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1. Milner R, Hung S, Erokwu B, Dore-Duffy P, LaManna JC, del Zoppo GJ: Increased expression of fibronectin and the alpha 5 beta 1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Mol Cell Neurosci; 2008 May;38(1):43-52
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  • [Title] Increased expression of fibronectin and the alpha 5 beta 1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia.
  • We showed previously that angiogenic capillaries in the developing CNS express high levels of fibronectin and its receptor alpha5beta1 integrin, and that this expression is developmentally downregulated.
  • As cerebral hypoxia leads to an angiogenic response, we sought to determine whether angiogenic vessels in the adult CNS re-express fibronectin and the alpha5beta1 integrin.
  • Immunofluorescent studies demonstrated that the alpha5 integrin was expressed by angiogenic endothelial cells.
  • In light of the defined angiogenic role for fibronectin in other systems, this work suggests that induction of fibronectin-alpha5beta1 integrin expression may be an important molecular switch driving angiogenesis in the hypoxic CNS.

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  • (PMID = 18343155.001).
  • [ISSN] 1095-9327
  • [Journal-full-title] Molecular and cellular neurosciences
  • [ISO-abbreviation] Mol. Cell. Neurosci.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R37 NS038710-08; United States / NINDS NIH HHS / NS / NS143627; United States / NIAID NIH HHS / AI / R01 AI043627-01A1; United States / PHS HHS / / NSO53716; United States / NINDS NIH HHS / NS / NS038632-01A1; United States / NINDS NIH HHS / NS / R01 NS038632; United States / NINDS NIH HHS / NS / R01 NS053716-01; United States / NINDS NIH HHS / NS / R37 NS038710; United States / NINDS NIH HHS / NS / NS047672; United States / NINDS NIH HHS / NS / R01 NS053716; United States / NINDS NIH HHS / NS / NS38632; United States / NINDS NIH HHS / NS / NS053716-01; United States / NINDS NIH HHS / NS / NS038710-08; United States / NINDS NIH HHS / NS / NS053716-04; United States / NINDS NIH HHS / NS / NS047672-01; United States / NINDS NIH HHS / NS / R01 NS047672; United States / NINDS NIH HHS / NS / R01 NS038632-01A1; United States / NINDS NIH HHS / NS / R01 NS053716-04; United States / NINDS NIH HHS / NS / R01 NS047672-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibronectins; 0 / Integrin alpha5beta1
  • [Other-IDs] NLM/ NIHMS78778; NLM/ PMC2588547
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2. Maruyama Y, Ono M, Kawahara A, Yokoyama T, Basaki Y, Kage M, Aoyagi S, Kinoshita H, Kuwano M: Tumor growth suppression in pancreatic cancer by a putative metastasis suppressor gene Cap43/NDRG1/Drg-1 through modulation of angiogenesis. Cancer Res; 2006 Jun 15;66(12):6233-42
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  • Cellular expression of matrix metalloproteinase-9 and two major angiogenic factors, vascular endothelial growth factor and interleukin-8, were also significantly decreased in cell lines with Cap43 overexpression as compared with their parental counterparts.
  • Thus, Cap43 could play a key role in the angiogenic on- or off-switch of tumor stroma in pancreatic ductal adenocarcinoma.

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  • (PMID = 16778198.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Interleukin-8; 0 / Intracellular Signaling Peptides and Proteins; 0 / N-myc downstream-regulated gene 1 protein; 0 / Proteins; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.35 / Matrix Metalloproteinase 9
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3. Merdzhanova G, Gout S, Keramidas M, Edmond V, Coll JL, Brambilla C, Brambilla E, Gazzeri S, Eymin B: The transcription factor E2F1 and the SR protein SC35 control the ratio of pro-angiogenic versus antiangiogenic isoforms of vascular endothelial growth factor-A to inhibit neovascularization in vivo. Oncogene; 2010 Sep 30;29(39):5392-403
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  • [Title] The transcription factor E2F1 and the SR protein SC35 control the ratio of pro-angiogenic versus antiangiogenic isoforms of vascular endothelial growth factor-A to inhibit neovascularization in vivo.
  • Besides being regulated by transcription, VEGF-A is also highly regulated by pre-mRNA alternative splicing, resulting in the expression of several VEGF isoforms with either pro-(VEGF(xxx)) or anti-(VEGF(xxx)b) angiogenic properties.
  • We further show that, strikingly, E2F1 alters the ratio of pro-VEGF(xxx) versus anti-VEGF(xxx)b angiogenic isoforms, favouring the antiangiogenic isoforms, by a mechanism involving the induction of SC35 expression.
  • Overall, these findings highlight E2F1 and SC35 as two regulators of the VEGF(xxx)/VEGF(xxx)b angiogenic switch in human cancer cells, a role that could be crucial during tumour progression, as well as in tumour response to antiangiogenic therapies.

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  • (PMID = 20639906.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / Proteins; 0 / RNA Precursors; 0 / RNA, Messenger; 0 / Ribonucleoproteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 147153-65-9 / SRSF2 protein, human
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4. Ribatti D: Endogenous inhibitors of angiogenesis: a historical review. Leuk Res; 2009 May;33(5):638-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In pathological states such as chronic inflammation and tumor growth, there is an imbalance between endogenous stimulator and inhibitor levels, leading to an "angiogenic switch".

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  • (PMID = 19117606.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 97
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5. Finetti F, Donnini S, Giachetti A, Morbidelli L, Ziche M: Prostaglandin E(2) primes the angiogenic switch via a synergic interaction with the fibroblast growth factor-2 pathway. Circ Res; 2009 Sep 25;105(7):657-66
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  • [Title] Prostaglandin E(2) primes the angiogenic switch via a synergic interaction with the fibroblast growth factor-2 pathway.
  • The magnitude of the angiogenic response to PGE(2) was directly related to FGF-2 availability which determined the extent of FGFR1 activation.
  • CONCLUSION: We propose a model for the angiogenic switch based on the autocrine/paracrine FGF-2/FGFR1 activation by PGE(2) and FGF-2 synergistic interaction.

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  • (PMID = 19713533.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FRS2alpha protein, mouse; 0 / Membrane Proteins; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type III; EC 1.14.13.39 / Nos3 protein, mouse; EC 2.7.10.1 / Fgfr1 protein, mouse; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.4.3 / Phospholipase C gamma; K7Q1JQR04M / Dinoprostone
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6. Elice F, Rodeghiero F, Falanga A, Rickles FR: Thrombosis associated with angiogenesis inhibitors. Best Pract Res Clin Haematol; 2009 Mar;22(1):115-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Five anti-angiogenic agents (thalidomide, lenalidomide, bevacizumab, sunitinib, sorafenib) have already obtained US Food and Drug Administration approval for clinical use, and many others have entered clinical trials.
  • Many new biological agents with anti-angiogenic properties appear to be associated with an increased risk for thrombosis and, paradoxically, bleeding.
  • Although the mechanisms underlying the increased thromboembolic risk remain ill defined, the main hypothesis is that perturbation of tumour-associated endothelial cells can switch the endothelium from a naturally anticoagulant surface to a prothrombotic surface, thus mediating the activation of systemic coagulation in cancer patients, who are already more susceptible to thromboembolism due to their underlying disease.
  • The toxicity profile differs between the anti-angiogenic agents.
  • The observation of these vascular toxicities suggests the need to establish, in randomized clinical trials, the usefulness of thrombosis prophylaxis when anti-angiogenic agents are used in cancer patients, especially when associated with chemotherapy.
  • In addition, careful reporting of haemostatic complications during treatment with new anti-angiogenic drugs is warranted.

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  • (PMID = 19285278.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 100
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7. Edelmann J, Klein-Hitpass L, Carpinteiro A, Führer A, Sellmann L, Stilgenbauer S, Dührsen U, Dürig J: Bone marrow fibroblasts induce expression of PI3K/NF-kappaB pathway genes and a pro-angiogenic phenotype in CLL cells. Leuk Res; 2008 Oct;32(10):1565-72
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  • [Title] Bone marrow fibroblasts induce expression of PI3K/NF-kappaB pathway genes and a pro-angiogenic phenotype in CLL cells.
  • STR as compared to TW conditions induced a significant up-regulation of PI3K/NF-kappaB pro-survival pathway genes and mediated a pro-angiogenetic switch in the CLL cells by up-regulation of vascular endothelial growth factor (VEGF) and osteopontin (OPN) and down-regulation of the anti-angiogenetic molecule thrombospondin-1 (TSP-1).
  • [MeSH-major] Angiogenic Proteins / metabolism. Fibroblasts / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / metabolism

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  • (PMID = 18407351.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / NF-kappa B; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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8. Huang H, Bhat A, Woodnutt G, Lappe R: Targeting the ANGPT-TIE2 pathway in malignancy. Nat Rev Cancer; 2010 Aug;10(8):575-85
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  • Angiopoietins (ANGPTs) are ligands of the endothelial cell receptor TIE2 and have crucial roles in the tumour angiogenic switch.

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  • (PMID = 20651738.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopoietins; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, TIE-2
  • [Number-of-references] 160
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9. Wang J, Milner R: Fibronectin promotes brain capillary endothelial cell survival and proliferation through alpha5beta1 and alphavbeta3 integrins via MAP kinase signalling. J Neurochem; 2006 Jan;96(1):148-59
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  • We showed previously that blood vessel maturation in the CNS is associated with a developmental switch in brain capillary endothelial cells (BCEC), from fibronectin signalling during angiogenesis to laminin signalling in the adult.
  • To investigate the functional significance of this switch, we have examined the response of BCEC to different extracellular matrix (ECM) proteins.
  • Taken together, these findings show that fibronectin exerts a strong angiogenic influence on endothelial cells (EC) in the CNS, and that this is mediated through the alpha5beta1 and alphavbeta3 integrins via MAP kinase signalling.

