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Article ; Online: Application of radiotherapy and chemotherapy protocols to pre-clinical tumor models.

Burd, Randy / Wachsberger, Phyllis

Current protocols in pharmacology

2007 Volume Chapter 14, Page(s) Unit 14.7

Abstract: This unit (1) provides background into understanding how agents that target specific molecules or receptors (molecular-targeted agents), in particular, agents affecting the tumor vasculature (perivasculature network in tumors), interact with and modify ... ...

Abstract	This unit (1) provides background into understanding how agents that target specific molecules or receptors (molecular-targeted agents), in particular, agents affecting the tumor vasculature (perivasculature network in tumors), interact with and modify radiation therapy; (2) details factors affecting interpretation of results in murine tumor model experiments utilizing radiation therapy and drug combinations; and (3) provides specific protocols for the application of radiation therapy, both alone and in combination with chemotherapy and/or molecular-targeted agents.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Animals ; Cell Hypoxia ; Disease Models, Animal ; Fluorodeoxyglucose F18 ; Humans ; Mice ; Mice, SCID ; Neoplasms, Experimental/drug therapy ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/radiotherapy ; Oxygen Consumption ; Xenograft Model Antitumor Assays
Chemical Substances	Angiogenesis Inhibitors ; Fluorodeoxyglucose F18 (0Z5B2CJX4D)
Language	English
Publishing date	2007-09
Publishing country	United States
Document type	Journal Article
ISSN	1934-8290
ISSN (online)	1934-8290
DOI	10.1002/0471141755.ph1407s38
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Article: Acoustic radiation force and optical spectroscopy for assessing tumor vessel normalization during anti-angiogenic therapy.

Yan, Kaiguo / Wachsberger, Phyllis / Yu, Yan

Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference

2009 Volume 2009, Page(s) 769–772

Abstract: Molecular oxygen is the best known mediator of radiation damage during radiation therapy. This paper investigates techniques for enhancing tumor oxygenation by use of anti-angiogenic therapy for better radiosensitivity. A noninvasive monitoring technique, ...

Abstract	Molecular oxygen is the best known mediator of radiation damage during radiation therapy. This paper investigates techniques for enhancing tumor oxygenation by use of anti-angiogenic therapy for better radiosensitivity. A noninvasive monitoring technique, Acoustic radiation force (ARF)-induced optical spectroscopy, was proposed in this paper to track tumor oxygen changes during anti-angiogenic therapy. Male NCR-NUM nude mice bearing human U87 glioblastoma (ATCC) xenografts on the right hind limb were used for the study. An anti-angiogenic regimen using the drug AZD2171 (AsraZeneca) was found capable of improving tissue oxygenation during the first week of drug treatment. The optical spectroscopy technique was shown to be able to track tumor oxygenation changes during anti-angiogenic therapy, as verified by direct pO2 measurement. By using anti-angiogenic therapy to improve tumor oxygenation prior to radiotherapy, tissue oxygenation may be altered in a way that favors radiation therapy.
MeSH term(s)	Acoustics ; Angiogenesis Inhibitors/administration & dosage ; Animals ; Biomarkers, Tumor/analysis ; Cell Line, Tumor ; Glioblastoma/blood supply ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Humans ; Male ; Mice ; Mice, Nude ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Oxygen/analysis ; Quinazolines/administration & dosage ; Reproducibility of Results ; Sensitivity and Specificity ; Spectrum Analysis/methods ; Treatment Outcome
Chemical Substances	Angiogenesis Inhibitors ; Biomarkers, Tumor ; Quinazolines ; cediranib (NQU9IPY4K9) ; Oxygen (S88TT14065)
Language	English
Publishing date	2009-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2375-7477
ISSN	2375-7477
DOI	10.1109/IEMBS.2009.5333814
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Article: Investigation of acoustic radiation force for radio-protecting normal tissues during radiation therapy.

Yan, Kaiguo / Wachsberger, Phyllis / Yu, Yan

Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference

2009 Volume 2009, Page(s) 2304–2307

Abstract: Radiation therapy (radiotherapy) is the medical use of ionizing radiation as part of cancer treatment to erradicate malignant cells. Normal tissue tolerance is currently a major dose-limiting factor. As molecular oxygen plays a critical role in creating ... ...

