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1. Lin EY, Li JF, Gnatovskiy L, Deng Y, Zhu L, Grzesik DA, Qian H, Xue XN, Pollard JW: Macrophages regulate the angiogenic switch in a mouse model of breast cancer. Cancer Res; 2006 Dec 1;66(23):11238-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Macrophages regulate the angiogenic switch in a mouse model of breast cancer.
  • We show that the onset of the angiogenic switch, identified as the formation of a high-density vessel network, is closely associated with the transition to malignancy.
  • More importantly, both the angiogenic switch and the progression to malignancy are regulated by infiltrated macrophages in the primary mammary tumors.
  • Inhibition of the macrophage infiltration into the tumor delayed the angiogenic switch and malignant transition whereas genetic restoration of the macrophage population specifically in these tumors rescued the vessel phenotype.
  • Furthermore, premature induction of macrophage infiltration into premalignant lesions promoted an early onset of the angiogenic switch independent of tumor progression.

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  • (PMID = 17114237.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 100324; United States / NCI NIH HHS / CA / CA 94173; United States / NCI NIH HHS / CA / P30 CA 13330
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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2. Wang J, Wang J, Dai J, Jung Y, Wei CL, Wang Y, Havens AM, Hogg PJ, Keller ET, Pienta KJ, Nor JE, Wang CY, Taichman RS: A glycolytic mechanism regulating an angiogenic switch in prostate cancer. Cancer Res; 2007 Jan 1;67(1):149-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A glycolytic mechanism regulating an angiogenic switch in prostate cancer.
  • The generation of an "angiogenic switch" is essential for tumor growth, yet its regulation is poorly understood.
  • At metastatic sites, however, high levels of CXCL12 signaling through CXCR4 reduced PGK1 expression, releasing the angiogenic response for metastastic growth.
  • These data suggest that PGK1 is a critical downstream target of the chemokine axis and an important regulator of an "angiogenic switch" that is essential for tumor and metastatic growth.

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  • (PMID = 17210694.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 93900; United States / NIDCR NIH HHS / DE / DE 13701
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Interleukin-8; 0 / Receptors, CXCR4; 0 / Vascular Endothelial Growth Factor A; 86090-08-6 / Angiostatins; EC 2.7.2.3 / Phosphoglycerate Kinase
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3. Hlushchuk R, Riesterer O, Baum O, Wood J, Gruber G, Pruschy M, Djonov V: Tumor recovery by angiogenic switch from sprouting to intussusceptive angiogenesis after treatment with PTK787/ZK222584 or ionizing radiation. Am J Pathol; 2008 Oct;173(4):1173-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor recovery by angiogenic switch from sprouting to intussusceptive angiogenesis after treatment with PTK787/ZK222584 or ionizing radiation.
  • Irradiation and anti-angiogenic therapy had similar effects on the tumor vasculature.
  • Quantification revealed that recovery was characterized by an angiogenic switch from sprouting to intussusception.
  • Both irradiation and anti-angiogenic therapy cause a switch from sprouting to intussusceptive angiogenesis, representing an escape mechanism and accounting for the development of resistance, as well as rapid recovery, after cessation of therapy.

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  • (PMID = 18787105.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, CD31; 0 / Antineoplastic Agents; 0 / Phthalazines; 0 / Pyridines; 5DX9U76296 / vatalanib
  • [Other-IDs] NLM/ PMC2543084
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4. Korsisaari N, Kasman IM, Forrest WF, Pal N, Bai W, Fuh G, Peale FV, Smits R, Ferrara N: Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc+/min mice. Proc Natl Acad Sci U S A; 2007 Jun 19;104(25):10625-30
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  • [Title] Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc+/min mice.
  • Therefore, VEGF-A inhibition may be a previously uncharacterized strategy for the prevention of the angiogenic switch and growth in intestinal adenomas.

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  • (PMID = 17553957.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC1888576
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5. Gao D, Nolan D, McDonnell K, Vahdat L, Benezra R, Altorki N, Mittal V: Bone marrow-derived endothelial progenitor cells contribute to the angiogenic switch in tumor growth and metastatic progression. Biochim Biophys Acta; 2009 Aug;1796(1):33-40
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  • [Title] Bone marrow-derived endothelial progenitor cells contribute to the angiogenic switch in tumor growth and metastatic progression.
  • EPCs regulate the angiogenic switch via paracrine secretion of proangiogenic growth factors and by direct luminal incorporation into sprouting nascent vessels.
  • In addition, EPCs are also being used as pharmacodynamic surrogate markers for monitoring cancer progression, as well as for optimizing efficacy of anti-angiogenic therapies in the clinic.

