DNA Damage in Human Endothelial Cells after Irradiation in Anoxia

Rosander, Kerstin; Zackrisson, Björn

doi:10.3109/02841869509093648

Cited by 16 publications

(5 citation statements)

References 23 publications

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“…Under acute hypoxia or anoxia, fewer breaks are generated due to the decreased oxygen which is normally required for the fixation of DNA damage under oxic conditions [35][36][37][38][39][40][41][42]. This is quantified by an oxygen enhancement ratio (OER), defined as the ratio of doses required for the same biological effect (e.g.…”

Section: Hypoxia Cellular Radiosensitivity and The Oxygen Enhancemenmentioning

confidence: 99%

Tumor Hypoxia as a Modifier of DNA Strand Break and Cross-Link Repair

Chan

Koch

Bristow

2009

CMM

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Hypoxia is a common characteristic of many solid tumors and is associated with poor prognosis. Cells with low oxygen levels can have altered sensitivity to radiotherapy and chemotherapy secondary to changes in the incidence of DNA single- and double-strand breaks (DNA-ssb, DNA-dsb), DNA base damage, DNA-DNA cross-links and DNA-protein cross-links. Recent evidence also supports that cells exposed to chronic hypoxia have a decreased capacity of DNA-dsb repair. This review will examine the influence of short-term and prolonged hypoxia on the two major pathways of DNA-dsb repair: homologous recombination (HR) and non-homologous end-joining (NHEJ). Novel treatment strategies designed to exploit the hypoxic tumor microenvironment are also discussed. Modification of DNA damage sensing and repair due to fluctuating oxygen levels within a dynamic tumor microenvironment may have profound implications for tumor progression and treatment.

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Section: Hypoxia Cellular Radiosensitivity and The Oxygen Enhancemenmentioning

confidence: 99%

Tumor Hypoxia as a Modifier of DNA Strand Break and Cross-Link Repair

Chan

Koch

Bristow

2009

CMM

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“…In order to investigate the mechanisms for irradiation of choroidal vessels, it might also be important to evaluate the radiosensitivity of human retinal pigment epithelial cell cultures. Interestingly, Rosander and Zackrisson [17] were able to show that hypoxia increased the radioresistance of vascular endothelial cells, resulting in less DNA damage. This could be especially relevant for the treatment of hypoxia-mediated vascular proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…To compare clinical results more effectively, we used a photon beam applied by a linear accelerator, a system which is employed in clinical routine irradiation. Apart from different irradiation modi, different experimental set-ups and treatment regimens have to be compared [16][17][18], both in in vivo as well as in vitro experiments. Johnson et al [14], for example, showed a progressive cell loss in endothelial cell monolayers after irradiation with 10 Gy.…”

Section: Discussionmentioning

confidence: 99%

Irradiation for Inhibition of Endothelial Cell Growth in vitro

et al. 2000

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The clinical effect of ionising radiation on ocular neovascularisations is controversial, not only because of the variety of treatment modalities. The aim of our study was to investigate an experimental model which allows to evaluate radiation parameters and to study the mechanism of the inhibitory effect on neoangiogenesis. In vitro experiments were performed using human umbilical vein endothelial cells and human corneal keratocytes. The cells were irradiated with different doses of photon beam radiation and counted daily after treatment. Cell cultures confirmed the efficiency of irradiation in inhibiting proliferation of vascular endothelial cells. Radiosensitivity was shown to be higher in vascular endothelial cells than in corneal stromal keratocytes. This might be helpful in investigating therapy parameters for treating ocular neovascularisations, as well as underlying mechanisms.

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“…Replicating human endothelial cells in culture have shown to be affected by radiation doses as low as 6 Gray (Gy), with complete inhibition of growth at 8.7 Gy [31]. After this low-dose radiation, vascular endothelium demonstrates morphologic [32] and DNA [33,34] changes, inhibition of replication [35], and apoptosis [28]. Fibroblast proliferation and subsequent scar formation, both integral parts of AMD disease activity and progression, are also inhibited [16,36].…”

Section: Role Of Radiation In Choroidal Neovascularizationmentioning

confidence: 98%

Brachytherapy in Neovascular AMD

Grewal

Vajzovic

2015

Curr Ophthalmol Rep

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Neovascular age-related macular degeneration (AMD) has a complex pathophysiology, and although anti-VEGF therapy has been one of the most significant and successful advances, it is not effective for all patients with neovascular AMD. The potential role of radiation in the management of neovascular AMD has been suggested for several years. While previous work focused on the role of radiation alone, recent trials have evaluated the role of ionizing radiation as a synergistic treatment with anti-VEGF drugs, with endpoints being to reduce choroidal neovascular lesions faster, preserve visual acuity, and extend the treatment interval between injections. We review the current evidence available for the safety and efficacy of radiation in conjunction with anti-VEGF treatment for neovascular AMD delivered using three approaches-epimacular brachytherapy involving a pars plana vitrectomy (Vidion Neovista, Inc., Newark, CA, USA), episcleral brachytherapy without a pars plana vitrectomy (Salutaris Medical Devices, Tucson, AZ), and low-voltage stereotactic radiotherapy (IRay,

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DNA Damage in Human Endothelial Cells after Irradiation in Anoxia

Cited by 16 publications

References 23 publications

Tumor Hypoxia as a Modifier of DNA Strand Break and Cross-Link Repair

Tumor Hypoxia as a Modifier of DNA Strand Break and Cross-Link Repair

Irradiation for Inhibition of Endothelial Cell Growth in vitro

Brachytherapy in Neovascular AMD

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