenon of excessive sensitivity to X ray doses <0.5 Gy. Docetaxel is a taxane shown to arrest cells in the G2/M phase of the cell cycle. Some previous studies suggested that HRS might result from the abrogation of the early G2 checkpoint arrest. First we tested whether HRS occurs in gastric cancer—derived cells, and whether pre-treatment of cells with low docetaxel concentrations can enhance the magnitude of HRS in gastric cancer cells. The results demonstrated HRS at ~0.3 Gy and the synergy between 0.3 Gy and docetaxel (3 nM for 24 h), and the additivity of other drug/dose combinations. The synergistic effect was associated with a significant docetaxel-induced G2 accumulation. Next, we evaluated in time-course experiments ATM kinase activity and proteins associated with the induction and maintenance of the early G2 checkpoint. The results of multi-immunoblot analysis demonstrate that HRS does not correlate with the ATM-dependent early G2 checkpoint arrest. We speculate that G2 checkpoint adaptation, a phenomenon associated with a prolonged cell cycle arrest, might be involved in HRS. Our results also suggest a new approach for the improvement the effectiveness of docetaxel-based radiotherapy using low doses per fraction.


2002 ◽  
Vol 277 (16) ◽  
pp. 13873-13882 ◽  
Author(s):  
Eleanore A. Gross ◽  
Marinella G. Callow ◽  
Linda Waldbaum ◽  
Suzanne Thomas ◽  
Rosamaria Ruggieri

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Wenjing Zhang ◽  
Yi Li ◽  
Rui Li ◽  
Yaya Wang ◽  
Mengwen Zhu ◽  
...  

The present study was designed to elucidate the key parameters associated with X-ray radiation induced oxidative stress and the effects of STS on X-ray-induced toxicity in H9c2 cardiomyocytes. Cytotoxicity of STS and radiation was assessed by MTT. Antioxidant activity was evaluated by SOD and MDA. Apoptosis was measured by the flow cytometry, Hoechst 33258, clonogenic survival assay, and western blot. It was found that the cell viability of H9c2 cells exposed to X-ray radiation was significantly decreased in a dose-dependent manner and was associated with cell cycle arrest at the G0/G1 phase as well as apoptosis. STS treatment significantly reversed the morphological changes, attenuated radiation-induced apoptosis, and improved the antioxidant activity in the H9c2 cells. STS significantly increased the Bcl-2 and Bcl-2/Bax levels and decreased the Bax and caspase-3 levels, compared with the cells treated with radiation alone. STS treatment also resulted in a significant increase in p38-MAPK activation. STS could protect the cells from X-ray-induced cell cycle arrest, oxidative stress, and apoptosis. Therefore, we suggest the STS could be useful for the treatment of radiation-induced cardiovascular injury.


2006 ◽  
Vol 2 (1/2) ◽  
pp. 111 ◽  
Author(s):  
B.N. Pandey ◽  
H.D. Sarma ◽  
D. Shukla ◽  
K.P. Mishra

2014 ◽  
Vol 10 (3) ◽  
pp. 1569-1575 ◽  
Author(s):  
YONG XIN ◽  
HAI-BIN ZHANG ◽  
TIAN-YOU TANG ◽  
GUI-HONG LIU ◽  
JIAN-SHE WANG ◽  
...  

2010 ◽  
Vol 173 (2) ◽  
pp. 125-137 ◽  
Author(s):  
Benjamin J. Blyth ◽  
Edouard I. Azzam ◽  
Roger W. Howell ◽  
Rebecca J. Ormsby ◽  
Alexander H. Staudacher ◽  
...  

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