Accumulation of DNA Damage and Cell Death after Fractionated Irradiation
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F11%3A10104927" target="_blank" >RIV/00216208:11150/11:10104927 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/68081707:_____/11:00367046 RIV/60162694:G44__/11:00002528
Výsledek na webu
<a href="http://www.rrjournal.org/doi/pdf/10.1667/RR2478.1" target="_blank" >http://www.rrjournal.org/doi/pdf/10.1667/RR2478.1</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1667/RR2478.1" target="_blank" >10.1667/RR2478.1</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Accumulation of DNA Damage and Cell Death after Fractionated Irradiation
Popis výsledku v původním jazyce
The purpose of this work was to determine how fractionated radiation used in the treatment of tumors affects the ability of cancer as well as normal cells to repair induced DNA double-strand breaks (DSBs) and how cells that have lost this ability die. Lymphocytic leukemia cells (MOLT4) were used as an experimental model, and the results were compared to those for normal cell types. The results show that cancer and normal cells were mostly unable to repair all DSBs before the next radiation dose inducednew DNA damage. Accumulation of DSBs was observed in normal human fibroblasts and healthy lymphocytes irradiated in vitro after the second radiation dose. The lymphocytic leukemia cells irradiated with 4 X 1 Gy and a single dose of 4 Gy had very similarsurvival; however, there was a big difference between human fibroblasts irradiated with 4 X 1.5 Gy and a single dose of 6 Gy. These results suggest that exponentially growing lymphocytic leukemia cells, similar to rapidly proliferating tu
Název v anglickém jazyce
Accumulation of DNA Damage and Cell Death after Fractionated Irradiation
Popis výsledku anglicky
The purpose of this work was to determine how fractionated radiation used in the treatment of tumors affects the ability of cancer as well as normal cells to repair induced DNA double-strand breaks (DSBs) and how cells that have lost this ability die. Lymphocytic leukemia cells (MOLT4) were used as an experimental model, and the results were compared to those for normal cell types. The results show that cancer and normal cells were mostly unable to repair all DSBs before the next radiation dose inducednew DNA damage. Accumulation of DSBs was observed in normal human fibroblasts and healthy lymphocytes irradiated in vitro after the second radiation dose. The lymphocytic leukemia cells irradiated with 4 X 1 Gy and a single dose of 4 Gy had very similarsurvival; however, there was a big difference between human fibroblasts irradiated with 4 X 1.5 Gy and a single dose of 6 Gy. These results suggest that exponentially growing lymphocytic leukemia cells, similar to rapidly proliferating tu
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
BO - Biofyzika
OECD FORD obor
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Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)
Ostatní
Rok uplatnění
2011
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Radiation Research
ISSN
0033-7587
e-ISSN
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Svazek periodika
175
Číslo periodika v rámci svazku
6
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
11
Strana od-do
708-718
Kód UT WoS článku
000291336500004
EID výsledku v databázi Scopus
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