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  • (PMID = 19460418.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100933
  • [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 / ID1 protein, human; 0 / Inhibitor of Differentiation Protein 1
  • [Number-of-references] 84
  • [Other-IDs] NLM/ NIHMS119200; NLM/ PMC3649840
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6. Shchors K, Shchors E, Rostker F, Lawlor ER, Brown-Swigart L, Evan GI: The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1beta. Genes Dev; 2006 Sep 15;20(18):2527-38
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  • [Title] The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1beta.
  • We have used a reversibly switchable mouse transgenic model of Myc-dependent beta-cell carcinogenesis to delineate the kinetics and causal sequence of angiogenic processes following acute Myc activation.
  • Endothelial cell proliferation is not indirectly induced by local tissue hypoxia but instead via a diffusible angiogenic signal produced by Myc-expressing beta cells.

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  • (PMID = 16980582.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / F32 CA106039; United States / NCI NIH HHS / CA / R01 CA098018; United States / NCI NIH HHS / CA / F32-CA106039; United States / NCI NIH HHS / CA / R01 CA98018
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bcl2l1 protein, mouse; 0 / Interleukin-1; 0 / Myc protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Vascular Endothelial Growth Factor A; 0 / bcl-X Protein; 0 / vascular endothelial growth factor A, mouse
  • [Other-IDs] NLM/ PMC1578676
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7. Slevin M, Krupinski J, Badimon L: Controlling the angiogenic switch in developing atherosclerotic plaques: possible targets for therapeutic intervention. J Angiogenes Res; 2009;1:4
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  • [Title] Controlling the angiogenic switch in developing atherosclerotic plaques: possible targets for therapeutic intervention.
  • However in more advanced plaques, inflammatory cell infiltration, and concomitant production of numerous pro-angiogenic cytokines may be responsible for induction of uncontrolled neointimal microvessel proliferation resulting in production of immature and fragile neovessels similar to that seen in tumour development.
  • Despite this, there is conflicting evidence regarding the causal relationship between neovessel expression and plaque thrombosis with some in vivo experimental models suggesting the contrary and as yet, few direct mediators of angiogenesis have been identified and associated with plaque instability in vivo.In recent years, an increasing number of angiogenic therapeutic targets have been proposed in order to facilitate modulation of neovascularization and its consequences in diseases such as cancer and macular degeneration.
  • A complete knowledge of the mechanisms responsible for initiation of adventitial vessel proliferation, their extension into the intimal regions and possible de-novo synthesis of neovessels following differentiation of bone-marrow-derived stem cells is required in order to contemplate potential single or combinational anti-angiogenic therapies.
  • In this review, we will examine the importance of angiogenesis in complicated plaque development, describe the current knowledge of molecular mechanisms of its initiation and maintenance, and discuss possible future anti-angiogenic therapies to control plaque stability.

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  • (PMID = 19946412.001).
  • [ISSN] 2040-2384
  • [Journal-full-title] Journal of angiogenesis research
  • [ISO-abbreviation] J Angiogenes Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2776234
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8. 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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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. Persano L, Moserle L, Esposito G, Bronte V, Barbieri V, Iafrate M, Gardiman MP, Larghero P, Pfeffer U, Naschberger E, Stürzl M, Indraccolo S, Amadori A: Interferon-alpha counteracts the angiogenic switch and reduces tumor cell proliferation in a spontaneous model of prostatic cancer. Carcinogenesis; 2009 May;30(5):851-60
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  • [Title] Interferon-alpha counteracts the angiogenic switch and reduces tumor cell proliferation in a spontaneous model of prostatic cancer.
  • Overall, these findings demonstrate that IFN-alpha is able to counteract the angiogenic switch and impairs tumor cell proliferation in preinvasive lesions.
  • Since the angiogenic switch also marks progression of human prostatic cancer, these results highlight the potential of angiogenesis inhibitors for the development of chemoprevention strategies in high-risk individuals.

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  • (PMID = 19237608.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GBP1 protein, human; 0 / Interferon-alpha; 0 / Myxovirus Resistance Proteins; 0 / RNA, Messenger; EC 3.6.1.- / GTP-Binding Proteins
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12. Narazaki M, Tosato G: Tumor cell populations differ in angiogenic activity: a model system for spontaneous angiogenic switch can tell us why. J Natl Cancer Inst; 2006 Mar 1;98(5):294-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor cell populations differ in angiogenic activity: a model system for spontaneous angiogenic switch can tell us why.

