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3. Hong YK, Chung DS, Joe YA, Yang YJ, Kim KM, Park YS, Yung WK, Kang JK: Efficient inhibition of in vivo human malignant glioma growth and angiogenesis by interferon-beta treatment at early stage of tumor development. Clin Cancer Res; 2000 Aug;6(8):3354-60
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  • [Title] Efficient inhibition of in vivo human malignant glioma growth and angiogenesis by interferon-beta treatment at early stage of tumor development.
  • Malignant gliomas are highly angiogenic and aggressive tumors.
  • IFN-beta has been used for the treatment of patients with malignant glioma; however, its antitumor mechanism in vivo remains unclear.
  • To understand the in vivo antitumor effect and mechanism of recombinant human IFN-beta (rhIFN-beta) depending on the stages of tumor development or progression, we used orthotopic xenograft brain tumors generated by stereotactic intracerebral implantation of U-87 human glioma cells in nude mice.
  • Tumor growth was suppressed by 69.6% in group 1 and 10.8% in group 2 compared with tumors of each control group treated with saline. rhIFN-beta-treated group 1 animals showed 38% reduction in vascularization along with a 2.5-fold increase of the apoptotic index and no change in the proliferative index as compared with untreated tumors.
  • The expression level of vascular endothelial cell growth factor and basic fibroblast growth factor was not affected by rhIFN-beta treatment. rhIFN-beta showed inhibitory activity on proliferation of U-87 cells, human umbilical vein endothelial cells, and PAM 212 murine keratinocytes in vitro.
  • Our results indicate that the in vivo antitumor effect of rhIFN-beta on malignant gliomas may be mediated, at least in part, via angiogenesis inhibition rather than antiproliferative activity and that rhIFN-beta may be more effective for the treatment of malignant glioma patients at an early stage with minimal or microscopic tumor burdens rather than at an advanced stage of tumor development.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Interferon Type I / pharmacology. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Division / drug effects. Endothelial Growth Factors / biosynthesis. Fibroblast Growth Factor 2 / biosynthesis. Humans. Immunohistochemistry. Lymphokines / biosynthesis. Mice. Mice, Nude. Recombinant Proteins. Stereotaxic Techniques. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors. Xenograft Model Antitumor Assays

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  • (PMID = 10955823.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Endothelial Growth Factors; 0 / Interferon Type I; 0 / Lymphokines; 0 / Recombinant Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2
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4. Wakimoto H, Kesari S, Farrell CJ, Curry WT Jr, Zaupa C, Aghi M, Kuroda T, Stemmer-Rachamimov A, Shah K, Liu TC, Jeyaretna DS, Debasitis J, Pruszak J, Martuza RL, Rabkin SD: Human glioblastoma-derived cancer stem cells: establishment of invasive glioma models and treatment with oncolytic herpes simplex virus vectors. Cancer Res; 2009 Apr 15;69(8):3472-81
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  • [Title] Human glioblastoma-derived cancer stem cells: establishment of invasive glioma models and treatment with oncolytic herpes simplex virus vectors.
  • Glioblastoma, the most malignant type of primary brain tumor, is one of the solid cancers where cancer stem cells have been isolated, and studies have suggested resistance of those cells to chemotherapy and radiotherapy.
  • They grew as neurospheres in serum-free medium with epidermal growth factor and fibroblast growth factor 2, varied in the level of CD133 expression and very efficiently formed highly invasive and/or vascular tumors upon intracerebral implantation into immunodeficient mice.
  • As a novel therapeutic strategy for glioblastoma-derived cancer stem-like cells (GBM-SC), we have tested oncolytic herpes simplex virus (oHSV) vectors.
  • We show that although ICP6 (UL39)-deleted mutants kill GBM-SCs as efficiently as wild-type HSV, the deletion of gamma34.5 significantly attenuated the vectors due to poor replication.
  • Importantly, despite the highly invasive nature of the intracerebral tumors generated by GBM-SCs, intratumoral injection of G47Delta significantly prolonged survival.
  • These results for the first time show the efficacy of oHSV against human GBM-SCs, and correlate this cytotoxic property with specific oHSV mutations.
  • Moreover, the new glioma models described in this study provide powerful tools for testing experimental therapeutics and studying invasion and angiogenesis.

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  • (PMID = 19351838.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS032677; United States / NCI NIH HHS / CA / K08 CA124804-01A1; United States / NINDS NIH HHS / NS / NS-032677; United States / NCI NIH HHS / CA / K08 CA124804; United States / NINDS NIH HHS / NS / R01 NS032677-06; United States / NINDS NIH HHS / NS / P01 NS024279-20A29010; United States / NINDS NIH HHS / NS / NS032677-06; United States / NINDS NIH HHS / NS / NS024279-20A29010
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS104249; NLM/ PMC2785462
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5. Trog D, Moenkemann H, Haertel N, Schüller H, Golubnitschaja O: Expression of ABC-1 transporter is elevated in human glioma cells under irradiation and temozolomide treatment. Amino Acids; 2005 Mar;28(2):213-9
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  • [Title] Expression of ABC-1 transporter is elevated in human glioma cells under irradiation and temozolomide treatment.
  • OBJECTIVE: Chemo-therapeutic treatment of glioma patients has minor success.
  • Little is known about mechanisms of a pronounced resistance of gliomas towards actual therapies, yet.
  • ABC-1 belongs to the group of transporters known to be involved in the export of hydrophobic substances and vascular regulation.
  • This study investigates an effect of both temozolomide (TMZ) treatment and/or irradiation on the expression of the ABC-1 transporter in human U87-MG glioma cells.
  • MATERIAL AND METHODS: In parallel experiments U87-MG cells underwent either irradiation (RT), chemo-treatment (CT) using TMZ, and combined chemo/radiation-treatment (CT/RT).
  • After each treatment the cells were incubated either 2 or 24 hours at 37 degrees C and counted before protein analysis using Western-Blot technique.
  • RESULTS AND CONCLUSIONS: An exponential growth of cellular density was observed for both untreated and irradiated cells being, however, about 2-times slower in irradiated compared to untreated cells.
  • In contrast the density increase of chemo-treated cells as well as that of cells, which underwent the combined CT/RT treatment was of linear nature.
  • Increasing cell density and all kinds of treatment resulted in a considerably enhanced ABC-1 expression.
  • CT treatment resulted in highly up-regulated ABC-1 expression especially in non-confluent cultures compared to untreated cells.
  • The highest expression rates were observed in cultures with high cellular density 2 hours after application of the combined treatment.
  • Strong up-regulation of ABC-1 expression under both irradiation and chemo-treatment might be a clue to multidrug and irradiation cross-resistance mechanisms of malignant glioma cells converting the ABC-1 transporter into an attractive pharmacological target for a clinical breakthrough in the therapy of malignant gliomas.
  • [MeSH-major] ATP-Binding Cassette Transporters / biosynthesis. Antineoplastic Agents, Alkylating / pharmacology. Dacarbazine / analogs & derivatives. Gamma Rays. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / radiation effects. Glioma / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Up-Regulation / drug effects. Up-Regulation / radiation effects