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  • (PMID = 16269008.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fibronectins; 0 / Integrin alpha5beta1; 0 / Integrin alphaVbeta3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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10. Siemerink MJ, Augustin AJ, Schlingemann RO: Mechanisms of ocular angiogenesis and its molecular mediators. Dev Ophthalmol; 2010;46:4-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Complex interactions are involved between non-vascular and microvascular cells, such as endothelial cells and pericytes, via several angiogenic growth factors and inhibitors.
  • During the angiogenic process, endothelial cells shift from a homogeneous quiescent population into a population of heterogeneous phenotypes, each with a distinct cellular fate.
  • So far, three angiogenic specialized phenotypes have been identified:.
  • In most of these conditions, angiogenesis is part of a wound healing response culminating, via an angiofibrotic switch, in fibrosis and scar formation which leads to blindness.

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  • (PMID = 20703029.001).
  • [ISSN] 1662-2790
  • [Journal-full-title] Developments in ophthalmology
  • [ISO-abbreviation] Dev Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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11. Gevertz JL, Torquato S: Modeling the effects of vasculature evolution on early brain tumor growth. J Theor Biol; 2006 Dec 21;243(4):517-31
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  • The properties of the vasculature and hence of each cell are determined by the relative concentrations of these key angiogenic factors.
  • The model exhibits an angiogenic switch consistent with experimental observations on the upregulation of angiogenesis.
  • Furthermore, we show that tumor expansion can occur in well-vascularized environments even when angiogenesis is inhibited, suggesting that anti-angiogenic therapies may not be sufficient to eliminate a population of actively dividing malignant cells.

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  • (PMID = 16938311.001).
  • [ISSN] 0022-5193
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiopoietins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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12. Carmeliet P: VEGF as a key mediator of angiogenesis in cancer. Oncology; 2005;69 Suppl 3:4-10
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  • The production of VEGF and other growth factors by the tumor results in the 'angiogenic switch', where new vasculature is formed in and around the tumor, allowing it to grow exponentially.

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16301830.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 45
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13. Rao VU, Shenoy AM, Karthikeyan B: Role of angiogenetic markers to predict neck node metastasis in head and neck cancers. J Cancer Res Ther; 2010 Apr-Jun;6(2):142-7
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  • The angiogenic switch may be one of the earliest events in conferring a metastatic potential to the tumor.
  • The present article reviews the utility value of various angiogenic parameters and markers that have been utilized to predict regional metastasis including micro vessel density, positive and negative regulators of angiogenesis, and genetic markers for angiogenesis.

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  • (PMID = 20622359.001).
  • [ISSN] 1998-4138
  • [Journal-full-title] Journal of cancer research and therapeutics
  • [ISO-abbreviation] J Cancer Res Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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14. Kim MS, Kim YK, Cho KH, Chung JH: Infrared exposure induces an angiogenic switch in human skin that is partially mediated by heat. Br J Dermatol; 2006 Dec;155(6):1131-8
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  • [Title] Infrared exposure induces an angiogenic switch in human skin that is partially mediated by heat.
  • OBJECTIVES: To elucidate the molecular regulation of the angiogenic switch by acute near-IR radiation or by a single heat treatment in human skin in vivo.
  • CONCLUSIONS: Our results suggest that IR radiation plays an important role in skin angiogenesis via regulation of the balance between the angiogenic inducer VEGF and the angiogenic inhibitor TSP-2, and that IR-induced skin angiogenesis might be partially caused by the effects of heat in human skin in vivo.

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  • (PMID = 17107379.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Thrombospondins; 0 / Vascular Endothelial Growth Factor A; 0 / thrombospondin 2
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15. Rosenblatt MI, Azar DT: Anti-angiogenic therapy: Prospects for treatment of ocular tumors. Semin Ophthalmol; 2006 Jul-Sep;21(3):151-60
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  • [Title] Anti-angiogenic therapy: Prospects for treatment of ocular tumors.
  • Angiogenesis research has identified a host of pro- and anti-angiogenic factors that regulate an "angiogenic switch," which when turned on, allows tumors to assume a more aggressive form.
  • Angiogensis inhibitors that target this switch are in clinical trials for a wide array of tumor types.

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  • (PMID = 16912013.001).
  • [ISSN] 0882-0538
  • [Journal-full-title] Seminars in ophthalmology
  • [ISO-abbreviation] Semin Ophthalmol
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY10101
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 51
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16. Glinskii OV, Abraha TW, Turk JR, Glinsky VV, Huxley VH: PDGF/VEGF system activation and angiogenesis following initial post ovariectomy meningeal microvessel loss. Cell Cycle; 2008 May 15;7(10):1385-90
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  • It appears that the latter serves as a molecular switch favoring angiogenic responses rather than further regression of destabilized microvessels.
  • Indeed, consistent with this idea, we have found a considerable angiogenic activity in meningeal microvascular networks that previously underwent regression.

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  • (PMID = 18418080.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL078816-04W1; United States / NHLBI NIH HHS / HL / R01 HL078816; United States / NHLBI NIH HHS / HL / HL-52490; United States / NHLBI NIH HHS / HL / T32 HL007094; United States / NHLBI NIH HHS / HL / R37 HL042528; United States / NHLBI NIH HHS / HL / P01 HL052490; United States / NHLBI NIH HHS / HL / R37 HL042528-15; United States / NHLBI NIH HHS / HL / 5R01 HL078816-03; United States / NHLBI NIH HHS / HL / T32 HL007094-30
  • [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
  • [Chemical-registry-number] 0 / Estrogens; 0 / Hypoxia-Inducible Factor 1; 0 / Platelet-Derived Growth Factor; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.4.3 / Phospholipase C gamma
  • [Other-IDs] NLM/ NIHMS370834; NLM/ PMC3332329
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17. Puri N, Khramtsov A, Ahmed S, Nallasura V, Hetzel JT, Jagadeeswaran R, Karczmar G, Salgia R: A selective small molecule inhibitor of c-Met, PHA665752, inhibits tumorigenicity and angiogenesis in mouse lung cancer xenografts. Cancer Res; 2007 Apr 15;67(8):3529-34
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  • PHA665752 also inhibited angiogenesis by >85% in all the abovementioned cell lines and caused an angiogenic switch which resulted in a decreased production of vascular endothelial growth factor and an increase in the production of the angiogenesis inhibitor thrombospondin-1.

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  • (PMID = 17440059.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 100750-04; United States / NCI NIH HHS / CA / CA 125541-01
  • [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 / 5-((2,6-dichlorobenzyl)sulfonyl)-3-((3,5-dimethyl-4-((2-(pyrrolidin-1-ylmethyl)pyrrolidin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-1,3-dihydro-2H-indol-2-one; 0 / Indoles; 0 / Sulfones; 0 / Thrombospondin 1; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
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18. Nozawa H, Chiu C, Hanahan D: Infiltrating neutrophils mediate the initial angiogenic switch in a mouse model of multistage carcinogenesis. Proc Natl Acad Sci U S A; 2006 Aug 15;103(33):12493-8
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  • [Title] Infiltrating neutrophils mediate the initial angiogenic switch in a mouse model of multistage carcinogenesis.
  • In this article, we have identified two inflammatory cell types that are major sources of MMP-9 in the angiogenic stages of pancreatic islet carcinogenesis that unfold in RIP1-Tag2 transgenic mice.
  • MMP-9-expressing neutrophils were predominantly found inside angiogenic islet dysplasias and tumors, whereas MMP-9-expressing macrophages were localized along the periphery of such lesions.
  • Transient depletion of neutrophils significantly suppressed VEGF:VEGF-receptor association, a signature of MMP-9 activity, and markedly reduced the frequency of initial angiogenic switching in dysplasias.

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  • (PMID = 16891410.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [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 / Biomarkers; 0 / GTPase-Activating Proteins; 0 / Gr-1 protein, mouse; 0 / Ralbp1 protein, mouse; 0 / Receptors, Chemokine; 0 / Vascular Endothelial Growth Factor A; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC1531646
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19. Banerjee S, Mehta S, Haque I, Sengupta K, Dhar K, Kambhampati S, Van Veldhuizen PJ, Banerjee SK: VEGF-A165 induces human aortic smooth muscle cell migration by activating neuropilin-1-VEGFR1-PI3K axis. Biochemistry; 2008 Mar 18;47(11):3345-51
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  • Collectively, these results establish, for the first time, a mechanistic link among VEGF-A 165, NRP-1, VEGFR1, and PI3K/Akt in the regulation of migration of human vascular smooth muscle cells that eventually could be involved in the angiogenic switch.

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  • (PMID = 18284215.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 1P20 RR15563
  • [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
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Peptide Fragments; 0 / Protein Isoforms; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A (138-165); 144713-63-3 / Neuropilin-1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.11.1 / Oncogene Protein v-akt
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20. Naumov GN, Folkman J, Straume O, Akslen LA: Tumor-vascular interactions and tumor dormancy. APMIS; 2008 Jul-Aug;116(7-8):569-85
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  • Tumor progression is dependent on a number of sequential steps, including initial tumor-vascular interactions and recruitment of blood vessels (i.e., the angiogenic switch), as well as tumor cells interacting with the surrounding microenvironment and its different components.

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  • (PMID = 18834403.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA45548
  • [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.; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor
  • [Number-of-references] 122
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21. Tacconelli A, Farina AR, Cappabianca L, Gulino A, Mackay AR: Alternative TrkAIII splicing: a potential regulated tumor-promoting switch and therapeutic target in neuroblastoma. Future Oncol; 2005 Oct;1(5):689-98
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  • [Title] Alternative TrkAIII splicing: a potential regulated tumor-promoting switch and therapeutic target in neuroblastoma.
  • TrkAIII exhibits neuroblastoma xenograft tumor-promoting activity associated with the induction of a more angiogenic and stress-resistant neuroblastoma phenotype and antagonises nerve growth factor/TrkAI antioncogenic signaling.

