Ionizing radiation modulates vascular endothelial growth factor (VEGF) expression through multiple mitogen activated protein kinase dependent pathways

Park, Jong‐Sung; Qiao, Li; Su, Zao-Zong; Hinman, Darin; Willoughby, Karen A.; McKinstry, Robert; Yacoub, Adly; Duigou, Gregory J.; Young, C. S. H.; Grant, Steven; Hagan, Michael P.; Ellis, Elliot F.; Fisher, Paul B.; Dent, Paul

doi:10.1038/sj.onc.1204258

Cited by 119 publications

(86 citation statements)

References 44 publications

(73 reference statements)

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“…Together with Davies et al's findings on the enhanced penetration and the improved intratumoral distribution of PEGylated liposomal doxorubicin in response to radiotherapy, these observations suggest that radiotherapy beneficially affects both arms of the EPR effect: on the one hand, by e.g. enhancing the expression of VEGF (Li et al, 2000;Park et al, 2001), it likely increases the permeability of the tumour blood vessels towards long-circulating nanomedicines, and on the other hand, by e.g. reducing the tumour cell density (Peschke et al, 1999) and the interstitial fluid pressure (Znati et al, 1996), it likely enhances their retention and their intratumoral distribution.…”

Section: Discussionmentioning

confidence: 97%

“…Besides reflecting, for instance, on the integrity and function of the tumour vasculature (V), and on the expression of certain cellular receptors (R), it is also known to affect several cell membrane-related (C), nuclear (N), mitochondrial (M) and signalling (S) processes. By eliciting such effects, radiotherapy has been shown to induce (I) an increase in the production of vascular endothelial growth factor (VEGF) (Park et al, 2001) and fibroblast growth factor (FGF) (Lee et al, 1995), (II) an increase in apoptosis and endothelial cell apoptosis (Garcia-Barros et al, 2003), (III) a decrease in tumour cell density (Peschke et al, 1999), and (IV) a reduction in interstitial fluid pressure (Znati et al, 1996). By means of the former phenomenon, radiotherapy is considered to be able to increase the permeability of the vasculature towards long-circulating nanomedicines (Samaniego et al, 1998;Feng et al, 1999), and by means of the latter three, it likely improves their penetration and their intratumoral distribution (Jain, 1994;Netti et al, 1995;Au et al, 2001).…”

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confidence: 99%

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Image-guided and passively tumour-targeted polymeric nanomedicines for radiochemotherapy

Subr²,

et al. 2008

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Drug targeting systems are nanometer-sized carrier materials designed for improving the biodistribution of systemically applied (chemo-) therapeutics. Reasoning that (I) the temporal and spatial interaction between systemically applied chemotherapy and clinically relevant fractionated radiotherapy is suboptimal, and that (II) drug targeting systems are able to improve the temporal and spatial parameters of this interaction, we have here set out to evaluate the potential of 'carrier-based radiochemotherapy'. N-(2-hydroxypropyl)methacrylamide (HPMA) copolymers were used as a model drug targeting system, doxorubicin and gemcitabine as model drugs, and the syngeneic and radio-and chemoresistant Dunning AT1 rat prostate carcinoma as a model tumour model. Using magnetic resonance imaging and g-scintigraphy, the polymeric drug carriers were first shown to circulate for prolonged periods of time, to localise to tumours both effectively and selectively, and to improve the tumour-directed delivery of low molecular weight agents. Subsequently, they were then shown to interact synergistically with radiotherapy, with radiotherapy increasing the tumour accumulation of the copolymers, and with the copolymers increasing the therapeutic index of radiochemotherapy (both for doxorubicin and for gemcitabine). Based on these findings, and on the fact that its principles are likely broadly applicable, we propose carrier-based radiochemotherapy as a novel concept for treating advanced solid malignancies.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

Image-guided and passively tumour-targeted polymeric nanomedicines for radiochemotherapy

Subr²,

et al. 2008

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“…The advantage of using the PEG-Prom in these cancer contexts is its apparent ubiquitous cancer specificity. PEA-3 and AP-1 transactivation and subsequently PEG-Prom activity are positively regulated by the ras-dependent signaling cascade (18,19,44). Because activation of the ras pathway is a frequent event in diverse cancers, including breast cancer, the ability of the PEG-Prom to drive transgene expression in these cancers will be robust and specific (45,46).…”