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  • (PMID = 15723240.001).
  • [ISSN] 0939-4451
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide
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6. Virrey JJ, Golden EB, Sivakumar W, Wang W, Pen L, Schönthal AH, Hofman FM, Chen TC: Glioma-associated endothelial cells are chemoresistant to temozolomide. J Neurooncol; 2009 Oct;95(1):13-22
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  • [Title] Glioma-associated endothelial cells are chemoresistant to temozolomide.
  • Temozolomide is considered the standard of care and drug of choice for the treatment of initially diagnosed malignant gliomas.
  • Following drug treatment, patient prognosis still remains poor; tumor recurrence is almost universal.
  • We hypothesized that this lack of effectiveness with temozolomide is because this drug does not target the glioma microenvironment, which is highly vascular in malignant gliomas.
  • We found that this drug did not affect the viability or proliferation rate of endothelial cells isolated from human glioma specimens, although temozolomide was highly cytotoxic to the glioma cell lines U87MG and U251.
  • Furthermore, temozolomide did not inhibit the migration of these glioma-associated endothelial cells, a key mechanism responsible for tumor angiogenesis.
  • In in vivo studies, using the intracranial glioma mouse model, temozolomide did not cause a pronounced effect on microvessel density.
  • Our findings show that temozolomide has no apparent effect on the glioma vascular microenvironment.
  • Thus combination therapy with anti-vascular agents may enhance temozolomide effectiveness as glioma therapeutic protocol.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Brain Neoplasms / pathology. Dacarbazine / analogs & derivatives. Endothelial Cells / drug effects. Glioma / pathology
  • [MeSH-minor] Animals. Antigens, CD31 / metabolism. Cell Death / drug effects. Cell Movement / drug effects. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Neoplasm Transplantation / methods. Neovascularization, Pathologic / drug therapy. Tetrazolium Salts. Thiazoles. Time Factors. Tumor Cells, Cultured


7. Miletic H, Niclou SP, Johansson M, Bjerkvig R: Anti-VEGF therapies for malignant glioma: treatment effects and escape mechanisms. Expert Opin Ther Targets; 2009 Apr;13(4):455-68
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  • [Title] Anti-VEGF therapies for malignant glioma: treatment effects and escape mechanisms.
  • BACKGROUND: Glioblastoma multiforme (GBM) has a very poor prognosis and novel treatment strategies are urgently needed.
  • GBM appears to be an optimal target for anti-angiogenic therapy as the tumour shows a high degree of endothelial cell proliferation and pro-angiogenic growth factor expression.
  • OBJECTIVE: To examine the role of angiogenic factors (particularly VEGF) in glioma and whether inhibition of these factors can be used as a treatment.
  • RESULTS/CONCLUSIONS: Anti-angiogenic therapy has fulfilled the proof of concept in glioma animal models.
  • In glioma patients, the efficacy of anti-angiogenic mono-therapies initially has been disappointing.
  • However recent clinical trials combining bevacizumab, an anti-VEGF antibody, with chemotherapy reported very encouraging response rates.
  • Although randomized phase III clinical trials with anti-angiogenic molecules are not yet available for GBM patients, this treatment regimen is already applied off protocol in several clinical centers.
  • In particular invasive cells, which migrate away from the highly vascularized tumour core, are not targeted by anti-angiogenic therapies.
  • In our opinion, the future of anti-angiogenic therapy will rely on a combination strategy including chemotherapy and drugs that target invasive glioma cells.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Neovascularization, Pathologic / drug therapy. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Aged. Angiogenic Proteins / secretion. Animals. Clinical Trials as Topic. Disease Progression. Drug Resistance, Neoplasm. Endothelium, Vascular / physiopathology. Glioblastoma / blood supply. Glioblastoma / drug therapy. Glioblastoma / secretion. Humans. Middle Aged. Neoplasm Invasiveness. Receptors, Vascular Endothelial Growth Factor / drug effects. Receptors, Vascular Endothelial Growth Factor / physiology. Xenograft Model Antitumor Assays