Abstract	Radiation therapy (radiotherapy) is the medical use of ionizing radiation as part of cancer treatment to erradicate malignant cells. Normal tissue tolerance is currently a major dose-limiting factor. As molecular oxygen plays a critical role in creating the radiation damage, we propose a novel approach, that is, the use of acoustic radiation force (ARF) to suppress the normal tissue oxygenation, for the purpose of protecting the normal tissue and increasing its tolerance during radiotherapy. This paper investigated the effects of ARF on tissue oxygenation. Both subcutaneous tissue and tumor were studied for comparison. Experiments have been carried out using a murine model. Preliminary results showed that ARF can effectively suppress normal tissue oxygenation, and at the same time had negligible effect on the tumor oxygenation. Further investigation is ongoing to characterize the time course of oxygen changes with different ultrasound parameters (frequency, intensity, ultrasound pulse duration, etc.), for the purpose of optimal control of tissue oxygenation.
MeSH term(s)	Acoustics ; Animals ; Biomedical Engineering/methods ; Cell Line, Tumor ; Equipment Design ; Fiber Optic Technology ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Oxygen/chemistry ; Radiation Injuries/prevention & control ; Radiation Tolerance ; Radiotherapy/adverse effects ; Ultrasonics
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2009-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2375-7477
ISSN	2375-7477
DOI	10.1109/IEMBS.2009.5335044
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Article: Epidermal growth factor receptor mutation status and rad51 determine the response of glioblastoma to multimodality therapy with cetuximab, temozolomide, and radiation.

Wachsberger, Phyllis Rachelle / Lawrence, Richard Yaacov / Liu, Yi / Rice, Barbara / Daskalakis, Constantine / Dicker, Adam P

Frontiers in oncology

2013 Volume 3, Page(s) 13

Abstract: Purpose: EGFR amplification and mutation (i.e., EGFRvIII) are found in 40% of primary GBM tumors and are believed to contribute to tumor development and therapeutic resistance. This study was designed to investigate how EGFR mutational status modulates ... ...

Abstract	Purpose: EGFR amplification and mutation (i.e., EGFRvIII) are found in 40% of primary GBM tumors and are believed to contribute to tumor development and therapeutic resistance. This study was designed to investigate how EGFR mutational status modulates response to multimodality treatment with cetuximab, an anti-EGFR inhibitor, the chemotherapeutic agent, temozolomide (TMZ), and radiation therapy (RT). Methods and materials: In vitro and in vivo experiments were performed on two isogenic U87 GBM cell lines: one overexpressing wildtype EGFR (U87wtEGFR) and the other overexpressing EGFRvIII (U87EGFRvIII). Results: Xenografts harboring EGFRvIII were more sensitive to TMZ alone and TMZ in combination with RT and/or cetuximab than xenografts expressing wtEGFR. In vitro experiments demonstrated that U87EGFRvIII-expressing tumors appear to harbor defective DNA homologous recombination repair in the form of Rad51 processing. Conclusion: The difference in sensitivity between EGFR-expressing and EGFRvIII-expressing tumors to combined modality treatment may help in the future tailoring of GBM therapy to subsets of patients expressing more or less of the EGFR mutant.
Language	English
Publishing date	2013-02-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2013.00013
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Article ; Online: Hsp90 inhibition enhances PI-3 kinase inhibition and radiosensitivity in glioblastoma.

Wachsberger, Phyllis R / Lawrence, Yaacov Richard / Liu, Yi / Rice, Barbara / Feo, Nicholas / Leiby, Benjamin / Dicker, Adam P

Journal of cancer research and clinical oncology

2014 Volume 140, Issue 4, Page(s) 573–582

Abstract: Purpose: Combined targeting with a PI3-kinase inhibitor, BKM120, and an Hsp90 inhibitor, HSP990, was investigated as a multi-targeted approach to potentiate cell death in glioblastoma (GBM). Additionally, the effect of dual drug treatment combined with ... ...