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  • [CommentOn] J Natl Cancer Inst. 2006 Mar 1;98(5):316-25 [16507828.001]
  • (PMID = 16507821.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
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13. Baeriswyl V, Christofori G: The angiogenic switch in carcinogenesis. Semin Cancer Biol; 2009 Oct;19(5):329-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The angiogenic switch in carcinogenesis.
  • Coined in the late eighties, the term "angiogenic switch" refers to a time-restricted event during tumor progression where the balance between pro- and anti-angiogenic factors tilts towards a pro-angiogenic outcome, resulting in the transition from dormant avascularized hyperplasia to outgrowing vascularized tumor and eventually to malignant tumor progression.
  • The molecular players and mechanisms underlying the angiogenic switch have been intensely investigated.
  • In particular, a large number of pro-angiogenic factors and angiogenic inhibitors activated and repressed, respectively, in their activities during the angiogenic switch have been identified and characterized.
  • Part of this research has lead to the development of various pro- and anti-angiogenic therapies that are currently tested in clinical trials or are already in clinical use.
  • Furthermore, they also offer the opportunity to assess the efficacy of novel anti-angiogenic cancer therapies and the nature of developing resistance mechanisms.
  • These experiments have provided first important concepts to improve anti-angiogenic therapy and thus directly contribute to their translation to the clinical setting.
  • [MeSH-major] Angiogenic Proteins / metabolism. Neoplasms / blood supply. Neovascularization, Pathologic / metabolism

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  • (PMID = 19482086.001).
  • [ISSN] 1096-3650
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiogenic Proteins
  • [Number-of-references] 112
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14. Chen W, Li F, Mead L, White H, Walker J, Ingram DA, Roman A: Human papillomavirus causes an angiogenic switch in keratinocytes which is sufficient to alter endothelial cell behavior. Virology; 2007 Oct 10;367(1):168-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human papillomavirus causes an angiogenic switch in keratinocytes which is sufficient to alter endothelial cell behavior.
  • We have previously reported that expression of human papillomavirus type 16 E6 and E7 (HPV16 E6E7) proteins in primary foreskin keratinocytes (HFKs) decreases expression of two inhibitors and increases expression of two angiogenic inducers [Toussaint-Smith, E., Donner, D.B., Roman, A., 2004.
  • Expression of human papillomavirus type 16 E6 and E7 oncoproteins in primary foreskin keratinocytes is sufficient to alter the expression of angiogenic factors.
  • In addition, introduction of the conditioned media into immunocompetent mice using a Matrigel plug model resulted in a clear angiogenic response.
  • These novel data support the hypothesis that HPV proteins contribute not only to the uncontrolled keratinocyte growth seen following HPV infection but also to the angiogenic response needed for tumor formation.

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  • (PMID = 17602722.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / PHS HHS / / NF043019; United States / NCI NIH HHS / CA / T32 CA111198; United States / NCI NIH HHS / CA / CA111198-02S1; United States / NCI NIH HHS / CA / T32 CA11 1198-02S1; United States / NCI NIH HHS / CA / P30 CA082709; United States / NINDS NIH HHS / NS / P50 NS0 52606; United States / NCI NIH HHS / CA / K08 CA096579-01; United States / NCI NIH HHS / CA / P30 CA82709; United States / NCI NIH HHS / CA / T32 CA111198-02S1; United States / NCI NIH HHS / CA / K08 CA096579; United States / NIAID NIH HHS / AI / U19 AI031494; United States / NIAID NIH HHS / AI / U19 AI031494-130005; United States / NIAID NIH HHS / AI / AI031494-130005; United States / NINDS NIH HHS / NS / P50 NS052606; United States / NIAID NIH HHS / AI / R01AI31494
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / E6 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Papillomavirus E7 Proteins; 0 / Repressor Proteins; 0 / oncogene protein E7, Human papillomavirus type 16
  • [Other-IDs] NLM/ NIHMS31797; NLM/ PMC2043482
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15. Felsher DW: Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switch. Lymphat Res Biol; 2008;6(3-4):149-54
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  • [Title] Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switch.

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  • (PMID = 19093787.001).
  • [ISSN] 1539-6851
  • [Journal-full-title] Lymphatic research and biology
  • [ISO-abbreviation] Lymphat Res Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 26
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16. 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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17. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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18. Ulanet DB, Hanahan D: Loss of p19(Arf) facilitates the angiogenic switch and tumor initiation in a multi-stage cancer model via p53-dependent and independent mechanisms. PLoS One; 2010 Aug 27;5(8):e12454
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of p19(Arf) facilitates the angiogenic switch and tumor initiation in a multi-stage cancer model via p53-dependent and independent mechanisms.
  • In a transgenic mouse model of multi-stage pancreatic neuroendocrine carcinogenesis (PNET) driven by inhibition of the canonical p53 and Rb tumor suppressors with SV40 large T-antigen (Tag), stochastic progression to tumors is limited in part by a requirement for initiation of an angiogenic switch.
  • Despite inhibition of p53 by Tag in this mouse PNET model, concomitant disruption of Arf via genetic knockout resulted in a significantly accelerated pathway to tumor formation that was surprisingly not driven by alterations in tumor cell proliferation or apoptosis, but rather via earlier activation of the angiogenic switch.

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  • (PMID = 20805995.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA045234; United States / NCI NIH HHS / CA / R01CA45234
  • [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 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2929208
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19. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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20. Bellmunt J, Trigo J, Calvo E, Carles J, Perez-Gracia J, Rubió J, Virizuela J, López R, Lázaro M, Albanell J: Activity of a multitargeted, metronomic, and maximum-tolerated dose "chemo-switch" regimen in metastatic renal cell carcinoma (mRCC): A phase II study of sorafenib, gemcitabine (Gem), and metronomic capecitabine (Cap) in patients with advanced mRCC (SOGUG-02-06). J Clin Oncol; 2009 May 20;27(15_suppl):5040

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of a multitargeted, metronomic, and maximum-tolerated dose "chemo-switch" regimen in metastatic renal cell carcinoma (mRCC): A phase II study of sorafenib, gemcitabine (Gem), and metronomic capecitabine (Cap) in patients with advanced mRCC (SOGUG-02-06).
  • : 5040 Background: Maximal tolerated dose (MTD) chemotherapy followed by metronomic chemotherapy (low doses administered on a frequent schedule) acts on tumor vascular endothelial cells and enhances the antitumor effect of anti-angiogenic agents (Pietras et al.
  • These findings confirm the synergistic activity of the "chemo-switch" concept seen in preclinical models.

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  • (PMID = 27962942.001).
  • [ISSN] 1527-7755
  • [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
  • [Publication-country] United States
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21. Ding W, Knox TR, Tschumper RC, Wu W, Schwager SM, Boysen JC, Jelinek DF, Kay NE: Platelet-derived growth factor (PDGF)-PDGF receptor interaction activates bone marrow-derived mesenchymal stromal cells derived from chronic lymphocytic leukemia: implications for an angiogenic switch. Blood; 2010 Oct 21;116(16):2984-93
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  • [Title] Platelet-derived growth factor (PDGF)-PDGF receptor interaction activates bone marrow-derived mesenchymal stromal cells derived from chronic lymphocytic leukemia: implications for an angiogenic switch.
  • These results show that PDGF-PDGFR signaling influences at least the MSC in the microenvironment of CLL and may play a role in the induction of an angiogenic switch known to be permissive for disease progression.

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  • (PMID = 20606160.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116237; United States / NCI NIH HHS / CA / R01 CA136591; United States / NCI NIH HHS / CA / CA116237; United States / NCI NIH HHS / CA / CA136591
  • [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 / Culture Media, Conditioned; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2974606
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22. Takahashi Y, Mai M: Antibody against vascular endothelial growth factor (VEGF) inhibits angiogenic switch and liver metastasis in orthotopic xenograft model with site-dependent expression of VEGF. J Exp Clin Cancer Res; 2005 Jun;24(2):237-43
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  • [Title] Antibody against vascular endothelial growth factor (VEGF) inhibits angiogenic switch and liver metastasis in orthotopic xenograft model with site-dependent expression of VEGF.
  • We previously reported that upregulation of angiogenesis, i.e. angiogenic switch (AS), may occur simultaneously to initiation of invasion in the early development of human colon cancer.