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  • (PMID = 16556046.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, trkA
  • [Number-of-references] 58
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22. Zhang X, Kazerounian S, Duquette M, Perruzzi C, Nagy JA, Dvorak HF, Parangi S, Lawler J: Thrombospondin-1 modulates vascular endothelial growth factor activity at the receptor level. FASEB J; 2009 Oct;23(10):3368-76
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  • Vascular endothelial growth factor (VEGF) is a well-established stimulator of vascular permeability and angiogenesis, whereas thrombospondin-1 (TSP-1) is a potent angiogenic inhibitor.
  • Thus, this complex may represent a molecular switch that regulates angiogenesis and determines endothelial cell behavior.

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  • (PMID = 19528255.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092644; United States / NCI NIH HHS / CA / R01 CA130895; United States / NCI NIH HHS / CA / CA92644; United States / NCI NIH HHS / CA / CA130895; United States / NCI NIH HHS / CA / K08 CA088965
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Receptors, Complement 3b; 0 / Thrombospondin 1; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC2747678
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23. Raica M, Mogoantă L, Cîmpean AM, Alexa A, Ioanovici S, Mărgăritescu C, Lazăr D, Izvernariu D: Immunohistochemical expression of vascular endothelial growth factor (VEGF) in intestinal type gastric carcinoma. Rom J Morphol Embryol; 2008;49(1):37-42
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  • It was demonstrated the expression of VEGF in intestinal metaplasia and gastric dysplasia, which could signify an early angiogenic switch during tumorigenesis.

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  • (PMID = 18273500.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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24. Ribatti D: The crucial role of vascular permeability factor/vascular endothelial growth factor in angiogenesis: a historical review. Br J Haematol; 2005 Feb;128(3):303-9
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  • It is controlled by the net balance between molecules that have positive and negative regulatory activity and this concept had led to the notion of the 'angiogenic switch', depending on an increased production of one or more of the positive regulators of angiogenesis.
  • Numerous inducers of angiogenesis have been identified and this review offers a historical account of the relevant literature concerning the discovery of one of the best characterized angiogenic factors, namely vascular endothelial growth factor (VEGF)/vascular permeability factor.

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  • (PMID = 15667531.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 63
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25. Agliano A, Martin-Padura I, Mancuso P, Marighetti P, Rabascio C, Pruneri G, Shultz LD, Bertolini F: Human acute leukemia cells injected in NOD/LtSz-scid/IL-2Rgamma null mice generate a faster and more efficient disease compared to other NOD/scid-related strains. Int J Cancer; 2008 Nov 1;123(9):2222-7
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  • The leukemia-related angiogenic switch (measured as the number of circulating endothelial cells and progenitors) was faster in NSG compared to NS and NSB mice.


26. Martínez JA, Tavárez JJ, Oliveira CM, Banerjee DK: Potentiation of angiogenic switch in capillary endothelial cells by cAMP: A cross-talk between up-regulated LLO biosynthesis and the HSP-70 expression. Glycoconj J; 2006 May;23(3-4):209-20
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  • [Title] Potentiation of angiogenic switch in capillary endothelial cells by cAMP: A cross-talk between up-regulated LLO biosynthesis and the HSP-70 expression.
  • The exact mechanism of switching to a new angiogenic phenotype is currently unknown.

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  • (PMID = 16691504.001).
  • [ISSN] 0282-0080
  • [Journal-full-title] Glycoconjugate journal
  • [ISO-abbreviation] Glycoconj. J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U54-CA096297
  • [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
  • [Chemical-registry-number] 0 / Glc(3)Man(9)(GlcNAc)(2)-diphosphate-dolichol; 0 / HSP70 Heat-Shock Proteins; 0 / HSP90 Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / Polyisoprenyl Phosphate Sugars; 0 / Polysaccharides; 0 / Proto-Oncogene Proteins c-bcl-2; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 9001-27-8 / Factor VIII; 9035-58-9 / Thromboplastin; E0399OZS9N / Cyclic AMP; EC 2.4.1.- / Mannosyltransferases; EC 2.4.1.83 / dolichyl-phosphate beta-D-mannosyltransferase; EC 3.4.22.- / Caspases
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27. Mundel TM, Kalluri R: Type IV collagen-derived angiogenesis inhibitors. Microvasc Res; 2007 Sep-Nov;74(2-3):85-9
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  • The concept of anti-angiogenesis therapy was introduced by Judah Folkman in 1971 and since then, a plethora of pro- and anti-angiogenic factors have been identified.
  • In the recent years, it has become clear that angiogenesis, the formation of new capillaries from a pre-existing capillary network, is highly regulated by the action of pro- and anti-angiogenic factors.
  • In the healthy adult organism the "angiogenic-switch" is likely turned "Off", i. e. anti-angiogenic factors are likely counteracting the pro-angiogenic factors resulting in a non-angiogenic state.

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  • (PMID = 17602710.001).
  • [ISSN] 0026-2862
  • [Journal-full-title] Microvascular research
  • [ISO-abbreviation] Microvasc. Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK61688; United States / NIDDK NIH HHS / DK / DK55001; United States / NIDDK NIH HHS / DK / R01 DK081576; United States / NIDDK NIH HHS / DK / R01 DK061688; United States / NIDDK NIH HHS / DK / R01 DK062987-04; United States / NIDDK NIH HHS / DK / R01 DK061688-03; United States / NIDDK NIH HHS / DK / R01 DK062987; United States / NIDDK NIH HHS / DK / R01 DK055001; United States / NIDDK NIH HHS / DK / R01 DK055001-07S1; United States / NIDDK NIH HHS / DK / DK62987; United States / NIAAA NIH HHS / AA / AA53194
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Collagen Type IV
  • [Number-of-references] 62
  • [Other-IDs] NLM/ NIHMS34602; NLM/ PMC3998721
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28. Moserle L, Amadori A, Indraccolo S: The angiogenic switch: implications in the regulation of tumor dormancy. Curr Mol Med; 2009 Nov;9(8):935-41
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  • [Title] The angiogenic switch: implications in the regulation of tumor dormancy.
  • A discrete event termed "the angiogenic switch" has been recognized as key in promoting the transition towards a clinically aggressive tumor.
  • This concept generally describes a permanent change in the angiogenic capacity of the tumor sustained by genetic events occurring in cancer cells.
  • Recent evidence, however, indicates that a transient angiogenic switch delivered by components of the tumor microenvironment can also convey tumorigenic properties to tumor cells.
  • Why is the angiogenic switch so fundamental in the promotion of tumor growth?
  • In this review, we discuss the possible implications of the angiogenic switch on our understanding of the regulation of tumor dormancy.
  • [MeSH-major] Angiogenic Proteins / metabolism. Neoplasms / blood supply. Neovascularization, Pathologic / metabolism

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  • (PMID = 19925406.001).
  • [ISSN] 1875-5666
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Biomarkers, Tumor; 0 / Thrombospondin 1
  • [Number-of-references] 88
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29. Kim MS, Oh YJ, Lee S, Kim JE, Kim KH, Chung JH: Ultraviolet radiation attenuates thrombospondin 1 expression via PI3K-Akt activation in human keratinocytes. Photochem Photobiol; 2006 May-Jun;82(3):645-50
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  • Recent studies have demonstrated that UV radiation induces an angiogenic switch, by which it alters the balance between pro- and anti-angiogenic factors in the skin.
  • [MeSH-minor] Angiogenic Proteins / genetics. Angiogenic Proteins / radiation effects. Down-Regulation / genetics. Down-Regulation / radiation effects. Humans. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 16478297.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Thrombospondin 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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30. Evensen L, Micklem DR, Link W, Lorens JB: A novel imaging-based high-throughput screening approach to anti-angiogenic drug discovery. Cytometry A; 2010 Jan;77(1):41-51
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  • [Title] A novel imaging-based high-throughput screening approach to anti-angiogenic drug discovery.
  • The successful progression to the clinic of angiogenesis inhibitors for cancer treatment has spurred interest in developing new classes of anti-angiogenic compounds.
  • Initially, EC are dependent on vSMC-derived VEGF and sensitive to clinical anti-angiogenic therapeutics.
  • A subsequent phenotypic VEGF-switch renders EC networks resistant to anti-VEGF therapeutics, demarcating a mature vascular phenotype.
  • Therefore, candidate anti-angiogenic compounds can be interrogated for their relative potency on immature and mature networks and classified as either vascular normalizing or vascular disrupting agents.
  • Here, we demonstrate that the EC-vSMC co-culture assay represents a robust high-content imaging high-throughput screening system for identification of novel anti-angiogenic agents.
  • High-throughput screening using the EC-vSMC co-culture assay establishes a new platform to screen for novel anti-angiogenic compounds for cancer therapy.

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  • (PMID = 19834964.001).
  • [ISSN] 1552-4930
  • [Journal-full-title] Cytometry. Part A : the journal of the International Society for Analytical Cytology
  • [ISO-abbreviation] Cytometry A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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31. Roth P, Hammer C, Piguet AC, Ledermann M, Dufour JF, Waelti E: Effects on hepatocellular carcinoma of doxorubicin-loaded immunoliposomes designed to target the VEGFR-2. J Drug Target; 2007 Nov;15(9):623-31
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  • These findings suggest that IL designed to bind specifically to VEGFR-2 can be used to deliver doxorubicin to the tumour endothelium and may impair the "angiogenic switch" of the tumours.

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  • (PMID = 17968716.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Liposomes; 80168379AG / Doxorubicin; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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32. Khan GN, Merajver SD: Modulation of angiogenesis for cancer prevention: strategies based on antioxidants and copper deficiency. Curr Pharm Des; 2007;13(35):3584-90
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  • The possibility of interfering very early in tumor progression by modulating the cancer angiogenic switch is appealing.
  • In this chapter, we review progress with in vitro and in vivo models that show that anti-angiogenic interventions may be amenable to long- term chemopreventive measures.