Abstract	Purpose: Combined targeting with a PI3-kinase inhibitor, BKM120, and an Hsp90 inhibitor, HSP990, was investigated as a multi-targeted approach to potentiate cell death in glioblastoma (GBM). Additionally, the effect of dual drug treatment combined with cytotoxic stress (radiation therapy) was examined. Methods: Four human GBM cell lines containing wild-type or mutated PTEN and/or p53 were studied. The effects of drug treatments on cell viability, apoptosis induction, pAKt activity, cell cycle arrest, clonogenicity, and tumor growth delay were studied. Results: Combined concurrent treatment with both drugs produced more cell killing in cell viability and apoptosis assays than either drug alone. BKM120 plus HSP990 induced suppression of baseline Akt signaling as well as radiation (RT)-induced pAkt signaling in all cell lines. Cell cycle analysis revealed that HSP990 and BKM120, singly or combined, induced G2/M arrest leading to apoptosis/necrosis and polyploidy. Additionally, the drugs radiosensitized GBM cells in clonogenic assays. In vivo tumor growth delay studies demonstrated the effectiveness of combined drug treatment with HSP990 and BKM120 over single drug treatment, as well as the effectiveness of combined drug treatment in enhancing the effectiveness of radiation therapy. Conclusions: In conclusion, HSP990 and BKM120, with and without RT, are active agents against glioma tumors. The sensitivity to these agents does not appear to depend on PTEN/p53status in the cell lines tested. We suggest that the combined action of both drugs is a viable multi-targeted strategy with the potential to improve clinical outcome for patients with high-grade glioma.
MeSH term(s)	Aminopyridines/pharmacology ; Animals ; Apoptosis/drug effects ; Blotting, Western ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Brain Neoplasms/radiotherapy ; Cell Proliferation/drug effects ; Flow Cytometry ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/radiation effects ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Glioblastoma/radiotherapy ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; HSP90 Heat-Shock Proteins/metabolism ; Humans ; Mice ; Mice, Nude ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Radiation Tolerance/drug effects ; Radiation-Sensitizing Agents/pharmacology ; Tumor Cells, Cultured
Chemical Substances	Aminopyridines ; HSP90 Heat-Shock Proteins ; Morpholines ; NVP-BKM120 ; Phosphoinositide-3 Kinase Inhibitors ; Radiation-Sensitizing Agents ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
Language	English
Publishing date	2014-02-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	134792-5
ISSN	1432-1335 ; 0171-5216 ; 0084-5353 ; 0943-9382
ISSN (online)	1432-1335
ISSN	0171-5216 ; 0084-5353 ; 0943-9382
DOI	10.1007/s00432-014-1594-6
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Article ; Online: Cediranib enhances control of wild type EGFR and EGFRvIII-expressing gliomas through potentiating temozolomide, but not through radiosensitization: implications for the clinic.

Wachsberger, Phyllis R / Lawrence, Richard Yaacov / Liu, Yi / Xia, Xu / Andersen, Barbara / Dicker, Adam P

Journal of neuro-oncology

2011 Volume 105, Issue 2, Page(s) 181–190

Abstract: Glioblastomas (GBM) frequently overexpress the epidermal growth factor receptor (wtEGFR) or its mutant, EGFRvIII, contributing to chemo- and radioresistance. The current standard of care is surgery followed by radiation therapy with concurrent ... ...

Abstract	Glioblastomas (GBM) frequently overexpress the epidermal growth factor receptor (wtEGFR) or its mutant, EGFRvIII, contributing to chemo- and radioresistance. The current standard of care is surgery followed by radiation therapy with concurrent temozolomide (TMZ) followed by adjuvant TMZ. New treatment strategies for GBM include blockade of EGFR signaling and angiogenesis. Cediranib is a highly potent receptor tyrosine kinase inhibitor that inhibits all three VEGF receptors. This study investigated the radiosensitizing potential of cediranib in combination with TMZ in U87 GBM xenografts expressing wtEGFR or EGFRvIII. U87 GBM cells stably transfected with either wtEGFR or EGFRvIII were injected into the hind limbs of nude mice. Cediranib was dosed at 3 mg/kg daily five times a week orally for 2 weeks. TMZ was dosed at 10 mg/kg once only on day 0. Radiotherapy (RT) consisted of 3 fractions of 5 Gy (days 0-2). Cediranib did not radiosensitize either tumor type; however, cediranib did enhance the effectiveness of TMZ in both transfectants. Our results suggest that combining cediranib with temozolomide in the clinic will lead to improved tumor control.
MeSH term(s)	Animals ; Antineoplastic Agents, Alkylating/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/radiotherapy ; Cell Survival/drug effects ; Cell Survival/radiation effects ; Dacarbazine/analogs & derivatives ; Dacarbazine/therapeutic use ; ErbB Receptors/metabolism ; Glioma/drug therapy ; Glioma/metabolism ; Glioma/radiotherapy ; Humans ; Immunoblotting ; Mice ; Mice, Nude ; Quinazolines/therapeutic use ; Radiation Tolerance/drug effects ; Temozolomide ; Tumor Cells, Cultured ; Tumor Stem Cell Assay ; Vascular Endothelial Growth Factor A/metabolism ; X-Rays
Chemical Substances	Antineoplastic Agents, Alkylating ; Quinazolines ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; epidermal growth factor receptor VIII ; Dacarbazine (7GR28W0FJI) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; cediranib (NQU9IPY4K9) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2011-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604875-4
ISSN	1573-7373 ; 0167-594X
ISSN (online)	1573-7373
ISSN	0167-594X
DOI	10.1007/s11060-011-0580-y
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Article: Improving tumor response to radiotherapy by targeting angiogenesis signaling pathways.