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  • (PMID = 16110757.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies; 0 / Oligonucleotides; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
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23. Yano K, Kadoya K, Kajiya K, Hong YK, Detmar M: Ultraviolet B irradiation of human skin induces an angiogenic switch that is mediated by upregulation of vascular endothelial growth factor and by downregulation of thrombospondin-1. Br J Dermatol; 2005 Jan;152(1):115-21
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  • [Title] Ultraviolet B irradiation of human skin induces an angiogenic switch that is mediated by upregulation of vascular endothelial growth factor and by downregulation of thrombospondin-1.
  • CONCLUSIONS: Together, these data indicate that a disruption of the balance between VEGF and TSP-1 expression leads to a UVB-induced angiogenic switch, facilitating the infiltration of elastase-producing leucocytes and cutaneous photodamage.

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  • (PMID = 15656811.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Thrombospondin 1; 0 / Vascular Endothelial Growth Factor A; EC 3.4.21.36 / Pancreatic Elastase
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24. Bellone G, Gramigni C, Vizio B, Mauri FA, Prati A, Solerio D, Dughera L, Ruffini E, Gasparri G, Camandona M: Abnormal expression of Endoglin and its receptor complex (TGF-β1 and TGF-β receptor II) as early angiogenic switch indicator in premalignant lesions of the colon mucosa. Int J Oncol; 2010 Nov;37(5):1153-65

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  • [Title] Abnormal expression of Endoglin and its receptor complex (TGF-β1 and TGF-β receptor II) as early angiogenic switch indicator in premalignant lesions of the colon mucosa.
  • The precise timing of the angiogenic switch in colorectal cancer development is still unclear.

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  • (PMID = 20878063.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / ENG protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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25. Ito TK, Ishii G, Chiba H, Ochiai A: The VEGF angiogenic switch of fibroblasts is regulated by MMP-7 from cancer cells. Oncogene; 2007 Nov 8;26(51):7194-203
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  • [Title] The VEGF angiogenic switch of fibroblasts is regulated by MMP-7 from cancer cells.
  • Here we report that the latent VEGF angiogenic activity of fibroblasts is activated by cancer cells, resulting in tumor-selective utilization of fibroblast-derived VEGF.
  • Suppression of MMP-7 in Capan-1 cells abrogates the tumor angiogenic activity of VA-13 fibroblasts, which is restored by suppression of CTGF in VA-13 fibroblasts.

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  • (PMID = 17525740.001).
  • [ISSN] 0950-9232
  • [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 / CTGF protein, human; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Vascular Endothelial Growth Factor A; 139568-91-5 / Connective Tissue Growth Factor; EC 3.4.24.23 / MMP7 protein, human; EC 3.4.24.23 / Matrix Metalloproteinase 7
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26. Okamoto R, Ueno M, Yamada Y, Takahashi N, Sano H, Suda T, Takakura N: Hematopoietic cells regulate the angiogenic switch during tumorigenesis. Blood; 2005 Apr 1;105(7):2757-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic cells regulate the angiogenic switch during tumorigenesis.
  • Our findings suggest that HCs are involved in tumor angiogenesis and regulate the angiogenic switch during tumorigenesis.

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  • (PMID = 15572584.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, TIE-2
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27. 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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28. Szarvas T, Jäger T, Tötsch M, vom Dorp F, Kempkensteffen C, Kovalszky I, Romics I, Ergün S, Rübben H: Angiogenic switch of angiopietins-Tie2 system and its prognostic value in bladder cancer. Clin Cancer Res; 2008 Dec 15;14(24):8253-62
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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  • [Title] Angiogenic switch of angiopietins-Tie2 system and its prognostic value in bladder cancer.

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  • (PMID = 19088043.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANGPT1 protein, human; 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, TIE-2
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29. Abdollahi A, Schwager C, Kleeff J, Esposito I, Domhan S, Peschke P, Hauser K, Hahnfeldt P, Hlatky L, Debus J, Peters JM, Friess H, Folkman J, Huber PE: Transcriptional network governing the angiogenic switch in human pancreatic cancer. Proc Natl Acad Sci U S A; 2007 Jul 31;104(31):12890-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional network governing the angiogenic switch in human pancreatic cancer.
  • A shift of the angiogenic balance to the proangiogenic state, termed the "angiogenic switch," is a hallmark of cancer progression.
  • Here we devise a strategy for identifying genetic participants of the angiogenic switch based on inverse regulation of genes in human endothelial cells in response to key endogenous pro- and antiangiogenic proteins.
  • We also demonstrate that the angiogenic switch is governed by simultaneous regulations of multiple genes organized as transcriptional circuitries.
  • In pancreatic cancer patients, we validate the transcriptome-derived switch of the identified "angiogenic network:" The angiogenic state in chronic pancreatitis specimens is intermediate between the normal (angiogenesis off) and neoplastic (angiogenesis on) condition, suggesting that aberrant proangiogenic environment contributes to the increased cancer risk in patients with chronic pancreatitis.
  • In knockout experiments in mice, we show that the targeted removal of a hub node (peroxisome proliferative-activated receptor delta) of the angiogenic network markedly impairs angiogenesis and tumor growth.
  • Our results therefore also may contribute to the rational design of antiangiogenic cancer agents; whereas "narrow" targeted cancer drugs may fail to shift the robust angiogenic regulatory network toward antiangiogenesis, the network may be more vulnerable to multiple or broad-spectrum inhibitors or to the targeted removal of the identified angiogenic "hub" nodes.


30. Lin EY, Pollard JW: Tumor-associated macrophages press the angiogenic switch in breast cancer. Cancer Res; 2007 Jun 1;67(11):5064-6
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] Tumor-associated macrophages press the angiogenic switch in breast cancer.
  • In a mouse model of breast cancer, we found that tumor-associated macrophages that are recruited to the tumor just before malignant conversion are essential for the angiogenic switch.

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  • (PMID = 17545580.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100324; United States / NCI NIH HHS / CA / CA94173; United States / NCI NIH HHS / CA / P30 CA13330
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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31. Soares AB, Juliano PB, Araujo VC, Metze K, Altemani A: Angiogenic switch during tumor progression of carcinoma ex-pleomorphic adenoma. Virchows Arch; 2007 Jul;451(1):65-71
COS Scholar Universe. author profiles.

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  • [Title] Angiogenic switch during tumor progression of carcinoma ex-pleomorphic adenoma.
  • We analyzed the tumor vascularization in carcinomas ex-pleomorphic adenoma (CXPA) to investigate the angiogenic switch during the malignant transformation of pleomorphic adenoma (PA) to carcinoma and during tumor progression.
  • In conclusion, the antibody CD105 reveals an angiogenic switch during the progression from adenoma to carcinoma in salivary glands.

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  • (PMID = 17593387.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / ENG protein, human; 0 / Receptors, Cell Surface
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32. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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33. Naumov GN, Akslen LA, Folkman J: Role of angiogenesis in human tumor dormancy: animal models of the angiogenic switch. Cell Cycle; 2006 Aug;5(16):1779-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of angiogenesis in human tumor dormancy: animal models of the angiogenic switch.
  • Tumor progression depends on sequential events, including a switch to the angiogenic phenotype (i.e., initial recruitment of blood vessels).
  • Because it is well established that tumor growth beyond the size of 1-2 mm is angiogenesis-dependent, we hypothesized that presentation of large tumors is attributed to a switch to the angiogenic phenotype in otherwise microscopic, dormant tumors.
  • The development of animal models which recapitulate the clinically observed timing and proportion of dormant tumors which switch to the angiogenic phenotype are reviewed here.
  • The contributing molecular mechanisms involved in the angiogenic switch and different strategies for isolation of both angiogenic and non-angiogenic tumor cell populations from otherwise heterogeneous human tumor cell lines or surgical specimens are also summarized.
  • The animal models employed here permitted further studies of the angiogenic switch.
  • These models also allowed development of an angiogenesis-based panel of blood and urine biomarkers that can be quantified and used to detect microscopic tumors before or during the angiogenic switch.
  • [MeSH-major] Angiogenic Proteins / metabolism. Biomarkers, Tumor / metabolism. Cell Proliferation. Neoplasms / blood supply. Neoplastic Stem Cells / metabolism. Neovascularization, Pathologic / metabolism. Thrombospondin 1 / metabolism