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  • (PMID = 18220795.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA77612
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Chelating Agents; 0 / Flavonoids; 0 / NF-kappa B; 0 / Phenols; 0 / Polyphenols; 0 / Reactive Oxygen Species; 36-88-4 / Carotenoids; 789U1901C5 / Copper; 81AH48963U / Molybdenum; 91U3TGV99T / tetrathiomolybdate
  • [Number-of-references] 75
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33. Lee H, Baek S, Joe SJ, Pyo SN: Modulation of IFN-gamma production by TNF-alpha in macrophages from the tumor environment: significance as an angiogenic switch. Int Immunopharmacol; 2006 Jan;6(1):71-8
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  • [Title] Modulation of IFN-gamma production by TNF-alpha in macrophages from the tumor environment: significance as an angiogenic switch.
  • BACKGROUND: The role of macrophages in tumor angiogenesis has been known to influence in the production of angiogenic cytokines and growth factors including TNF-alpha.
  • Recently, macrophages were also found to produce INF-gamma, which were found to be involved in angiogenic inhibition.
  • Thus, the importance of macrophages in tumor angiogenesis might be the angiogenic switch.
  • The hypothesis tested here is that TNF-alpha can modulate the INF-gamma production in macrophages in tumor environment as part of the tumor angiogenic switch.
  • CONCLUSION: The overall data suggest that the macrophages in tumor environment might play an important role not only in angiogenic signal but also in anti-angiogenic signal by producing related cytokines.
  • Moreover, TNF-alpha might be a key cytokine functioning as a tumor angiogenic switch.

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  • (PMID = 16332515.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 82115-62-6 / Interferon-gamma
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34. Siekmann AF, Lawson ND: Notch signalling and the regulation of angiogenesis. Cell Adh Migr; 2007 Apr-Jun;1(2):104-6
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  • During angiogenic sprouting, endothelial cells exhibit a diverse array of cellular behaviors.
  • In particular, this work has identified a conserved role for the Notch signalling pathway in limiting the cellular angiogenic response, in part by reducing the level of vascular endothelial growth factor receptors in endothelial cells.
  • In this overview, we discuss the emerging concepts elucidated by these studies and propose a model in which Notch acts reiteratively throughout the angiogenic process, likely by acting as a switch to determine a cell's response to Vegf.

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  • (PMID = 19329884.001).
  • [ISSN] 1933-6926
  • [Journal-full-title] Cell adhesion & migration
  • [ISO-abbreviation] Cell Adh Migr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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  • [Other-IDs] NLM/ PMC2633979
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35. Furness MS, Robinson TP, Ehlers T, Hubbard RB 4th, Arbiser JL, Goldsmith DJ, Bowen JP: Antiangiogenic agents: studies on fumagillin and curcumin analogs. Curr Pharm Des; 2005;11(3):357-73
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  • Alteration of the delicate balance of angiogenic stimulating factors and angiogenic inhibitors results in the phenotypic change from quiescence to active endothelial proliferation.
  • To date, this angiogenic switch is not completely understood.

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  • (PMID = 15723631.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclohexanes; 0 / Fatty Acids, Unsaturated; 0 / Sesquiterpenes; 7OW73204U1 / fumagillin; IT942ZTH98 / Curcumin
  • [Number-of-references] 51
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36. Lucerna M, Pomyje J, Mechtcheriakova D, Kadl A, Gruber F, Bilban M, Sobanov Y, Schabbauer G, Breuss J, Wagner O, Bischoff M, Clauss M, Binder BR, Hofer E: Sustained expression of early growth response protein-1 blocks angiogenesis and tumor growth. Cancer Res; 2006 Jul 01;66(13):6708-13
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  • Transient induction of the transcription factor early growth response protein-1 (EGR-1) plays a pivotal role in the transcriptional response of endothelial cells to the angiogenic growth factors vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), which are produced by most tumors and are involved in the angiogenic switch.

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  • (PMID = 16818645.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / S 9403
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2882226; NLM/ UKMS30448
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37. Pinto AV, Martins PR, Romagnoli GG, Campanelli AP, Terezan AP, Filho ER, Ferreira da Eira A, Kaneno R: Polysaccharide fraction of Agaricus brasiliensis avoids tumor-induced IL-10 production and changes the microenvironment of subcutaneous Ehrlich adenocarcinoma. Cell Immunol; 2009;256(1-2):27-38
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  • Analysis of in situ expression of angiogenic growth factors showed a slight decrease of FGF-2 mRNA in Ehr-ATF animals (7th day) but not of VEGF-A or TGF-beta expression.
  • This fraction could not directly lyse either lymphocytes or tumor cells and we speculate that antitumor effect of ATF could be due to induction of a selective migration of immunocompetent cells from the spleen to the tumor site and to the switch of cytokine production.
  • [MeSH-minor] Angiogenic Proteins / genetics. Animals. Cytokines / biosynthesis. In Vitro Techniques. Interferon-gamma / biosynthesis. Lymphocyte Activation / drug effects. Lymphocytes, Tumor-Infiltrating / drug effects. Lymphocytes, Tumor-Infiltrating / pathology. Magnetic Resonance Spectroscopy. Male. Mice. Mice, Inbred BALB C. Molecular Structure. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism

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  • (PMID = 19243740.001).
  • [ISSN] 1090-2163
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Cytokines; 0 / Polysaccharides; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 130068-27-8 / Interleukin-10; 82115-62-6 / Interferon-gamma
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38. Munaut C, Colige AC, Lambert CA: Alternative splicing: a promising target for pharmaceutical inhibition of pathological angiogenesis? Curr Pharm Des; 2010;16(35):3864-76
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  • In this issue, we discuss some key examples showing how alternative splicing may induce a switch from anti-angiogenic to pro-angiogenic functions and reciprocally.
  • The emergence of strategies enabling to regulate alternative splicing opens new routes for anti-angiogenic therapies.

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  • (PMID = 21158727.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Messenger
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39. Yue F, Zhang GP, Jin HM: Effects of basic fibroblast growth factor on the expressions of angiogenic gene profile and cyclooxygenase-2 in brain microvascular endothelial cells. Sheng Li Xue Bao; 2006 Apr 25;58(2):124-8
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  • [Title] Effects of basic fibroblast growth factor on the expressions of angiogenic gene profile and cyclooxygenase-2 in brain microvascular endothelial cells.
  • The effects of bFGF (10 ng/ml) on mRNA and protein expressions of cyclooxygenase-2 (COX-2), an angiogenesis bystander molecule, were further investigated. cDNA microarray was employed to study the effects of bFGF on the expressions of angiogenic genes in a high throughput pattern.
  • The results showed that, 2 h after bFGF treatment, pro-angiogenic genes (Adamts1, MMP-9, Ang-1, PDGF B, G-CSF, FGF16, IGF-1, etc.) were significantly upregulated, whereas anti-angiogenic genes (TIMP-2, TSP-3, etc.) were significantly downregulated.
  • The bystander molecule in angiogenic pathway COX-2 mRNA and protein expressions were significantly upregulated after bFGF treatment.
  • It is suggested that triggering angiogensis switch through upregulating pro-angiogenic gene and downregulating anti-angiogenic gene expression is one of the major mechanisms of bFGF-induced angiogenesis.

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  • (PMID = 16628358.001).
  • [ISSN] 0371-0874
  • [Journal-full-title] Sheng li xue bao : [Acta physiologica Sinica]
  • [ISO-abbreviation] Sheng Li Xue Bao
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
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40. Perrin RM, Konopatskaya O, Qiu Y, Harper S, Bates DO, Churchill AJ: Diabetic retinopathy is associated with a switch in splicing from anti- to pro-angiogenic isoforms of vascular endothelial growth factor. Diabetologia; 2005 Nov;48(11):2422-7
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  • [Title] Diabetic retinopathy is associated with a switch in splicing from anti- to pro-angiogenic isoforms of vascular endothelial growth factor.
  • VEGF is alternatively spliced to form the angiogenic (VEGF(xxx)) and potentially anti-angiogenic (VEGF(xxx)b) family of isoforms.
  • CONCLUSIONS/INTERPRETATION: Since VEGF(xxx)b inhibits VEGF(xxx)-induced angiogenesis in a one-to-one stoichiometric manner, these results show that in the eye of diabetic patients VEGF splicing was switched from an anti-angiogenic to a pro-angiogenic environment.

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  • (PMID = 16193288.001).
  • [ISSN] 0012-186X
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / VEGFB protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor B
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41. Kopp HG, Hooper AT, Broekman MJ, Avecilla ST, Petit I, Luo M, Milde T, Ramos CA, Zhang F, Kopp T, Bornstein P, Jin DK, Marcus AJ, Rafii S: Thrombospondins deployed by thrombopoietic cells determine angiogenic switch and extent of revascularization. J Clin Invest; 2006 Dec;116(12):3277-91
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  • [Title] Thrombospondins deployed by thrombopoietic cells determine angiogenic switch and extent of revascularization.
  • However, the molecular determinants controlling the angiogenic phenotype of thrombopoietic cells remain unknown.
  • Here, we show that expression and release of thrombospondins (TSPs) by megakaryocytes and platelets function as a major antiangiogenic switch.

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  • (PMID = 17143334.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR45418; United States / NHLBI NIH HHS / HL / P01 HL046403; United States / NINDS NIH HHS / NS / R01 NS041462; United States / NHLBI NIH HHS / HL / R01 HL59312; United States / NHLBI NIH HHS / HL / P01 HL067839; United States / NINDS NIH HHS / NS / R01 NS41462; United States / Howard Hughes Medical Institute / / ; United States / NHLBI NIH HHS / HL / P01 HL059312; United States / NHLBI NIH HHS / HL / R01 HL061849; United States / NHLBI NIH HHS / HL / R01 HL67839; United States / NHLBI NIH HHS / HL / R37 HL047073; United States / NHLBI NIH HHS / HL / R01 HL61849; United States / NHLBI NIH HHS / HL / R01 HL075234; United States / NIAMS NIH HHS / AR / R01 AR045418; United States / NHLBI NIH HHS / HL / R37 HL47073; United States / NHLBI NIH HHS / HL / P01 HL46403; United States / NHLBI NIH HHS / HL / R21 HL083222
  • [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
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Stilbenes; 0 / Thrombospondin 1; 0 / Thrombospondins; 0 / thrombospondin 2; 9014-42-0 / Thrombopoietin; I5590ES2QZ / fosbretabulin
  • [Other-IDs] NLM/ PMC1679710
  •  go-up   go-down


42. Coulon C, Georgiadou M, Roncal C, De Bock K, Langenberg T, Carmeliet P: From vessel sprouting to normalization: role of the prolyl hydroxylase domain protein/hypoxia-inducible factor oxygen-sensing machinery. Arterioscler Thromb Vasc Biol; 2010 Dec;30(12):2331-6
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  • At the forefront of a vessel sprout, "tip cells" guide the sprouting vessel toward an angiogenic stimulus.
  • For this purpose, endothelial cells switch to the "phalanx" cell fate, which is characterized by quiescent and nonproliferating cells aligned in a tight cobblestonelike layer.

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  • (PMID = 20966400.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / endothelial PAS domain-containing protein 1; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; S88TT14065 / Oxygen
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43. Li Calzi S, Neu MB, Shaw LC, Kielczewski JL, Moldovan NI, Grant MB: EPCs and pathological angiogenesis: when good cells go bad. Microvasc Res; 2010 May;79(3):207-16
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  • EPCs provide both instructive (release of pro-angiogenic cytokines) and structural (vessel incorporation and stabilization) functions that contribute to the initiation of neo-angiogenesis.
  • Since the EPCs may be responsible for turning on the "angiogenic switch," strategies have been employed to keep this switch in the "off" position for diseases like cancer, retinopathy, and wet AMD.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20188747.001).
  • [ISSN] 1095-9319
  • [Journal-full-title] Microvascular research
  • [ISO-abbreviation] Microvasc. Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK090730; United States / NEI NIH HHS / EY / R01 EY007739; United States / NEI NIH HHS / EY / R01 EY012601; United States / NHLBI NIH HHS / HL / R01 HL110170; United States / NEI NIH HHS / EY / R21 EY014818
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 73
  • [Other-IDs] NLM/ NIHMS192917; NLM/ PMC3650470
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44. Tassi E, Wellstein A: The angiogenic switch molecule, secreted FGF-binding protein, an indicator of early stages of pancreatic and colorectal adenocarcinoma. Semin Oncol; 2006 Dec;33(6 Suppl 11):S50-6
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  • [Title] The angiogenic switch molecule, secreted FGF-binding protein, an indicator of early stages of pancreatic and colorectal adenocarcinoma.

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  • (PMID = 17178288.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL068686; United States / NCI NIH HHS / CA / R01 CA071508; United States / NCI NIH HHS / CA / R01 CA108440; United States / NCI NIH HHS / CA / R01 CA71508
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Intercellular Signaling Peptides and Proteins; 139946-12-6 / FGFBP1 protein, human
  • [Number-of-references] 98
  • [Other-IDs] NLM/ NIHMS15609; NLM/ PMC1781498
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45. Galiè M, Konstantinidou G, Peroni D, Scambi I, Marchini C, Lisi V, Krampera M, Magnani P, Merigo F, Montani M, Boschi F, Marzola P, Orrù R, Farace P, Sbarbati A, Amici A: Mesenchymal stem cells share molecular signature with mesenchymal tumor cells and favor early tumor growth in syngeneic mice. Oncogene; 2008 Apr 17;27(18):2542-51
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  • We also found that MTCs and MSCs have the same molecular signature for stemness-related genes, and that when co-implanted with cancer cells in syngeneic animals MSCs determine early tumor appearance, probably by favoring the angiogenic switch.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Gene Expression Regulation, Neoplastic. Mammary Neoplasms, Animal / metabolism. Mesenchymal Stem Cell Transplantation / adverse effects. Mesenchymal Stromal Cells / metabolism. Neovascularization, Pathologic / metabolism

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  • (PMID = 17998939.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenic Proteins
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46. Ardi VC, Van den Steen PE, Opdenakker G, Schweighofer B, Deryugina EI, Quigley JP: Neutrophil MMP-9 proenzyme, unencumbered by TIMP-1, undergoes efficient activation in vivo and catalytically induces angiogenesis via a basic fibroblast growth factor (FGF-2)/FGFR-2 pathway. J Biol Chem; 2009 Sep 18;284(38):25854-66
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  • By quantifying the levels of host angiogenic factors, we demonstrated that basic fibroblast growth factor (FGF-2) was a major cytokine becoming bioavailable in the onplant tissue undergoing a neutrophil proMMP-9-mediated angiogenic switch.

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  • (PMID = 19608737.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA105412; United States / NHLBI NIH HHS / HL / T32 HL007195; United States / NCI NIH HHS / CA / CA105412; United States / NCI NIH HHS / CA / CA55852; United States / NHLBI NIH HHS / HL / 5T32 HL07195-31; United States / NCI NIH HHS / CA / R01 CA055852; United States / NCI NIH HHS / CA / R01 CA129484
  • [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 / Enzyme Precursors; 0 / Tissue Inhibitor of Metalloproteinase-1; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / Fgfr2 protein, mouse; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 3.4.24.- / pro-matrix metalloproteinase 9; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2757987
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47. Shojaei F, Singh M, Thompson JD, Ferrara N: Role of Bv8 in neutrophil-dependent angiogenesis in a transgenic model of cancer progression. Proc Natl Acad Sci U S A; 2008 Feb 19;105(7):2640-5
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  • Also, the role of neutrophils in RIP-Tag angiogenic switching, as assessed by systemic ablation using anti-Gr1 antibodies at different stages of tumor progression, has been recently described.
  • Here, we show that early treatment of RIP-Tag mice with anti-Bv8 antibodies resulted in a significant reduction in the number of angiogenic islets relative to control antibody-treated mice, implicating Bv8 in the angiogenic switch during neoplasia.
  • Histological analysis showed a significant reduction in vascular surface areas in hyperplastic and angiogenic lesions in pancreatic islets from anti-Bv8-treated mice.

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  • (PMID = 18268320.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Gastrointestinal Hormones; 0 / Insulin; 0 / Neuropeptides; 0 / Prok2 protein, mouse
  • [Other-IDs] NLM/ PMC2268189
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48. Yoder MC, Ingram DA: Endothelial progenitor cell: ongoing controversy for defining these cells and their role in neoangiogenesis in the murine system. Curr Opin Hematol; 2009 Jul;16(4):269-73
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  • RECENT FINDINGS: Highlighted articles identify a critical role for these cells in promoting the angiogenic switch for growth of metastatic tumors or find no role at all for these circulating cells as engrafting cells in vascular endothelium or as promoters of tumor growth.

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  • (PMID = 19417649.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 41
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49. Giuriato S, Ryeom S, Fan AC, Bachireddy P, Lynch RC, Rioth MJ, van Riggelen J, Kopelman AM, Passegué E, Tang F, Folkman J, Felsher DW: Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch. Proc Natl Acad Sci U S A; 2006 Oct 31;103(44):16266-71
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  • [Title] Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch.

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  • (PMID = 17056717.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 105102; United States / NCI NIH HHS / CA / U56 CA112973; United States / NCI NIH HHS / CA / 1P20 CA 112973; United States / NCI NIH HHS / CA / R01 CA089305; United States / NCI NIH HHS / CA / R01 CA105102; United States / NCI NIH HHS / CA / 3R01 CA 089305-03S1; United States / NCI NIH HHS / CA / R01 CA 85610; United States / NCI NIH HHS / CA / R01 CA085610
  • [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 / Proto-Oncogene Proteins c-myc; 0 / Thrombospondin 1; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC1637571
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50. Schipani E: Hypoxia and HIF-1 alpha in chondrogenesis. Semin Cell Dev Biol; 2005 Aug-Oct;16(4-5):539-46
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  • The chondrocytic growth plate is a unique mesenchymal tissue, as it is avascular but it requires blood vessel invasion, i.e. the angiogenic switch, in order to be replaced by bone.
  • The findings overall highlight the usefulness of studying fetal growth plate development as a model to address issues such as adaptation of normal tissues to hypoxia, survival of hypoxic cells, and regulation of the angiogenic switch.

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  • (PMID = 16144691.001).
  • [ISSN] 1084-9521
  • [Journal-full-title] Seminars in cell & developmental biology
  • [ISO-abbreviation] Semin. Cell Dev. Biol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR 048191
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit
  • [Number-of-references] 54
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51. Taveau JC, Dubois M, Le Bihan O, Trépout S, Almagro S, Hewat E, Durmort C, Heyraud S, Gulino-Debrac D, Lambert O: Structure of artificial and natural VE-cadherin-based adherens junctions. Biochem Soc Trans; 2008 Apr;36(Pt 2):189-93
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  • This novel link is labile and promotes the endothelial cell switch from a quiescent to an angiogenic state.

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  • (PMID = 18363560.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Cadherins; 0 / Membranes, Artificial
  • [Number-of-references] 27
  • [Other-IDs] NLM/ HALMS433365; NLM/ PMC2798065
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52. Teodoro JG, Evans SK, Green MR: Inhibition of tumor angiogenesis by p53: a new role for the guardian of the genome. J Mol Med (Berl); 2007 Nov;85(11):1175-86
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  • The combination of these effects allows p53 to efficiently shut down the angiogenic potential of cancer cells.
  • Thus, the loss of functional p53 during tumorigenesis likely represents an essential step in the switch to an angiogenic phenotype that is displayed by aggressive tumors.