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  • (PMID = 19335067.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 124
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8. Goudar RK, Shi Q, Hjelmeland MD, Keir ST, McLendon RE, Wikstrand CJ, Reese ED, Conrad CA, Traxler P, Lane HA, Reardon DA, Cavenee WK, Wang XF, Bigner DD, Friedman HS, Rich JN: Combination therapy of inhibitors of epidermal growth factor receptor/vascular endothelial growth factor receptor 2 (AEE788) and the mammalian target of rapamycin (RAD001) offers improved glioblastoma tumor growth inhibition. Mol Cancer Ther; 2005 Jan;4(1):101-12
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  • [Title] Combination therapy of inhibitors of epidermal growth factor receptor/vascular endothelial growth factor receptor 2 (AEE788) and the mammalian target of rapamycin (RAD001) offers improved glioblastoma tumor growth inhibition.
  • Malignant gliomas are highly lethal tumors that display striking genetic heterogeneity.
  • Novel therapies that inhibit a single molecular target may slow tumor progression, but tumors are likely not dependent on a signal transduction pathway.
  • AEE788 is a novel orally active tyrosine kinase inhibitor that decreases the kinase activity associated with the epidermal growth factor receptor and, at higher concentrations, the vascular endothelial growth factor receptor 2 (kinase domain region).
  • We hypothesized that combined inhibition of upstream epidermal growth factor receptor and kinase domain region receptors with AEE788 and inhibition of the downstream mTOR pathway with RAD001 would result in increased efficacy against gliomas compared with single-agent therapy.
  • Combined AEE788 and RAD001 given orally to athymic mice bearing established human malignant glioma tumor xenografts resulted in greater tumor growth inhibition and greater increases in median survival than monotherapy.
  • These studies suggest that simultaneous inhibition of growth factor receptor and mTOR pathways offer increased benefit in glioma therapy.
  • [MeSH-major] Cell Division / drug effects. Glioma / pathology. Protein Kinases / metabolism. Purines / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA Replication / drug effects. Humans. Mice. Mice, Nude. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. TOR Serine-Threonine Kinases. Transplantation, Heterologous

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  • (PMID = 15657358.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 P20 CA096890; United States / NCI NIH HHS / CA / CA11898; United States / NCI NIH HHS / CA / CA14236; United States / NCI NIH HHS / CA / CA94231-02; United States / NCRR NIH HHS / RR / M01 RR 30; United States / NINDS NIH HHS / NS / NS047409; United States / NINDS NIH HHS / NS / NS20023; United States / NINDS NIH HHS / NS / NS30245-15
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AEE 788; 0 / Purines; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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9. Brastianos PK, Batchelor TT: Vascular endothelial growth factor inhibitors in malignant gliomas. Target Oncol; 2010 Sep;5(3):167-74
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  • [Title] Vascular endothelial growth factor inhibitors in malignant gliomas.
  • Glioblastomas are highly vascularized tumors.
  • Treatment strategies targeting angiogenesis have demonstrated promising results in preclinical studies and clinical trials in patients with malignant gliomas.
  • Anti-VEGF agents, either alone or in combination with chemotherapy, have been associated with reduction in vasogenic brain edema, and prolonged progression-free survival.
  • Unfortunately, antiangiogenic treatment inevitably fails in most patients.
  • Further studies are needed to understand the molecular pathways that enable a tumor to evade antiangiogenic therapy.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Brain Neoplasms / blood supply. Glioma / blood supply. Neovascularization, Pathologic / prevention & control. Vascular Endothelial Growth Factors / antagonists & inhibitors

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  • (PMID = 20821351.001).
  • [ISSN] 1776-260X
  • [Journal-full-title] Targeted oncology
  • [ISO-abbreviation] Target Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factors
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10. Kirches E, Warich-Kirches M: 2-methoxyestradiol as a potential cytostatic drug in gliomas? Anticancer Agents Med Chem; 2009 Jan;9(1):55-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 2-methoxyestradiol as a potential cytostatic drug in gliomas?
  • Gliomas of astrocytic origin show only a limited chemotherapy response.
  • Chemoresistance is most pronounced in glioblastoma multiforme, the most common and most malignant glioma, with median survival times not much longer than one year.
  • Failure of chemotherapy partly relies on protective mechanisms against the commonly used DNA alkylating agents, but also on the constitutive activation of the pro-survival PI3K-Akt pathway in glioma cells, which inhibits apoptosis.
  • Therefore, new drugs with an alternative mechanism, independent of DNA alkylation, are required.
  • The microtubule targeting drug 2-methoxyestradiol (2-ME) efficiently induces mitotic arrest, apoptosis, but also autophagic cell death in glioma cells in vitro.
  • Moreover, it may be able to inhibit vascularization of the highly vascular gliobastomas, because the drug influences blood vessel sprouting via a HIF-1-dependent mechanism.
  • Although high doses of i.p. injected 2-ME were recently shown to be effective in an orthothopic rat glioma model, clinical phase I/II trials revealed low oral bioavailability.
  • [MeSH-major] Estradiol / analogs & derivatives. Glioma / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Autophagy / drug effects. Humans. Treatment Outcome. Tubulin Modulators / therapeutic use

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  • (PMID = 19149482.001).
  • [ISSN] 1875-5992
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tubulin Modulators; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
  • [Number-of-references] 79
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11. de Groot JF, Yung WK: Bevacizumab and irinotecan in the treatment of recurrent malignant gliomas. Cancer J; 2008 Sep-Oct;14(5):279-85
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  • [Title] Bevacizumab and irinotecan in the treatment of recurrent malignant gliomas.
  • Rapidly dividing glioma cells maintain adequate oxygen and nutrient delivery through co-opting existing host blood vessels or promoting the formation of new vessels, a process called angiogenesis.
  • Vascular endothelial growth factor is a mediator of hypoxia-induced endothelial cell proliferation and migration and is highly expressed in gliomas, where it acts as a potent regulator of angiogenesis.
  • The use of vascular endothelial growth factor receptor antagonists and vascular endothelial growth factor scavenging antibodies has generated excitement in neuro-oncology because of the rapid but reversible decrease in vascular permeability.
  • This decrease in vascular permeability is marked by a decrease in cerebral edema and a decrease in contrast enhancement visualized on magnetic resonance imaging.
  • Despite the difficulties in accurately measuring the effect of antivascular endothelial growth factor therapy on tumor viability, several studies confirm that the antivascular endothelial growth factor human monoclonal antibody bevacizumab combined with irinotecan can significantly improve 6-month progression free survival of patients with malignant gliomas compared with historical controls.
  • The impact of cytotoxic chemotherapy on the efficacy of bevacizumab and the effect of this therapy on overall survival are important questions that remain to be answered.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / analogs & derivatives. Glioma / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Bevacizumab. Biomarkers. Brain Neoplasms / drug therapy. Clinical Trials as Topic. Humans. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 18836331.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
  • [Number-of-references] 42
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12. Chamberlain MC: Emerging clinical principles on the use of bevacizumab for the treatment of malignant gliomas. Cancer; 2010 Sep 1;116(17):3988-99
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  • [Title] Emerging clinical principles on the use of bevacizumab for the treatment of malignant gliomas.
  • Despite advances in adjuvant therapy, the prognosis for most patients with high-grade glioma (HGG) is poor, and almost all HGGs have a likelihood of disease recurrence.
  • HGGs are highly vascularized tumors with elevated expression levels of vascular endothelial growth factor (VEGF), an important mediator of angiogenesis.
  • A compelling biologic rationale, a pressing need for improved therapeutics and positive results from studies of bevacizumab in other tumor types, led to the evaluation of bevacizumab in the treatment of HGG.
  • It was demonstrated previously that bevacizumab, which is a humanized monoclonal antibody that targets VEGF, improved outcomes when combined with chemotherapy (most commonly irinotecan) in patients with recurrent HGG; and, on the basis of an improved objective response rate in 2 prospective phase 2 studies, bevacizumab was granted accelerated approval by the US Food and Drug Administration as a single agent in patients with previously treated glioblastoma (GB).
  • Bevacizumab-containing therapy has been associated with manageable, class-specific toxicity; however, severe treatment-related adverse events are observed in a minority of patients.
  • Preliminary data on bevacizumab-based therapy in recurrent anaplastic gliomas, in the frontline treatment of GB, and in additional patient populations are also encouraging.
  • With the goal of addressing unanswered questions regarding the optimal use of bevacizumab, the objective of the current review was to provide a summary of the clinical efficacy and safety data on bevacizumab in patients with HGG, the practical issues surrounding the administration of bevacizumab, and ongoing investigations of bevacizumab in additional brain tumor treatment settings.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / adverse effects. Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bevacizumab. Clinical Trials as Topic. Humans. Recurrence. Treatment Outcome

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  • [Copyright] Cancer 2010. (c) 2010 American Cancer Society.
  • (PMID = 20564141.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
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13. Mentlein R, Held-Feindt J: Angiogenesis factors in gliomas: a new key to tumour therapy? Naturwissenschaften; 2003 Sep;90(9):385-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiogenesis factors in gliomas: a new key to tumour therapy?
  • Gliomas, the most common brain tumours, are particularly highly vascularized and, therefore, serve as a model to elucidate the process of tumour angiogenesis and to investigate new anti-angiogenic therapies.
  • This review describes the role of angiogenic factors in glioma angiogenesis and new strategies to inhibit glioma growth by application of anti-angiogenic substances.
  • We focus on vascular endothelial growth factor (VEGF), but also examine the role of angiopoietin and pleiotropic factors such as platelet-derived growth factor (PDGF), pleiotrophin and transforming growth factor-beta (TGF-beta).
  • Strategies to inhibit glioma growth by reducing the action of angiogenic factors, by the application of anti-angiogenic substances such as angiostatin or endostatin, or inactivation of endothelial cells, are discussed.
  • These new anti-angiogenic therapies appear to have a high potential not only for the treatment of gliomas, but also of other tumours.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Glioma / blood supply. Glioma / drug therapy. Neovascularization, Pathologic / drug therapy

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  • (PMID = 14504780.001).
  • [ISSN] 0028-1042
  • [Journal-full-title] Die Naturwissenschaften
  • [ISO-abbreviation] Naturwissenschaften
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 89
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14. Rolhion C, Penault-Llorca F, Kémény JL, Lemaire JJ, Jullien C, Labit-Bouvier C, Finat-Duclos F, Verrelle P: Interleukin-6 overexpression as a marker of malignancy in human gliomas. J Neurosurg; 2001 Jan;94(1):97-101
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  • OBJECT: Glioblastomas multiforme (GBMs) grow rapidly and are highly resistant to treatment compared with other glioma types and grades.
  • Consequently, it is of major interest to identify markers of aggressiveness in these tumors that could represent new therapeutic targets.
  • Expression of IL-6 may be involved in cell growth, resistance to chemotherapy and radiotherapy (via an antiapoptotic pathway), and angiogenesis.
  • This study was conducted to test this hypotheses and to evaluate the suitability of IL-6 as a target in the treatment of GBMs.
  • METHODS: The authors studied the relationship between the level of IL-6 gene expression as assessed using semiquantitative reverse transcription-polymerase chain reaction and by determining various histological types and grades in a series of 59 gliomas.
  • It was found that GBMs displayed a significantly higher level of IL-6 expression than other types of glioma (p < 0.001).
  • Immunohistochemical analysis revealed that IL-6 was produced mainly by malignant cells and a few vascular endothelial cells.
  • CONCLUSIONS: It can be inferred from these findings that IL-6 gene expression is related to glioma aggressiveness and that IL-6 may play a central role in GBM behavior.
  • Interleukin-6, therefore, could be considered as a new potential target in the treatment of GBMs.
  • [MeSH-major] Central Nervous System Neoplasms / metabolism. Glioma / metabolism. Interleukin-6 / metabolism

