Non-Problematic Risks from Low-Dose Radiation-Induced DNA Damage Clusters

Hayes, Daniel P.
March 2008
Dose-Response;2008, Vol. 6 Issue 1, p30
Academic Journal
Radiation-induced DNA damage clusters have been proposed and are usually considered to pose the threat of serious biological damage. This has been attributed to DNA repair debilitation or cessation arising from the complexity of cluster damage. It will be shown here, contrary to both previous suggestions and perceived wisdom, that radiation induced damage clusters contribute to non-problematic risks in the low-dose, low-LET regime. The very complexity of cluster damage which inhibits and/or compromises DNA repair will ultimately be responsible for the elimination and/or diminution of precancerous and cancerous cells.


Related Articles

  • Dose-Dependent Reactive Species Accumulation and Preferential Double-Strand Breaks Repair are Featured in the γ-ray Response in Medicago truncatula Cells. Donà, Mattia; Ventura, Lorenzo; Balestrazzi, Alma; Buttafava, Armando; Carbonera, Daniela; Confalonieri, Massimo; Giraffa, Giorgio; Macovei, Anca // Plant Molecular Biology Reporter;Feb2014, Vol. 32 Issue 1, p129 

    In plants, there are issues related to the effects of gamma (γ)-rays that are still poorly explored, particularly as concerns the biological response to irradiation delivered at a low dose rate. In the present work, the effects of exposure to increasing γ-ray total doses (6, 12, 25, and 50...

  • Spatio-temporal analysis of DNA damage repair using the X-ray microbeam. Schettino, G.; Ghita, M.; Prise, K. M. // European Physical Journal D -- Atoms, Molecules, Clusters & Opti;Nov2010, Vol. 60 Issue 1, p157 

    Cellular response to radiation damage is made by a complex network of pathways and feedback loops whose spatiotemporal organization is still unclear despite its decisive role in determining the fate of the damaged cell. The single-cell approach and the high spatial resolution offered by...

  • Is DNA Damage Response Ready for Action Anywhere? Terradas, Mariona; Martín, Marta; Hernández, Laia; Tusell, Laura; Genescà, Anna // International Journal of Molecular Sciences;Sep2012, Vol. 13 Issue 9, p11569 

    Organisms are continuously exposed to DNA damaging agents, consequently, cells have developed an intricate system known as the DNA damage response (DDR) in order to detect and repair DNA lesions. This response has to be rapid and accurate in order to keep genome integrity. It has been observed...

  • CHK1 inhibition as a strategy for targeting fanconi anemia (FA) DNA repair pathway deficient tumors. Chen, Clark C.; Kennedy, Richard D.; Sidi, Samuel; Look, A. Thomas; D'Andrea, Alan // Molecular Cancer;2009, Vol. 8, Special section p1 

    Background: DNA repair deficient tumor cells have been shown to accumulate high levels of DNA damage. Consequently, these cells become hyper-dependent on DNA damage response pathways, including the CHK1-kinase-mediated response. These observations suggest that DNA repair deficient tumors should...

  • Effect of prolonging radiation delivery time on retention of gammaH2AX. Moiseenko, Vitali; Banáth, Judit P.; Duzenli, Cheryl; Olive, Peggy L. // Radiation Oncology;2008, Vol. 3, Special section p1 

    Background and purpose: Compared to conventional external beam radiotherapy, IMRT requires significantly more time to deliver the dose. Prolonging dose delivery potentially increases DNA repair which would reduce the biological effect. We questioned whether retention of γH2AX, a measure of...

  • Relationship between clonogenic radiosensitivity, radiation-induced apoptosis and DNA damage/repair in human colon cancer cells. Dunne, A.L.; Price, M.E.; Mothersill, C.; McKeown, S.R.; Robson, T.; Hirst, D.G. // British Journal of Cancer;12/15/2003, Vol. 89 Issue 12, p2277 

    The intrinsic radiation sensitivity of normal and tumour tissue is a major determinant of the outcome of radiotherapy. There is currently no established test that can be used routinely to measure the radiosensitivity of the cells in an individual patient's cancer in a manner that can inform...

  • Novel HSP90 inhibitors, NVP-AUY922 and NVP-BEP800, radiosensitise tumour cells through cell-cycle impairment, increased DNA damage and repair protraction. Stingl, L.; Stühmer, T.; Chatterjee, M.; Jensen, M. R.; Flentje, M.; Djuzenova, C. S. // British Journal of Cancer;5/25/2010, Vol. 102 Issue 11, p1578 

    Background:Heat-shock protein 90 (Hsp90) has a crucial role in both the stabilisation and regulation of various proteins, including those related to radioresistance. Inhibition of Hsp90 may therefore provide a strategy for enhancing the radiosensitivity of tumour cells. This study explores the...

  • Microarray analysis of DNA damage repair gene expression profiles in cervical cancer cells radioresistant to 252Cf neutron and X-rays. Yi Qing; Xue-Qin Yang; Zhao-Yang Zhong; Xin Lei; Jia-Yin Xie; Meng-Xia Li; De-Bing Xiang; Zeng-Peng Li; Zhen-Zhou Yang; Ge Wang; Dong Wang // BMC Cancer;2010, Vol. 10, p71 

    Background: The aim of the study was to obtain stable radioresistant sub-lines from the human cervical cancer cell line HeLa by prolonged exposure to 252Cf neutron and X-rays. Radioresistance mechanisms were investigated in the resulting cells using microarray analysis of DNA damage repair...

  • DNA repair pathways as targets for cancer therapy. Helleday, Thomas; Petermann, Eva; Lundin, Cecilia; Hodgson, Ben; Sharma, Ricky A. // Nature Reviews Cancer;Mar2008, Vol. 8 Issue 3, p193 

    DNA repair pathways can enable tumour cells to survive DNA damage that is induced by chemotherapeutic treatments; therefore, inhibitors of specific DNA repair pathways might prove efficacious when used in combination with DNA-damaging chemotherapeutic drugs. In addition, alterations in DNA...


Read the Article


Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics