R. E. Langley
Harvard University
5 Papers
100 Citations
R. E. Langley is an academic researcher from Harvard University. The author has contributed to research in topics: Apoptosis & Endothelial stem cell. The author has an hindex of 5, co-authored 5 publications.
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Papers
Radiation-induced apoptosis in microvascular endothelial cells.
TL;DR: These studies show that either bF GF withdrawal or ionizing radiation can induce apoptosis in confluent monolayers of capillary endothelial cells and that radiation-induced apoptosis can be modified by the presence of bFGF.
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Modifiers of Radiation-Induced Apoptosis'
TL;DR: It is found that internucleosomal DNA fragmentation, characteristics of apoptosis, can result from treatment of EL4 and F9 cells with agents that have diverse modes of action: tert-butyl hydroperoxide, diazenedicarboxylic acid bis(N,N-piperidide), and etoposide.
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Effect of cell cycle stage, dose rate and repair of sublethal damage on radiation-induced apoptosis in F9 teratocarcinoma cells.
TL;DR: It was found that the fraction of the radiation-killed F9 cells that died by apoptosis did not vary when cells were irradiated at different stages of the cell cycle despite large variations in overall survival, suggesting that the factors that influence radiation sensitivity throughout thecell cycle have an equal impact on apoptosis and classical reproductive cell death.
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Novel concepts in modification of radiation sensitivity
Edward A. Bump,Susan J. Braunhut,Sanjeewani T. Palayoor,Diane Medeiros,Leon L. Lai,Beth A. Cerce,R. E. Langley,C. Norman Coleman +7 more
TL;DR: The results raise the possibility that radiation could induce apoptosis by an oxidative stress mechanism that is different from that involved in classical clonogenic cell killing.
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Modification of the aerobic cytotoxicity of etanidazole
Sanjeewani T. Palayoor,Edward A. Bump,Kamal Malaker,R. E. Langley,Daniel Saroff,John R. Delfs,Selwyn J. Hurwitz,Selwyn J. Hurwitz,C. Norman Coleman +8 more
TL;DR: The results suggest that it might be possible to modify the neurotoxicity of etanidazole with agents that would not be expected to interfere with the tumoricidal action of radiation plus etanodazole.
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