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  • (PMID = 11147905.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-6
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15. van Eekelen M, Sasportas LS, Kasmieh R, Yip S, Figueiredo JL, Louis DN, Weissleder R, Shah K: Human stem cells expressing novel TSP-1 variant have anti-angiogenic effect on brain tumors. Oncogene; 2010 Jun 3;29(22):3185-95
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  • Novel therapeutic agents combined with innovative modes of delivery and non-invasive imaging of drug delivery, pharmacokinetics and efficacy are crucial in developing effective clinical anticancer therapies.
  • In this study, we have created and characterized multiple novel variants of anti-angiogenic protein thrombospondin (aaTSP-1) that comprises unique regions of three type-I-repeats of TSP-1 and used engineered human neural stem cells (hNSC) to provide sustained on-site delivery of secretable aaTSP-1 to tumor-vasculature.
  • We show that hNSC-aaTSP-1 has anti-angiogenic effect on human brain and dermal microvascular endothelial cells co-cultured with established glioma cells and CD133+ glioma-initiating cells.
  • Using human glioma cells and hNSC engineered with different combinations of fluorescent and bioluminescent marker proteins and employing multi-modality imaging techniques, we show that aaTSP-1 targets the vascular-component of gliomas and a single administration of hNSC-aaTSP-1 markedly reduces tumor vessel-density that results in inhibition of tumor-progression and increased survival in mice bearing highly malignant human gliomas.
  • We also show that therapeutic hNSC do not proliferate and remain in an un-differentiated state in the brains of glioma-bearing mice.
  • This study provides a platform for accelerated development of future cell-based therapies for cancer.

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  • (PMID = 20305695.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA131980; United States / NCI NIH HHS / CA / P50 CA086355; United States / NINDS NIH HHS / NS / R01 NS071197; United States / NCI NIH HHS / CA / R21CA131980; United States / NCI NIH HHS / CA / P50 CA86355
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Thrombospondin 1
  • [Other-IDs] NLM/ NIHMS387544; NLM/ PMC3390229
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16. Iwamoto FM, Fine HA: Bevacizumab for malignant gliomas. Arch Neurol; 2010 Mar;67(3):285-8
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  • Despite optimal treatment with surgery, radiotherapy, and temozolomide, tumor recurrences are frequent and patients with malignant gliomas continue to have poor prognoses.
  • Malignant gliomas are often highly vascularized, and significant advances have been made in the last few decades in our understanding of the mechanisms of tumor angiogenesis.
  • Recently, bevacizumab, an antibody against vascular endothelial growth factor, has demonstrated significant activity in recurrent glioblastomas, resulting in US Food and Drug Administration approval and raising the prospect for other antiangiogenic drugs now entering clinical trials.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / therapy. Glioma / therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal, Humanized. Bevacizumab. Humans. Neovascularization, Pathologic / therapy. Vascular Endothelial Growth Factors / metabolism

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  • (PMID = 20212225.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Vascular Endothelial Growth Factors; 2S9ZZM9Q9V / Bevacizumab
  • [Number-of-references] 32
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17. Bradley DP, Tessier JJ, Lacey T, Scott M, Jürgensmeier JM, Odedra R, Mills J, Kilburn L, Wedge SR: Examining the acute effects of cediranib (RECENTIN, AZD2171) treatment in tumor models: a dynamic contrast-enhanced MRI study using gadopentate. Magn Reson Imaging; 2009 Apr;27(3):377-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Examining the acute effects of cediranib (RECENTIN, AZD2171) treatment in tumor models: a dynamic contrast-enhanced MRI study using gadopentate.
  • Cediranib (RECENTIN, AZD2171) is a highly potent inhibitor of the tyrosine kinase activity associated with all three vascular endothelial growth factor (VEGF) receptors and is currently in Phase II/III clinical trials.
  • Clinically, changes observed using dynamic contrast-enhanced MRI (DCE-MRI) with gadopentate suggest that acute cediranib treatment compromises tumor hemodynamics.
  • In this study, a DCE-MRI baseline scan using gadopentate was performed in nude rats bearing Lovo (human colorectal carcinoma) or C6 (rat glioma) tumors.
  • Mean values for K(trans) (Tofts and Kermode-derived) [Magn Reson Med 17 (1991) 357-67] and the initial area under the gadolinium concentration curve over the first 60 s (iAUC) were reduced significantly following cediranib treatment: K(trans) by 33% (P<.05) in both tumor models and iAUC by 23% (P>.05) and 33% (P>.005) in Lovo and C6, respectively.
  • This is the first preclinical investigation to examine the effect of cediranib treatment on tumors by DCE-MRI with gadopentate.
  • [MeSH-major] Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / drug therapy. Disease Models, Animal. Gadolinium DTPA. Glioma / diagnosis. Glioma / drug therapy. Magnetic Resonance Imaging / methods. Quinazolines / administration & dosage
  • [MeSH-minor] Administration, Oral. Angiogenesis Inhibitors / administration & dosage. Animals. Contrast Media. Dose-Response Relationship, Drug. Humans. Rats. Rats, Nude. Treatment Outcome

