Radiation activates HIF-1 to regulate vascular radiosensitivity in tumors: role of reoxygenation, free radicals, and stress granules
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TLDR
Novel pathways contributing significantly to the understanding of HIF-1 regulation which may be major determinants of tumor radiosensitivity, potentially having high clinical relevance are described.About:
This article is published in Cancer Cell.The article was published on 2004-05-01 and is currently open access. It has received 928 citations till now. The article focuses on the topics: Radiosensitivity & Angiogenesis.read more
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Safety and Efficacy of Stereotactic Radiosurgery and Adjuvant Bevacizumab in Patients With Recurrent Malignant Gliomas
Kyle C. Cuneo,James J. Vredenburgh,John H. Sampson,David A. Reardon,Annick Desjardins,Katherine B. Peters,Henry S. Friedman,Christopher G. Willett,John P. Kirkpatrick +8 more
TL;DR: The combination of salvage radiosurgery and bevacizumab to treat recurrent malignant gliomas is well tolerated and seems to be associated with improved outcomes.
Journal ArticleDOI
Cancer cells that survive radiation therapy acquire HIF-1 activity and translocate towards tumour blood vessels
Hiroshi Harada,Masahiro Inoue,Satoshi Itasaka,Kiichi Hirota,Akiyo Morinibu,Kazumi Shinomiya,Lihua Zeng,Lihua Zeng,Guangfei Ou,Yuxi Zhu,Michio Yoshimura,Michio Yoshimura,W. Gillies McKenna,Ruth J. Muschel,Masahiro Hiraoka +14 more
TL;DR: For the first time, the HIF-1-dependent cellular dynamics during post-irradiation tumour recurrence are unveiled and provide a rational basis for targeting Hif-1 after radiation therapy.
Journal ArticleDOI
How Can We Overcome Tumor Hypoxia in Radiation Therapy
TL;DR: Fundamental problems surrounding tumor hypoxia in current radiation therapy, the function of HIF-1 in tumor radioresistance, the dynamics of hypoxic tumor cells during tumor growth and after radiation Therapy, and how to overcome the difficulties with radiation therapy using innovative interdisciplinary technologies are overviewed.
Journal ArticleDOI
Codependent functions of RSK2 and the apoptosis-promoting factor TIA-1 in stress granule assembly and cell survival.
T.S. Karin Eisinger-Mathason,Josefa Andrade,Angela L. Groehler,David E. Clark,Tara L. Muratore-Schroeder,Lejla Pasic,Jeffrey A. Smith,Jeffrey Shabanowitz,Donald F. Hunt,Ian G. Macara,Deborah A. Lannigan +10 more
TL;DR: Surprisingly, nuclear localization of RSK2 is sufficient to enhance proliferation through induction of cyclin D1, in the absence of other active signaling pathways, and is a pivotal factor linking the stress response to survival and proliferation.
Journal ArticleDOI
Hypoxia-induced genetic instability—a calculated mechanism underlying tumor progression
TL;DR: It is proposed that tumor development is a result of expansion and progression—two complementary aspects that collaborate with the tumor microenvironment—hypoxia in particular, on genetic alterations through the induction of genetic instability.
References
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Role of angiogenesis in tumor growth and metastasis
TL;DR: Preclinical studies have shown that endostatin effectively inhibits tumor growth and shrinks existing tumor blood vessels and therapy with endogenous inhibitors of angiogenesis, such asendostatin and angiostatin may reverse the angiogenic switch preventing growth of tumor vasculature.
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Mitochondrial reactive oxygen species trigger hypoxia-induced transcription
Navdeep S. Chandel,Emin Maltepe,Eugene Goldwasser,Carol Mathieu,M. C. Simon,Paul T. Schumacker +5 more
TL;DR: In this paper, the authors tested whether mitochondria act as O2 sensors during hypoxia and whether cobalt activated transcription by increasing the generation of reactive oxygen species (ROS).
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Reactive oxygen species generated at mitochondrial complex III stabilize hypoxia-inducible factor-1alpha during hypoxia: a mechanism of O2 sensing.
Navdeep S. Chandel,David S. McClintock,C E Feliciano,T M Wood,J A Melendez,A M Rodriguez,Paul T. Schumacker +6 more
TL;DR: Findings reveal that mitochondria-derived ROS are both required and sufficient to initiate HIF-1α stabilization during hypoxia and that catalase abolishes hypoxic response element-luciferase expression during Hypoxia.
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Tumor Response to Radiotherapy Regulated by Endothelial Cell Apoptosis
Monica Garcia-Barros,François Paris,Carlos Cordon-Cardo,David Lyden,Shahin Rafii,Adriana Haimovitz-Friedman,Zvi Fuks,Richard Kolesnick +7 more
TL;DR: Microvascular damage regulates tumor cell response to radiation at the clinically relevant dose range, indicating that endothelial apoptosis is a homeostatic factor regulating angiogenesis-dependent tumor growth.
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Vascular Endothelial Growth Factor
TL;DR: A historic account of the challenges associated with the discovery of VEGF and the early steps in elucidating the role of this molecule in the regulation of angiogenesis is provided.