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  • (PMID = 17589818.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 98
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53. Jouanneau E: Angiogenesis and gliomas: current issues and development of surrogate markers. Neurosurgery; 2008 Jan;62(1):31-50; discussion 50-2
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  • Hypoxia and genetic anomalies within a glioma trigger the angiogenic switch, thus upregulating angiogenic factors and downregulating antiangiogenic factors.
  • This article summarizes the mechanisms of the angiogenic switch based on tumor grade and subtype, reviews completed and ongoing clinical trials, and details the present and the future of surrogate markers for angiogenesis in gliomas.

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  • (PMID = 18300890.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors; 0 / Biomarkers
  • [Number-of-references] 216
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54. Maione F, Molla F, Meda C, Latini R, Zentilin L, Giacca M, Seano G, Serini G, Bussolino F, Giraudo E: Semaphorin 3A is an endogenous angiogenesis inhibitor that blocks tumor growth and normalizes tumor vasculature in transgenic mouse models. J Clin Invest; 2009 Nov;119(11):3356-72
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  • Pharmacologic inhibition of endogenous Sema3A during the angiogenic switch, the point when pretumoral lesions initiate an angiogenic phase that persists throughout tumor growth, enhanced angiogenesis and accelerated tumor progression.

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  • (PMID = 19809158.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP04127; Italy / Telethon / / GGP09175; United States / NIDDK NIH HHS / DK / DK59936; United States / NIAAA NIH HHS / AA / P60 AA11999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD29; 0 / Semaphorin-3A
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55. Rojas A, Silva R, Figueroa H, Morales MA: Oxidative stress in tumor microenvironment--Its role in angiogenesis. Zhongguo Fei Ai Za Zhi; 2008 Jun 20;11(3):297-305
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  • The tumor angiogenesis process is believed to be dependent on an "angiogenic switch" formed by a cascade of biologic events as a consequence of the "cross-talk" between tumor cells and several components of local microenvironment including endothelial cells, macrophages, mast cells and stromal components.
  • Oxidative stress represents an important stimulus that widely contributes to this angiogenic switch, which is particularly relevant in lungs, where oxidative stress is originated from different sources including the incomplete reduction of oxygen during respiration, exposure to hypoxia/reoxygenation, stimulated resident or chemoattracted immune cells to lung tissues, as well as by a variety of chemicals compounds.

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  • (PMID = 20731924.001).
  • [ISSN] 1999-6187
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] China
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56. Pietras K, Hanahan D: A multitargeted, metronomic, and maximum-tolerated dose "chemo-switch" regimen is antiangiogenic, producing objective responses and survival benefit in a mouse model of cancer. J Clin Oncol; 2005 Feb 10;23(5):939-52
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  • [Title] A multitargeted, metronomic, and maximum-tolerated dose "chemo-switch" regimen is antiangiogenic, producing objective responses and survival benefit in a mouse model of cancer.
  • PURPOSE: A transgenic mouse model has revealed parameters of the angiogenic switch during multistep tumorigenesis of pancreatic islets, and demonstrated efficacy of antiangiogenic therapies.
  • A "chemo-switch" protocol, involving sequential MTD and then metronomic chemotherapy, overlaid with multitargeted inhibition of PDGFR and VEGFR, gave complete responses and unprecedented survival advantage in this model.

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  • (PMID = 15557593.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [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 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Indoles; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Pyrroles; 0 / sunitinib; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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57. Prahst C, Héroult M, Lanahan AA, Uziel N, Kessler O, Shraga-Heled N, Simons M, Neufeld G, Augustin HG: Neuropilin-1-VEGFR-2 complexing requires the PDZ-binding domain of neuropilin-1. J Biol Chem; 2008 Sep 12;283(37):25110-4
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  • Vascular endothelial growth factor (VEGF) acts as a hierarchically high switch of the angiogenic cascade by interacting with its high affinity VEGF receptors and with neuropilin co-receptors.

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  • (PMID = 18628209.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL 084619
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / GIPC1 protein, human; 0 / Gipc protein, mouse; 0 / Neuropeptides; 0 / Vascular Endothelial Growth Factor A; 144713-63-3 / Neuropilin-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC2533068
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58. Zaslavsky A, Baek KH, Lynch RC, Short S, Grillo J, Folkman J, Italiano JE Jr, Ryeom S: Platelet-derived thrombospondin-1 is a critical negative regulator and potential biomarker of angiogenesis. Blood; 2010 Jun 3;115(22):4605-13
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  • The sequential events leading to tumor progression include a switch to the angiogenic phenotype, dependent on a shift in the balance between positive and negative angiogenic regulators produced by tumor and stromal cells.

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  • (PMID = 20086246.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA045548; United States / NHLBI NIH HHS / HL / R01 HL068130; United States / NCI NIH HHS / CA / P01 CA045548-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Thrombospondin 1
  • [Other-IDs] NLM/ PMC2881490
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59. Almog N: Molecular mechanisms underlying tumor dormancy. Cancer Lett; 2010 Aug 28;294(2):139-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although cancer can arise through multiple pathways, it is assumed that essentially most tumors begin as microscopic, non-angiogenic neoplasms which cannot expand in size until vasculature is established.
  • Additionally, analogies and distinctions between the concepts of "tumor dormancy" and that of the "cellular dormancy" of tumor cells, as well as between the "exit from tumor dormancy" and the "onset of the angiogenic switch" are discussed.

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20363069.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Ireland
  • [Number-of-references] 69
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60. Miyazawa M, Dong Z, Zhang Z, Neiva KG, Cordeiro MM, Oliveira DT, Nör JE: Effect of PTK/ZK on the angiogenic switch in head and neck tumors. J Dent Res; 2008 Dec;87(12):1166-71
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  • [Title] Effect of PTK/ZK on the angiogenic switch in head and neck tumors.
  • Transformation of small avascular masses of tumor cells into rapidly progressive cancers is triggered by the angiogenic switch, a process that involves vascular endothelial growth factor (VEGF) signaling.
  • We have shown that VEGF enhances the survival and angiogenic potential of endothelial cells by activating the Bcl-2-CXCL8 signaling axis.
  • Analysis of these data demonstrates that PTK/ZK blocks downstream targets of VEGF signaling in endothelial cells, and suggests that PTK/ZK may inhibit the angiogenic switch in head and neck tumors.

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  • (PMID = 19029087.001).
  • [ISSN] 1544-0591
  • [Journal-full-title] Journal of dental research
  • [ISO-abbreviation] J. Dent. Res.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / R01-DE15948; United States / NIDCR NIH HHS / DE / R01 DE014601-01; United States / NIDCR NIH HHS / DE / R01 DE014601; United States / NIDCR NIH HHS / DE / R01 DE016586-01; United States / NIDCR NIH HHS / DE / R01-DE14601; United States / NIDCR NIH HHS / DE / R01 DE016586; United States / NIDCR NIH HHS / DE / R01 DE015948-01; United States / NIDCR NIH HHS / DE / R01-DE16586; United States / NIDCR NIH HHS / DE / R01 DE015948
  • [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 / Interleukin-8; 0 / Phthalazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 5DX9U76296 / vatalanib; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Other-IDs] NLM/ NIHMS96082; NLM/ PMC2654254
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61. Zhang N, Zhong R, Perez-Pinera P, Herradon G, Ezquerra L, Wang ZY, Deuel TF: Identification of the angiogenesis signaling domain in pleiotrophin defines a mechanism of the angiogenic switch. Biochem Biophys Res Commun; 2006 May 5;343(2):653-8
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  • [Title] Identification of the angiogenesis signaling domain in pleiotrophin defines a mechanism of the angiogenic switch.
  • The appearance of new blood vessels in malignant tumors is known as the "angiogenic switch."
  • The angiogenic switch triggers a stage of rapid tumor growth supported by extensive tumor angiogenesis and a more aggressive tumor phenotype and its onset is a poor prognostic indicator for host survival.
  • Identification of the factors that stimulate the angiogenic switch thus is of high importance.
  • Pleiotrophin (PTN the protein, Ptn the gene) is an angiogenic factor and the Ptn gene has been found to be constitutively expressed in many human tumors of different cell types.
  • These studies use a nude mouse model to test if Ptn constitutively expressed in premalignant cells is sufficient to trigger an angiogenic switch in vivo.
  • SW-13 Ptn cell subcutaneous tumor implants grew very rapidly and had a striking increase in the density of new blood vessels compared to the SW-13 cell tumor implants, suggesting that constitutive PTN signaling in the premalignant SW-13 cell implants in the nude mouse recapitulates fully the angiogenic switch.
  • It was found also that ectopic expression of the C-terminal domain of PTN in SW-13 cell implants was equally effective in initiating an angiogenic switch as the full-length PTN whereas implants of SW-13 cells in nude mice that express the N-terminal domain of PTN grew rapidly but failed to develop tumor angiogenesis.
  • The data suggest the possibility that mutations that activate Ptn in premalignant cells are sufficient to stimulate an angiogenic switch in vivo and, since these mutations are frequently found in human malignancies, that constitutive PTN signaling may be an important contributor to progression of human tumors.

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  • (PMID = 16554021.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 2 T32 DK007022-26; United States / NCI NIH HHS / CA / CA 66029; United States / NCI NIH HHS / CA / CA 84400; United States / NIDDK NIH HHS / DK / DK 53557; United States / PHS HHS / / NHLBI 31102
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytokines; 134034-50-7 / pleiotrophin
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62. Maier JA, Nasulewicz-Goldeman A, Simonacci M, Boninsegna A, Mazur A, Wolf FI: Insights into the mechanisms involved in magnesium-dependent inhibition of primary tumor growth. Nutr Cancer; 2007;59(2):192-8
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  • The inhibition of LLC tumor growth in Mg-deficient mice is due to a direct effect of low Mg on LLC cell proliferation and to an impairment of the angiogenic switch.

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  • Hazardous Substances Data Bank. MAGNESIUM, ELEMENTAL .
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  • (PMID = 18001214.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.14.13.39 / Nitric Oxide Synthase; I38ZP9992A / Magnesium
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63. Chen SH, Babichev Y, Rodrigues N, Voskas D, Ling L, Nguyen VP, Dumont DJ: Gene expression analysis of Tek/Tie2 signaling. Physiol Genomics; 2005 Jul 14;22(2):257-67
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  • Using semiquantitative PCR, the differential expression of eight genes was confirmed that included Elk3, an important angiogenic switch gene which was upregulated in the absence of Tie2 signaling.
  • The results of this study provide valuable insight into the potential association between Tie2 signaling and other known angiogenic pathways as well as genes that might have novel functions in vascular remodeling.

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  • (PMID = 15899944.001).
  • [ISSN] 1531-2267
  • [Journal-full-title] Physiological genomics
  • [ISO-abbreviation] Physiol. Genomics
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-63224-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, TIE-2
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64. Hemberger M: IFPA award in placentology lecture - characteristics and significance of trophoblast giant cells. Placenta; 2008 Mar;29 Suppl A:S4-9
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  • Giant cells are highly polyploid as a result of a switch from a mitotic to an endoreduplicative cell cycle.
  • Their angiogenic and vasodilatory properties, combined with the ability to remodel arterial walls, enable them to redirect maternal blood flow towards the implantation site.

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  • (PMID = 18083226.001).
  • [ISSN] 0143-4004
  • [Journal-full-title] Placenta
  • [ISO-abbreviation] Placenta
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBS/E/B/0000M100; United Kingdom / Medical Research Council / / G120/824; United Kingdom / Medical Research Council / /
  • [Publication-type] Lectures; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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65. Giatromanolaki A, Sivridis E, Simopoulos C, Polychronidis A, Gatter KC, Harris AL, Koukourakis MI: Hypoxia inducible factors 1alpha and 2alpha are associated with VEGF expression and angiogenesis in gallbladder carcinomas. J Surg Oncol; 2006 Sep 1;94(3):242-7
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  • AIMS: To investigate the significance of the hypoxia inducible factors HIF-1alpha and HIF-2alpha in gallbladder adenocarcinomas and their relation to angiogenesis and to the expression of VEGF, an angiogenic factor transcriptionally regulated by HIFalphas.
  • In addition, the vascular density (VD) and the expression of the angiogenic factors VEGF and thymidine phosphorylase (TP) were examined.
  • Although HIFs did not relate significantly with prognosis, patients with HIF-1/2 expression who failed to switch-on VEGF or intratumoral angiogenesis had a favorable outcome.

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  • [Copyright] 2006 Wiley-Liss, Inc.
  • (PMID = 16900513.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1
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66. Schaffner F, Versteeg HH, Schillert A, Yokota N, Petersen LC, Mueller BM, Ruf W: Cooperation of tissue factor cytoplasmic domain and PAR2 signaling in breast cancer development. Blood; 2010 Dec 23;116(26):6106-13
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  • Simultaneous deletion of PAR2 in TF(ΔCT) mice did not further delay tumor appearance, consistent with overlapping roles of TF and PAR2 in promoting the angiogenic switch in early stages of breast cancer.
  • In advanced carcinomas, tumor-associated macrophages were reduced in TF(ΔCT) and TF(ΔCT)/PAR2(-/-) mice, and increased tumor vessel diameters of TF(ΔCT) mice were partially reversed by PAR2-deficiency, indicating that the TF cytoplasmic domain has additional roles that are interdependent with PAR2 signaling in regulating host angiogenic responses.

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  • (PMID = 20861457.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL060742; United States / NHLBI NIH HHS / HL / HL-60742
  • [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 / Receptor, PAR-2; 9035-58-9 / Thromboplastin
  • [Other-IDs] NLM/ PMC3031395
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67. Ria R, Reale A, Castrovilli A, Mangialardi G, Dammacco F, Ribatti D, Vacca A: Angiogenesis and progression in human melanoma. Dermatol Res Pract; 2010;2010:185687
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  • Secretion of various angiogenic cytokines, i.e.
  • VEGF-A, FGF-2, PGF-1 and -2, IL-8, and TGF-1 by melanoma cells promote the angiogenic switch and has been correlated to transition from the radial to the vertical growth phase, and to the metastatic phase.

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  • (PMID = 20631829.001).
  • [ISSN] 1687-6113
  • [Journal-full-title] Dermatology research and practice
  • [ISO-abbreviation] Dermatol Res Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2901609
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68. Vacca A, Scavelli C, Serini G, Di Pietro G, Cirulli T, Merchionne F, Ribatti D, Bussolino F, Guidolin D, Piaggio G, Bacigalupo A, Dammacco F: Loss of inhibitory semaphorin 3A (SEMA3A) autocrine loops in bone marrow endothelial cells of patients with multiple myeloma. Blood; 2006 Sep 01;108(5):1661-7
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  • Here we show that the VEGF165-driven angiogenic potential of multiple myeloma (MM) ECs is significantly higher than that of monoclonal gammopathy of undetermined significance (MGUS) ECs (MGECs) and human umbilical vein (HUV) ECs.
  • Moreover, by counteracting VEGF165 activity as efficiently as an anti-VEGFR-2 antibody, exogenous SEMA3A restrains the over-angiogenic potential of MMECs.
  • Our data indicate that loss of endothelial SEMA3A in favor of VEGF165 could be responsible for the angiogenic switch from MGUS to MM.

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  • (PMID = 16684957.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP04127
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / SEMA3A protein, human; 0 / Semaphorin-3A; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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69. Parsons-Wingerter P, Chandrasekharan UM, McKay TL, Radhakrishnan K, DiCorleto PE, Albarran B, Farr AG: A VEGF165-induced phenotypic switch from increased vessel density to increased vessel diameter and increased endothelial NOS activity. Microvasc Res; 2006 Nov;72(3):91-100
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  • [Title] A VEGF165-induced phenotypic switch from increased vessel density to increased vessel diameter and increased endothelial NOS activity.
  • Although vascular endothelial growth factor-165 (VEGF(165)) regulates numerous angiogenic cellular activities, its complex effects on vascular morphology are not highly quantified.
  • The VEGF-dependent phenotypic switch from normal vessels displaying increased vessel density to abnormal, dilated vessels typical of tumor vasculature and other pathologies resulted from an approximate threefold increase in VEGF concentration (1.25 to 5 microg/CAM) and correlated positively with increased eNOS activity.
  • In summary, VEGF(165) induced a phenotypic switch from increased vessel density associated with low VEGF concentration, to increased vessel diameter and increased eNOS activity at high VEGF concentration.

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  • (PMID = 16872639.001).
  • [ISSN] 0026-2862
  • [Journal-full-title] Microvascular research
  • [ISO-abbreviation] Microvasc. Res.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM-40711
  • [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
  • [Chemical-registry-number] 0 / Recombinant Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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70. Simantov R, Febbraio M, Silverstein RL: The antiangiogenic effect of thrombospondin-2 is mediated by CD36 and modulated by histidine-rich glycoprotein. Matrix Biol; 2005 Feb;24(1):27-34
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  • These data suggest that modulation of the TSR/CD36 system may play an important role in the regulation of the angiogenic "switch," and may provide a target for therapeutic interventions.

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  • (PMID = 15748999.001).
  • [ISSN] 0945-053X
  • [Journal-full-title] Matrix biology : journal of the International Society for Matrix Biology
  • [ISO-abbreviation] Matrix Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD36; 0 / Cell Adhesion Molecules; 0 / Macromolecular Substances; 0 / Peptides; 0 / Platelet Membrane Glycoproteins; 0 / Proteins; 0 / Recombinant Fusion Proteins; 0 / Thrombospondins; 0 / histidine-rich proteins; 0 / thrombospondin 2; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.5.1.18 / Glutathione Transferase
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71. Diaz-Gonzalez JA, Russell J, Rouzaut A, Gil-Bazo I, Montuenga L: Targeting hypoxia and angiogenesis through HIF-1alpha inhibition. Cancer Biol Ther; 2005 Oct;4(10):1055-62
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  • HIF-1alpha plays a major role in the response of tumors to hypoxia, and it is mainly responsible for the "angiogenic switch".

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  • (PMID = 16294030.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1
  • [Number-of-references] 105
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72. North S, Moenner M, Bikfalvi A: Recent developments in the regulation of the angiogenic switch by cellular stress factors in tumors. Cancer Lett; 2005 Jan 31;218(1):1-14
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  • [Title] Recent developments in the regulation of the angiogenic switch by cellular stress factors in tumors.
  • Angiogenesis in tumors is controlled by the so-called 'angiogenic switch' which allows the passage from low invasive and poorly vascularized tumors to highly invasive and angiogenic tumors.
  • A number of cellular stress factors such as hypoxia, nutrient deprivation or inducers of reactive oxygen species (ROS) are important stimuli of angiogenic signalling.
  • In addition, HIF-independent mechanisms have been described which involved number of other molecules and transcription factors such as nuclear factor-(kappa)B (NF-(kappa)B) and p53. p53 is an important intracellular mediator of the stress response and is now also recognized as a modifier of the angiogenic response. p53 may interact with the HIF system but may also have direct effects on angiogenesis regulators or interfere with translation mechanisms of angiogenesis factors.

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  • (PMID = 15639335.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Micronutrients; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 125
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73. Islam A, Banerjee S, Kambhampati S, Baranda J, Banerjee S, Weston AP, Saxena NK, Banerjee SK: Angiogenic switch in Barrett's adenocarcinoma: the role of vascular endothelial growth factor. Front Biosci; 2006;11:2336-48
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  • [Title] Angiogenic switch in Barrett's adenocarcinoma: the role of vascular endothelial growth factor.
  • Activation of "Angiogenic switch" or formation of new blood vessels is one of the upshots of these abuses.
  • Multiple factors are associated with the activation of angiogenic switch.