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  • (PMID = 18814988.001).
  • [ISSN] 1873-5894
  • [Journal-full-title] Magnetic resonance imaging
  • [ISO-abbreviation] Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Contrast Media; 0 / Quinazolines; K2I13DR72L / Gadolinium DTPA; NQU9IPY4K9 / cediranib
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18. Yamada K, Goto S, Kochi M, Ushio Y: Stereotactic biopsy for multifocal, diffuse, and deep-seated brain tumors using Leksell's system. J Clin Neurosci; 2004 Apr;11(3):263-7
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  • However, we avoided subjecting the patients with lesions adjacent to major vascular trunks or complex vascular structures such as the cavernous sinus, peri-insular regions and the pineal regions to stereotactic biopsy.
  • Thirteen (14.3%) cases had previously undergone radiation and/or chemotherapy for brain tumors, seven had recurrent glioma (five with malignant transformation) and six manifested radiation necrosis.
  • None of the patients died due to the stereotactic procedure; one (1.1%) exhibited morbidity due to complicated hemorrhage.
  • All five patients younger than 15 years underwent the procedure without complications.
  • The Leksell stereotactic system is useful for diagnostic tissue sampling and contributes effectively to the selection of appropriate therapy in patients with malignant brain tumors.
  • While it carries a low morbidity rate without mortality in our series, care must be taken for selected target sites in highly vascularized lesions exhibiting positive tumor stains.
  • [MeSH-minor] Adolescent. Adult. Aged. Cerebral Angiography. Cerebral Hemorrhage / epidemiology. Cerebral Hemorrhage / etiology. Cerebral Hemorrhage / pathology. Child. Child, Preschool. Electric Stimulation. Female. Humans. Infant. Male. Middle Aged. Neoplasm Recurrence, Local. Neurosurgical Procedures. Postoperative Care. Tomography, X-Ray Computed

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  • (PMID = 14975414.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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19. Li J, Di C, Mattox AK, Wu L, Adamson DC: The future role of personalized medicine in the treatment of glioblastoma multiforme. Pharmgenomics Pers Med; 2010;3:111-27
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  • [Title] The future role of personalized medicine in the treatment of glioblastoma multiforme.
  • Personalized therapeutic approaches have not become standard of care for GBM, but science is fast approaching this goal.
  • GBM's heterogeneous genomic landscape and resistance to radiotherapy and chemotherapy make this tumor one of the most challenging to treat.
  • Instead, future therapies will likely require personalization for each patient's tumor genotype or proteomic profile.
  • Over the past year, many investigations specifically focused simultaneously on strategies to target oncogenic pathways, angiogenesis, tumor immunology, epigenomic events, glioma stem cells (GSCs), and the highly migratory glioma cell population.
  • Combination therapy targeting multiple pathways is becoming a fast growing area of research, and many studies put special attention on small molecule inhibitors.
  • Because GBM is a highly vascular tumor, therapy that directs monoclonal antibodies or small molecule tyrosine kinase inhibitors toward angiogenic factors is also an area of focus for the development of new therapies.
  • GSCs can be useful targets to stop tumor recurrence and proliferation, and recent research has found key molecules that regulate GBM cell migration that can be targeted by therapy.
  • Current standard of care for GBM remains nonspecific; however, pharmacogenomic studies are underway to pave the way for patient-specific therapies that are based on the unique aberrant pathways in individual patients.
  • In conclusion, recent studies in GBM have found many diverse molecular targets possible for therapy.
  • The next obstacle in treating this fatal tumor is ascertaining which molecules in each patient should be targeted and how best to target them, so that we can move our current nonspecific therapies toward the realm of personalized medicine.

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  • (PMID = 23226047.001).
  • [ISSN] 1178-7066
  • [Journal-full-title] Pharmacogenomics and personalized medicine
  • [ISO-abbreviation] Pharmgenomics Pers Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3513213
  • [Keywords] NOTNLM ; GBM / genetics / oncogenomics / pharmacogenomics / signaling cascades
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20. Chi AS, Sorensen AG, Jain RK, Batchelor TT: Angiogenesis as a therapeutic target in malignant gliomas. Oncologist; 2009 Jun;14(6):621-36
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  • [Title] Angiogenesis as a therapeutic target in malignant gliomas.
  • Currently, adult glioblastoma (GBM) patients have poor outcomes with conventional cytotoxic treatments.
  • Because GBMs are highly angiogenic tumors, inhibitors that target tumor vasculature are considered promising therapeutic agents in these patients.
  • Encouraging efficacy and tolerability in preliminary clinical trials suggest that targeting angiogenesis may be an effective therapeutic strategy in GBM patients.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Glioma / blood supply. Glioma / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Cell Movement / drug effects. Clinical Trials as Topic. Drug Resistance, Neoplasm. Edema / drug therapy. Endothelial Cells / drug effects. Humans. Protein Kinase Inhibitors / therapeutic use. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 19487335.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 175
  • [Other-IDs] NLM/ NIHMS765709; NLM/ PMC4790121
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22. Virrey JJ, Dong D, Stiles C, Patterson JB, Pen L, Ni M, Schönthal AH, Chen TC, Hofman FM, Lee AS: Stress chaperone GRP78/BiP confers chemoresistance to tumor-associated endothelial cells. Mol Cancer Res; 2008 Aug;6(8):1268-75
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  • The tumor vasculature is essential for tumor growth and survival and is a key target for anticancer therapy.
  • Glioblastoma multiforme, the most malignant form of brain tumor, is highly vascular and contains abnormal vessels, unlike blood vessels in normal brain.
  • Previously, we showed that primary cultures of human brain endothelial cells, derived from blood vessels of malignant glioma tissues (TuBEC), are physiologically and functionally different from endothelial cells derived from nonmalignant brain tissues (BEC) and are substantially more resistant to apoptosis.
  • Resistance of TuBEC to a wide range of current anticancer drugs has significant clinical consequences as it represents a major obstacle toward eradication of residual brain tumor.
  • We report here that the endoplasmic reticulum chaperone GRP78/BiP is generally highly elevated in the vasculature derived from human glioma specimens, both in situ in tissue and in vitro in primary cell cultures, compared with minimal GRP78 expression in normal brain tissues and blood vessels.
  • Conversely, overexpression of GRP78 in BEC rendered these cells resistant to drug treatments.
  • Our findings provide the proof of principle that targeting GRP78 will sensitize the tumor vasculature to chemotherapeutic drugs, thus enhancing the efficacy of these drugs in combination therapy for glioma treatment.