Section: Discussionmentioning

confidence: 99%

Dual cancer-specific targeting strategy cures primary and distant breast carcinomas in nude mice

Sarkar

Vozhilla

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

117

185

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Limitations of current viral-based gene therapies for malignant tumors include lack of cancer-specific targeting and insufficient tumor delivery. To ameliorate these problems and develop a truly effective adenovirus gene-based therapy for cancer, we constructed a conditionally replication competent adenovirus (CRCA) manifesting the unique properties of tumor-specific virus replication in combination with production of a cancer-selective cytotoxic cytokine, melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24), which embodies potent bystander antitumor activity. Cancer cell selective tropism was ensured by engineering the expression of the adenoviral E1A protein, necessary for viral replication, under the control of a minimal promoter region of progression elevated gene-3 (PEG-3), which functions selectively in diverse cancer cells with minimal activity in normal cells. In the E3 region of this CRCA, we introduced the mda-7/IL-24 gene, thereby mediating robust production of this cytokine as a function of adenovirus replication. Infection of this CRCA (designated Ad.PEG-E1A-mda-7) in normal mammary epithelial cells and breast cancer cells confirmed cancer cell selective adenoviral replication, mda-7/ IL-24 expression, growth inhibition, and apoptosis induction. Injecting Ad.PEG-E1A-mda-7 into human breast cancer xenografts in athymic nude mice completely eradicated not only the primary tumor but also distant tumors (established on the opposite flank of the animal) thereby implementing a cure. This dual cancer-specific targeting strategy provides an effective approach for treating breast and other human neoplasms with the potential for eradicating both primary tumors and metastatic disease. Additionally, these studies support the potential use of mda-7/IL-24 in the therapy of malignant cancers.bystander antitumor activity ͉ conditionally replication competent adenovirus ͉ PEG-Prom ͉ mda-7͞IL-24 ͉ in vivo tumorigenesis

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“…Proteasome inhibition would be expected to prevent NF-kB activation, but numerous studies have shown radiation to activate it (Li and Karin, 1998;Raju et al, 1998). Activation of NF-kB is considered to mediate radiation-induced proinflammatory responses, and irradiation of cells and tissues increases expression of proinflammatory chemokines (Johnston et al, 2002) and cytokines such as TNF-a (Hallahan et al, 1989;Chiang et al, 1993), IL-1a and -b (Hong et al, 1994;Hosoi et al, 2001), IL-5 (Lu-Hesselmann et al, 1997), IL-6 (Abeyama et al, 1995;Beetz et al, 1997), GM-CSF (Zhang et al, 1994), IFN-a (Woloschak et al, 1990), bFGF (Haimovitz-Friedman et al, 1991), and VEGF (Gorski et al, 1999;Park et al, 2001), as well as proinflammatory cell adhesion molecules (ICAM-1 (Behrends et al, 1994;Hong et al, 1994;Gaugler et al, 1997), E-selectin (Hallahan et al, 1995), and VCAM-1 (Heckmann et al, 1998)), prostaglandins and leukotrienes (Eisen et al, 1977;Iwamoto and McBride, 1992), proteases (Hong et al, 1994;Patel et al, 1998;Fittkau et al, 2001), and prooxidant species. If the damage is not too severe, this is normally counterbalanced in time by production of anti-inflammatory cytokines, antiproteases, antioxidants, and heat-shock proteins leading to resolution of the inflammation (Barcellos-Hoff, 1993;Sierra-Rivera et al, 1993;Broski and Halloran, 1994;Sadekova et al, 1997;Roedel et al, 2002).…”

Section: Cellular Consequences Of Modulation Of Proteasome Activity Bmentioning

confidence: 99%

The role of the ubiquitin/proteasome system in cellular responses to radiation

et al. 2003

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Ionizing radiation modulates vascular endothelial growth factor (VEGF) expression through multiple mitogen activated protein kinase dependent pathways

Cited by 119 publications

References 44 publications

Image-guided and passively tumour-targeted polymeric nanomedicines for radiochemotherapy

Image-guided and passively tumour-targeted polymeric nanomedicines for radiochemotherapy

Dual cancer-specific targeting strategy cures primary and distant breast carcinomas in nude mice

The role of the ubiquitin/proteasome system in cellular responses to radiation

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