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  • (PMID = 16720317.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 87680; United States / NCRR NIH HHS / RR / P20 RR015563
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 123
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74. Heckman-Stoddard BM, Vargo-Gogola T, McHenry PR, Jiang V, Herrick MP, Hilsenbeck SG, Settleman J, Rosen JM: Haploinsufficiency for p190B RhoGAP inhibits MMTV-Neu tumor progression. Breast Cancer Res; 2009;11(4):R61
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  • To examine gene expression of potential mediators of the angiogenic switch, an angiogenesis PCR array was utilized and results were confirmed using immunohistochemistry.
  • Angiogenesis was decreased in the p190B heterozygous tumors, and expression of a potent angiogenic inhibitor, thrombospondin-1, was elevated in p190B+/-Neu mammary glands.

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  • (PMID = 19703301.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K99CA127361; United States / NCI NIH HHS / CA / CA030195-22; United States / NCI NIH HHS / CA / R00 CA127361; United States / NCI NIH HHS / CA / P01 CA030195; United States / NCI NIH HHS / CA / K99 CA127361; United States / NCI NIH HHS / CA / R00 CA127361-04; United States / NCI NIH HHS / CA / CA127361-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arhgap5 protein, mouse; 0 / GTPase-Activating Proteins; 0 / Neoplasm Proteins; 0 / Thrombospondin 1; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2750123
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75. Almog N, Ma L, Raychowdhury R, Schwager C, Erber R, Short S, Hlatky L, Vajkoczy P, Huber PE, Folkman J, Abdollahi A: Transcriptional switch of dormant tumors to fast-growing angiogenic phenotype. Cancer Res; 2009 Feb 1;69(3):836-44
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  • [Title] Transcriptional switch of dormant tumors to fast-growing angiogenic phenotype.
  • We have developed models in which human tumors remain dormant for a prolonged period of time (>120 days) until they switch to rapid growth and become strongly angiogenic.
  • These angiogenic tumors retain their ability to grow fast once injected in new mice.
  • We hypothesized that dormant tumors undergo a stable genetic reprogramming during their switch to the fast-growing phenotype.
  • Genome-wide transcriptional analysis was done to dissect the molecular mechanisms underlying the switch of dormant breast carcinoma, glioblastoma, osteosarcoma, and liposarcoma tumors.
  • The switch of dormant tumors was associated with down-regulation of angiogenesis inhibitor thrombospondin and decreased sensitivity of angiogenic tumors to angiostatin.


76. Rajcevic U, Petersen K, Knol JC, Loos M, Bougnaud S, Klychnikov O, Li KW, Pham TV, Wang J, Miletic H, Peng Z, Bjerkvig R, Jimenez CR, Niclou SP: iTRAQ-based proteomics profiling reveals increased metabolic activity and cellular cross-talk in angiogenic compared with invasive glioblastoma phenotype. Mol Cell Proteomics; 2009 Nov;8(11):2595-612
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  • [Title] iTRAQ-based proteomics profiling reveals increased metabolic activity and cellular cross-talk in angiogenic compared with invasive glioblastoma phenotype.
  • We have developed a human glioblastoma xenograft model in nude rats that is characterized by a highly infiltrative non-angiogenic phenotype.
  • Upon serial transplantation this phenotype will develop into a highly angiogenic tumor.
  • Here we aimed at identifying potential biomarkers expressed by the non-angiogenic and the angiogenic phenotypes and elucidating the molecular pathways involved in the switch from invasive to angiogenic growth.
  • Focusing on membrane-associated proteins, we profiled protein expression during the progression from an invasive to an angiogenic phenotype by analyzing serially transplanted glioma xenografts in rats.
  • Known and novel candidate proteins were identified that characterize the switch from a non-angiogenic to a highly angiogenic phenotype.
  • The data point to enhanced intercellular cross-talk and metabolic activity adopted by tumor cells in the angiogenic compared with the non-angiogenic phenotype.
  • In conclusion, we describe molecular profiles that reflect the change from an invasive to an angiogenic brain tumor phenotype.

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  • (PMID = 19674965.001).
  • [ISSN] 1535-9484
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2773724
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77. McDonnell K, Bowden ET, Cabal-Manzano R, Hoxter B, Riegel AT, Wellstein A: Vascular leakage in chick embryos after expression of a secreted binding protein for fibroblast growth factors. Lab Invest; 2005 Jun;85(6):747-55
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  • Secreted FGF-binding proteins (FGF-BPs) can release immobilized FGFs, enhance the activity of locally stored FGFs and can thus serve as an angiogenic switch molecule in cancer.

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  • (PMID = 15806140.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA71508
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Fibroblast Growth Factor; 147336-22-9 / Green Fluorescent Proteins; 62031-54-3 / Fibroblast Growth Factors
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78. Sakao S, Tatsumi K, Voelkel NF: Reversible or irreversible remodeling in pulmonary arterial hypertension. Am J Respir Cell Mol Biol; 2010 Dec;43(6):629-34
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  • Here we ask the question: which forms of pulmonary vascular remodeling are reversible and can such remodeling caused by angiogenic proliferation of EC be reversed?
  • Whereas it is suggested that the proliferative state of SMC may be reversible, it remains unknown whether phenotypically altered EC can switch back to a normal monolayer-forming EC.

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  • (PMID = 20008280.001).
  • [ISSN] 1535-4989
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / 5P01 HL66254-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2993084
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79. Connor KM, Subbaram S, Regan KJ, Nelson KK, Mazurkiewicz JE, Bartholomew PJ, Aplin AE, Tai YT, Aguirre-Ghiso J, Flores SC, Melendez JA: Mitochondrial H2O2 regulates the angiogenic phenotype via PTEN oxidation. J Biol Chem; 2005 Apr 29;280(17):16916-24
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  • [Title] Mitochondrial H2O2 regulates the angiogenic phenotype via PTEN oxidation.
  • Our findings provide the first evidence for the involvement of mitochondrial H2O2 in regulating PTEN function and the angiogenic switch, indicating that Sod2 can serve as an alternative physiological source of the potent signaling molecule, H2O2.

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  • (PMID = 15701646.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI49822; United States / NCI NIH HHS / CA / CA095011; United States / NCI NIH HHS / CA / CA77068
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Fluoresceins; 0 / Phosphatidylinositol Phosphates; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / phosphatidylinositol 3,4,5-triphosphate; 63368-54-7 / 5-iodoacetamidofluorescein; BBX060AN9V / Hydrogen Peroxide; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.15.1.1 / superoxide dismutase 2; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; S88TT14065 / Oxygen
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80. Grinberg S, Hasko G, Wu D, Leibovich SJ: Suppression of PLCbeta2 by endotoxin plays a role in the adenosine A(2A) receptor-mediated switch of macrophages from an inflammatory to an angiogenic phenotype. Am J Pathol; 2009 Dec;175(6):2439-53
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  • [Title] Suppression of PLCbeta2 by endotoxin plays a role in the adenosine A(2A) receptor-mediated switch of macrophages from an inflammatory to an angiogenic phenotype.
  • Toll-like receptor (TLR) 2, 4, 7, and 9 agonists, together with adenosine A(2A) receptor (A(2A)R) agonists, switch macrophages from an inflammatory (M1) to an angiogenic (M2-like) phenotype.
  • This switch involves induction of A(2A)Rs by TLR agonists, down-regulation of tumor necrosis factor alpha (TNFalpha) and interleukin-12, and up-regulation of vascular endothelial growth factor (VEGF) and interleukin-10 expression.

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  • (PMID = 19850892.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL080706-15; United States / NHLBI NIH HHS / HL / R01 HL080706-10; United States / NHLBI NIH HHS / HL / R01 HL080706-12; United States / NHLBI NIH HHS / HL / R01 HL080706; United States / NHLBI NIH HHS / HL / HL080706-13; United States / NHLBI NIH HHS / HL / T32 HL069752; United States / NHLBI NIH HHS / HL / R01 HL080706-13; United States / NHLBI NIH HHS / HL / R01 HL080706-11; United States / NHLBI NIH HHS / HL / 5 T32 HL069752; United States / NIGMS NIH HHS / GM / R01 GM054597; United States / NIGMS NIH HHS / GM / R01GM06836; United States / NHLBI NIH HHS / HL / HL080706-14; United States / NHLBI NIH HHS / HL / R01 HL080706-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Lipopolysaccharides; 0 / Myd88 protein, mouse; 0 / Myeloid Differentiation Factor 88; 0 / RNA, Small Interfering; 0 / Receptor, Adenosine A2A; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; EC 3.1.4.11 / Phospholipase C beta; EC 3.1.4.11 / Plcb2 protein, mouse
  • [Other-IDs] NLM/ PMC2789640
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81. Aurora AB, Biyashev D, Mirochnik Y, Zaichuk TA, Sánchez-Martinez C, Renault MA, Losordo D, Volpert OV: NF-kappaB balances vascular regression and angiogenesis via chromatin remodeling and NFAT displacement. Blood; 2010 Jul 22;116(3):475-84
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  • Extracellular factors control the angiogenic switch in endothelial cells (ECs) via competing survival and apoptotic pathways.
  • Previously, we showed that proangiogenic and antiangiogenic factors target the same signaling molecules, which thereby become pivots of angiogenic balance.
  • Here we show that in remodeling endothelium (ECs and EC precursors) natural angiogenic inhibitors enhance nuclear factor-kappaB (NF-kappaB) DNA binding, which is critical for antiangiogenesis, and that blocking the NF-kappaB pathway abolishes multiple antiangiogenic events in vitro and in vivo.
  • Our study defines an interactive transcriptional network underlying angiogenic balance and points to HDACi as tools to manipulate the angiogenic switch.