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  • (PMID = 18708359.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA111700; United States / NIA NIH HHS / AG / P50 AG005142; United States / NCI NIH HHS / CA / R01 CA111700-03; United States / NCI NIH HHS / CA / R01 CA111700; United States / NCI NIH HHS / CA / CA027607-27A2; United States / NCI NIH HHS / CA / CA111700-03; United States / NCI NIH HHS / CA / R01 CA027607-26S1; United States / NCI NIH HHS / CA / R01 CA111700-04; United States / NCI NIH HHS / CA / CA111700-04; United States / NCI NIH HHS / CA / R01 CA027607; United States / NCI NIH HHS / CA / R01 CA027607-27A2; United States / NCI NIH HHS / CA / CA027607; United States / NCI NIH HHS / CA / CA027607-26S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / RNA, Small Interfering; 0 / molecular chaperone GRP78; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS72229; NLM/ PMC2593417
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23. Chi AS, Norden AD, Wen PY: Antiangiogenic strategies for treatment of malignant gliomas. Neurotherapeutics; 2009 Jul;6(3):513-26
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  • [Title] Antiangiogenic strategies for treatment of malignant gliomas.
  • Numerous antiangiogenic agents with diverse mechanisms of action are currently under investigation for the treatment of patients with glioblastoma (GBM), a diagnosis that continues to carry a poor prognosis despite maximal conventional therapy.
  • Early clinical trials suggest that antiangiogenic drugs, which target the blood vessels of these highly angiogenic tumors, may have clinical benefit in GBM patients.
  • Antiangiogenic agents have potent antiedema and steroid-sparing effects in patients, and emerging data suggest that these drugs may modestly improve progression-free survival.
  • Interpretation of the radiographic changes that occur after treatment with antiangiogenic agents presents a major challenge.
  • Still lacking are reliable radiographic and biologic markers that can predict which patients will benefit from treatment and that accurately indicate response and progression during therapy.
  • In addition, most patients treated with antiangiogenic drugs eventually progress, and the mechanisms by which tumors escape from therapy are only beginning to be understood.
  • Here, we summarize the clinical experience with antiangiogenic therapy in patients with malignant gliomas (MG), review the major issues concerning the use and development of these agents, and discuss strategies that may build upon the initial gains observed with antiangiogenic agents.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Biomarkers / metabolism. Disease Progression. Glioblastoma / drug therapy. Glioblastoma / metabolism. Humans. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / metabolism. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19560741.001).
  • [ISSN] 1933-7213
  • [Journal-full-title] Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
  • [ISO-abbreviation] Neurotherapeutics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 126
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24. Ohlfest JR, Demorest ZL, Motooka Y, Vengco I, Oh S, Chen E, Scappaticci FA, Saplis RJ, Ekker SC, Low WC, Freese AB, Largaespada DA: Combinatorial antiangiogenic gene therapy by nonviral gene transfer using the sleeping beauty transposon causes tumor regression and improves survival in mice bearing intracranial human glioblastoma. Mol Ther; 2005 Nov;12(5):778-88
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  • [Title] Combinatorial antiangiogenic gene therapy by nonviral gene transfer using the sleeping beauty transposon causes tumor regression and improves survival in mice bearing intracranial human glioblastoma.
  • Glioblastoma is a fatal brain tumor that becomes highly vascularized by secreting proangiogenic factors and depends on continued angiogenesis to increase in size.
  • Consequently, a successful antiangiogenic therapy should provide long-term inhibition of tumor-induced angiogenesis, suggesting long-term gene transfer as a therapeutic strategy.
  • In this study a soluble vascular endothelial growth factor receptor (sFlt-1) and an angiostatin-endostatin fusion gene (statin-AE) were codelivered to human glioblastoma xenografts by nonviral gene transfer using the Sleeping Beauty (SB) transposon.
  • In subcutaneously implanted xenografts, co-injection of both transgenes showed marked anti-tumor activity as demonstrated by reduction of tumor vessel density, inhibition or abolition of glioma growth, and increase in animal survival (P = 0.003).
  • We show that SB can be used to increase animal survival significantly (P = 0.008) by combinatorial antiangiogenic gene transfer in an intracranial glioma model.

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  • (PMID = 16150649.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM063904-01; United States / NIGMS NIH HHS / GM / R01 GM063904; United States / NIGMS NIH HHS / GM / R01 GM063904-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / DNA Transposable Elements; 0 / Endostatins; 86090-08-6 / Angiostatins; EC 1.13.12.- / Luciferases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.7.- / Transposases; EC 2.7.7.- / sleeping beauty transposase, human
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25. Wild R, Dhanabal M, Olson TA, Ramakrishnan S: Inhibition of angiogenesis and tumour growth by VEGF121-toxin conjugate: differential effect on proliferating endothelial cells. Br J Cancer; 2000 Oct;83(8):1077-83
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  • Vascular endothelial growth factor (VEGF) plays an important role in tumour angiogenesis.
  • Therefore, VEGF can be used to target toxin molecules to tumour vessels for anti-angiogenic therapy.
  • NP-1 is widely expressed in normal tissue and presents a potential target for unwanted toxicity.
  • Treatment of endothelial cells with a VEGF121-diphtheria toxin (DT385) conjugate selectively inhibited proliferating endothelial cells, whereas confluent cultures were completely resistant to the construct.
  • In addition, VEGF121-DT385 conjugate treatment completely prevented tumour cell induced angiogenesis in vivo.
  • Most importantly, the conjugate inhibited tumour growth in athymic mice and induced tumour-specific vascular damage.
  • There was also no apparent toxicity associated with the treatment.
  • Our results suggest that proliferating endothelial cells are highly sensitive to VEGF121-toxin conjugates and that the binding to NP-1 receptors is not necessary for efficient inhibition of tumour growth.