Wachsberger, Phyllis / Burd, Randy / Dicker, Adam P

Hematology/oncology clinics of North America

2004 Volume 18, Issue 5, Page(s) 1039–57, viii

Abstract: Radiotherapy is one of the most widely used treatments for cancer; however, the development of tumor radioresistance is an ongoing problem. Agents that target tumor angiogenesis are being used in combination with radiotherapy to improve the therapeutic ... ...

Abstract	Radiotherapy is one of the most widely used treatments for cancer; however, the development of tumor radioresistance is an ongoing problem. Agents that target tumor angiogenesis are being used in combination with radiotherapy to improve the therapeutic index without a clear understanding of how these agents may affect radiosensitization. This article discusses recently published studies that may shed some light on the underlying signaling mechanisms that are involved in the interactions of antiangiogenic agents with ionizing radiation.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Animals ; Humans ; Neoplasms/blood supply ; Neoplasms/radiotherapy ; Neovascularization, Pathologic/radiotherapy ; Signal Transduction
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2004-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	93115-9
ISSN	1558-1977 ; 0889-8588
ISSN (online)	1558-1977
ISSN	0889-8588
DOI	10.1016/j.hoc.2004.06.007
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Article ; Online: Epidermal growth factor receptor (EGFR) mutation status and Rad51 determine the response of glioblastoma (GBM) to multimodality therapy with cetuximab, temozolomide and radiation

PhyllisRachelleWachsberger / RichardYaacovLawrence / ConstantineDaskalakis

Frontiers in Oncology, Vol

2013 Volume 3

Abstract	Purpose: EGFR amplification and mutation (i.e., EGFRvIII) are found in 40% of primary GBM tumors and are believed to contribute to tumor development and therapeutic resistance. This study was designed to investigate how EGFR mutational status modulates response to multimodality treatment with cetuximab, an anti-EGFR inhibitor, the chemotherapeutic agent, temozolamide (TMZ) and radiation therapy (RT) Methods and Materials: In vitro and in vivo experiments were performed on two isogenic U87 GBM cell lines: one overexpressing wildtype EGFR (U87wtEGFR) and the other overexpressing EGFRvIII (U87EGFRvIII). Results: Xenografts harboring EGFRvIII were more sensitive to TMZ alone and TMZ in combination with RT and/or cetuximab than xenografts expressing wtEGFR. In vitro experiments demonstrated that U87EGFRvIII-expressing tumors appear to harbor defective DNA homologous recombination repair in the form of Rad51 processing, Conclusions: The difference in sensitivity between EGFR-expressing and EGFRvIII-expressing tumors to combined modality treatment may help in the future tailoring of GBM therapy to subsets of patients expressing more or less of the EGFR mutant.
Keywords	radiation therapy ; EGFR ; cetuximab ; GBM ; RAD51 ; temozolomide ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R
Subject code	616
Language	English
Publishing date	2013-02-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Epidermal growth factor receptor expression modulates antitumor efficacy of vandetanib or cediranib combined with radiotherapy in human glioblastoma xenografts.

Wachsberger, Phyllis R / Lawrence, Yaacov R / Liu, Yi / Daroczi, Borbala / Xu, Xia / Dicker, Adam P

International journal of radiation oncology, biology, physics

2010 Volume 82, Issue 1, Page(s) 483–491

Abstract: Purpose: The purpose of this study was to determine the ability of radiation therapy (RT) combined with the tyrosine kinase inhibitors (TKI) vandetanib (antiepidermal growth factor receptor [EGFR] plus antivascular endothelial growth factor receptor [ ... ...

Abstract	Purpose: The purpose of this study was to determine the ability of radiation therapy (RT) combined with the tyrosine kinase inhibitors (TKI) vandetanib (antiepidermal growth factor receptor [EGFR] plus antivascular endothelial growth factor receptor [anti-VEGFR]) and cediranib (anti-VEGFR) to inhibit glioblastoma multiforme (GBM) growth. A secondary aim was to investigate how this regimen is modulated by tumor EGFR expression. Methods and materials: Radiosensitivity was assessed by clonogenic cell survival assay. VEGF secretion was quantified by enzyme-linked immunosorbent assay. GBM (U87MG wild-type EGFR [wtEGFR] and U87MG EGFR-null) xenografts were treated with vandetanib, cediranib, and RT, alone or in combinations. Excised tumor sections were stained for proliferative and survival biomarkers. Results: In vitro, U87MG wtEGFR and U87 EGFR-null cells had similar growth kinetics. Neither TKI affected clonogenic cell survival following RT. However, in vivo, exogenous overexpression of wtEGFR decreased tumor doubling time (T2x) in U87MG xenografts (2.70 vs. 4.41 days for U87MG wtEGFR vs. U87MG vector, respectively). In U87MG EGFR-null cells, TKI combined with radiation was no better than radiation therapy alone. In U87MG wtEGFR, RT in combination with vandetanib (but not with cediranib) significantly increased tumor T2x compared with RT alone (T2x, 10.4 days vs. 4.8 days; p < 0.001). In vivo, growth delay correlated with suppression of pAkt, survivin, and Ki67 expression in tumor samples. The presence of EGFR augmented RT-stimulated VEGF release; this effect was inhibited by vandetanib. Conclusions: EGFR expression promoted tumor growth in vivo but not in vitro, suggesting a microenvironmental effect. GBM xenografts expressing EGFR exhibited greater sensitivity to both cediranib and vandetanib than EGFR-null tumors. Hence EGFR status plays a major role in determining a tumor's in vivo response to radiation combined with TKI, supporting a "personalized" approach to GBM management.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor ; Chemoradiotherapy/methods ; Drug Administration Schedule ; ErbB Receptors/metabolism ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Glioblastoma/therapy ; Humans ; Mice ; Mice, Nude ; Neoplasm Proteins/metabolism ; Piperidines/therapeutic use ; Quinazolines/therapeutic use ; Radiation Tolerance ; Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors ; Tumor Burden ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor ; Neoplasm Proteins ; Piperidines ; Quinazolines ; ErbB Receptors (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; cediranib (NQU9IPY4K9) ; vandetanib (YO460OQ37K)
Language	English
Publishing date	2010-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	197614-x
ISSN	1879-355X ; 0360-3016
ISSN (online)	1879-355X
ISSN	0360-3016
DOI	10.1016/j.ijrobp.2010.09.019
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Article: Tumor response to ionizing radiation combined with antiangiogenesis or vascular targeting agents: exploring mechanisms of interaction.

Wachsberger, Phyllis / Burd, Randy / Dicker, Adam P

Clinical cancer research : an official journal of the American Association for Cancer Research

2003 Volume 9, Issue 6, Page(s) 1957–1971

Abstract: Recent preclinical studies have suggested that radiotherapy in combination with antiangiogenic/vasculature targeting agents enhances the therapeutic ratio of ionizing radiation alone. Because radiotherapy is one of the most widely used treatments for ... ...

Abstract	Recent preclinical studies have suggested that radiotherapy in combination with antiangiogenic/vasculature targeting agents enhances the therapeutic ratio of ionizing radiation alone. Because radiotherapy is one of the most widely used treatments for cancer, it is important to understand how best to use these two modalities to aid in the design of rational patient protocols. The mechanisms of interaction between antiangiogenic/vasculature targeting agents and ionizing radiation are complex and involve interactions between the tumor stroma and vasculature and the tumor cells themselves. Vascular targeting agents are aimed specifically at the existing tumor vasculature. Antiangiogenic agents target angiogenesis or the new growth of tumor vessels. These agents can decrease overall tumor resistance to radiation by affecting both tumor cells and tumor vasculature, thereby breaking the codependent cycle of tumor growth and angiogenesis. The hypoxic microenvironment of the tumor also contributes to the mechanisms of interactions between antiangiogenic/vasculature targeting agents and ionizing radiation. Hypoxia stimulates up-regulation of angiogenic and tumor cell survival factors, giving rise to tumor proliferation, radioresistance, and angiogenesis. Preclinical evidence suggests that antiangiogenic agents reduce tumor hypoxia and provides a rationale for combining these agents with ionizing radiation. Optimal scheduling of combined treatment with these agents and ionizing radiation will ultimately depend on understanding how tumor oxygenation changes as tumors regress and regrow during exposure to these agents. This review article explores the complex interactions between antiangiogenic/vasculature targeting agents and radiation and offers insight into the mechanisms of interaction that may be responsible for improved tumor response to radiation.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Animals ; Apoptosis/drug effects ; Clinical Trials as Topic ; Combined Modality Therapy ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/pharmacology ; Humans ; Isoenzymes ; Membrane Proteins ; Neoplasm Metastasis ; Neoplasms/blood supply ; Neoplasms/metabolism ; Neoplasms/radiotherapy ; Prostaglandin-Endoperoxide Synthases ; Receptors, Vascular Endothelial Growth Factor/physiology ; Signal Transduction ; Vascular Endothelial Growth Factor A/physiology
Chemical Substances	Angiogenesis Inhibitors ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; Isoenzymes ; Membrane Proteins ; Vascular Endothelial Growth Factor A ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2003-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
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