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  • [Copyright] Copyright 2000 Cancer Research Campaign.
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  • (PMID = 10993657.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 71803
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiogenic Proteins; 0 / Diphtheria Toxin; 0 / Endothelial Growth Factors; 0 / Immunotoxins; 0 / Lymphokines; 0 / VEGF121-diphtheria toxin conjugate; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors
  • [Other-IDs] NLM/ PMC2363558
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26. Charalambous C, Chen TC, Hofman FM: Characteristics of tumor-associated endothelial cells derived from glioblastoma multiforme. Neurosurg Focus; 2006;20(4):E22
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  • Glioblastomas multiforme (GBMs) are highly vascular brain tumors characterized by abnormal vessel structures in vivo.
  • This finding supports the theory that glioma-associated endothelial cells (ECs) have intrinsically different properties from ECs in normal human brain.
  • Therefore, identification of the functional and phenotypic characteristics of tumor-associated ECs is essential for designing a rational antiangiogenic therapy.
  • Although the tumor ECs have the typical markers, they proliferate more slowly than these cell types in normal brain.
  • The GBM-associated ECs are resistant to cytotoxic drugs, and they undergo less apoptosis than control cells.
  • Also, GBM-associated ECs migrate faster than controls and constitutively produce high levels of growth factors such as endothelin-1, interleukin-8, and vascular endothelial growth factor.
  • An understanding of these unique characteristics of glioma-associated ECs is important for the development of novel antiangiogenic agents that specifically target tumor-associated ECs in gliomas.
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Biomarkers, Tumor / metabolism. Cell Proliferation. Drug Resistance, Neoplasm / physiology. Humans

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  • (PMID = 16709028.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Endothelial Growth Factors
  • [Number-of-references] 35
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27. Kirsch M, Schackert G, Black PM: Anti-angiogenic treatment strategies for malignant brain tumors. J Neurooncol; 2000 Oct-Nov;50(1-2):149-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-angiogenic treatment strategies for malignant brain tumors.
  • The use of angiogenesis inhibitors may offer novel strategies in brain tumor therapy.
  • In contrast to traditional cancer treatments that attack tumor cells directly, angiogenesis inhibitors target at the formation of tumor-feeding blood vessels that provide continuous supply of nutrients and oxygen.
  • With respect to brain tumor therapy, inhibitors of angiogenesis display unique features that are unknown to conventional chemotherapeutic agents.
  • The most important features are independence of the blood-brain barrier, cell type specificity, and reduced resistance.
  • Despite multimodal therapeutic approaches, the prognosis remains dismal.
  • Thus, angiogenesis inhibitors may be highly effective drugs against these tumors.
  • In a clinical setting, they could be applied in the treatment of multiple tumors or postsurgically as an adjuvant therapy to prevent recurrence.
  • This article provides an overview of current anti-angiogenic treatment strategies with emphasis on substances already in clinical trials or candidate substances for clinical trials.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Angiopoietin-1. Angiopoietin-2. Angiostatins. Chemotherapy, Adjuvant. Clinical Trials as Topic. Collagen / chemistry. Collagen / therapeutic use. Combined Modality Therapy. Cyclohexanes. Endostatins. Endothelial Growth Factors / antagonists & inhibitors. Endothelial Growth Factors / physiology. Fatty Acids, Unsaturated / therapeutic use. Humans. Integrins / antagonists & inhibitors. Integrins / physiology. Lymphokines / antagonists & inhibitors. Lymphokines / physiology. Matrix Metalloproteinase 2 / chemistry. Matrix Metalloproteinase Inhibitors. Matrix Metalloproteinases / physiology. Membrane Glycoproteins / antagonists & inhibitors. Membrane Glycoproteins / physiology. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Proteins / physiology. Peptide Fragments / therapeutic use. Plasminogen / therapeutic use. Proteins / antagonists & inhibitors. Proteins / physiology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / physiology. Receptor, TIE-2. Receptors, Cell Surface / antagonists & inhibitors. Receptors, Cell Surface / physiology. Receptors, Growth Factor / antagonists & inhibitors. Receptors, Growth Factor / physiology. Receptors, TIE. Receptors, Vascular Endothelial Growth Factor. Sesquiterpenes. Suramin / therapeutic use. Thalidomide / therapeutic use. Thrombospondins / therapeutic use. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 11245274.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / Cyclohexanes; 0 / Endostatins; 0 / Endothelial Growth Factors; 0 / Fatty Acids, Unsaturated; 0 / Integrins; 0 / Lymphokines; 0 / Matrix Metalloproteinase Inhibitors; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, Growth Factor; 0 / Sesquiterpenes; 0 / Thrombospondins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 4Z8R6ORS6L / Thalidomide; 6032D45BEM / Suramin; 7OW73204U1 / fumagillin; 86090-08-6 / Angiostatins; 9001-91-6 / Plasminogen; 9007-34-5 / Collagen; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Receptors, TIE; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Number-of-references] 156
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