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  • (PMID = 16931911.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Luminescent Agents; 0 / Thrombospondin 1; EC 1.13.12.- / Luciferases
  • [Number-of-references] 49
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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. Ribatti D, Nico B, Crivellato E, Roccaro AM, Vacca A: The history of the angiogenic switch concept. Leukemia; 2007 Jan;21(1):44-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The history of the angiogenic switch concept.
  • Spontaneously arising tumor cells are not usually angiogenic at first.
  • The phenotypic switch to angiogenesis is usually accomplished by a substet that induces new capillaries that then converge toward the tumor.
  • The switch clearly involves more than simple upregulation of angiogenic activity and is thought to be the result of a net balance of positive and negative regulators.
  • Tumor growth is although to require disruption of this balance and hence this switch must turned on for cancer progression.
  • Progenitor endothelial cells, the crosstalk between angiogenic factors and their receptors and the interaction between vasculogenesis and lymphangiogenesis are all factors that may contribute to the switch.
  • This review describes the history of the angiogenic switch illustrated in the literature and with particular reference to the three transgenic mouse models, namely RIP1-TAG2, keratin-14 (K14) (human papilloma virus) HPV16 and papilloma virus, used for stage-specific assessment of the effects of antiangiogenic and antitumorigenic agents.

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  • (PMID = 16990761.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Keratin-14; 0 / Vascular Endothelial Growth Factors
  • [Number-of-references] 106
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36. Asosingh K, Swaidani S, Aronica M, Erzurum SC: Th1- and Th2-dependent endothelial progenitor cell recruitment and angiogenic switch in asthma. J Immunol; 2007 May 15;178(10):6482-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Th1- and Th2-dependent endothelial progenitor cell recruitment and angiogenic switch in asthma.
  • EPC recruitment was Th1 and Th2 dependent and was temporally associated with an increased microvessel density that was noted within 48 h of allergen challenge, indicating an early switch to an angiogenic lung environment.
  • Thus, a Th1- and Th2-dependent angiogenic switch with EPC mobilization, recruitment, and increased lung vessel formation occurs early but becomes a sustained and cumulative component of the allergen-induced asthmatic response.

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  • (PMID = 17475878.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI067816; United States / NIAID NIH HHS / AI / AI70649; United States / NHLBI NIH HHS / HL / HL04449; United States / NHLBI NIH HHS / HL / HL081064; United States / NHLBI NIH HHS / HL / HL60917; United States / NHLBI NIH HHS / HL / HL69170; United States / NCRR NIH HHS / RR / M01 RR018390
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides
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37. Mitra SK, Mikolon D, Molina JE, Hsia DA, Hanson DA, Chi A, Lim ST, Bernard-Trifilo JA, Ilic D, Stupack DG, Cheresh DA, Schlaepfer DD: Intrinsic FAK activity and Y925 phosphorylation facilitate an angiogenic switch in tumors. Oncogene; 2006 Sep 28;25(44):5969-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intrinsic FAK activity and Y925 phosphorylation facilitate an angiogenic switch in tumors.
  • These studies provide the first biological support for Y925 FAK phosphorylation and define a novel role for FAK activity in promoting a MAPK-associated angiogenic switch during tumor progression.

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  • (PMID = 16682956.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA087652; United States / NCI NIH HHS / CA / CA102310; United States / NCI NIH HHS / CA / CA107263; United States / NCI NIH HHS / CA / CA45726; United States / NCI NIH HHS / CA / CA50286; United States / NCI NIH HHS / CA / CA78045; United States / NCI NIH HHS / CA / CA95262; United States / NEI NIH HHS / EY / EY14174; United States / NIAID NIH HHS / AI / T32 AI07606
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 42HK56048U / Tyrosine; EC 2.7.1.- / FAK-related nonkinase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
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38. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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39. 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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40. Tassi E, Wellstein A: Tumor angiogenesis: initiation and targeting - therapeutic targeting of an FGF-binding protein, an angiogenic switch molecule, and indicator of early stages of gastrointestinal adenocarcinomas -. Cancer Res Treat; 2006 Dec;38(4):189-97

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor angiogenesis: initiation and targeting - therapeutic targeting of an FGF-binding protein, an angiogenic switch molecule, and indicator of early stages of gastrointestinal adenocarcinomas -.
  • In particular, the activity of angiogenic factors is crucial for tumor progression.

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  • (PMID = 19771241.001).
  • [ISSN] 1598-2998
  • [Journal-full-title] Cancer research and treatment : official journal of Korean Cancer Association
  • [ISO-abbreviation] Cancer Res Treat
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL068686; United States / NCI NIH HHS / CA / R01 CA071508
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2741650
  • [Keywords] NOTNLM ; Antiangiogenic agents / Colonic neoplasms / FGF-binding protein / Pancreatic neoplasms / Tumor angiogenesis
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41. Kupatt C, Hinkel R, von Brühl ML, Pohl T, Horstkotte J, Raake P, El Aouni C, Thein E, Dimmeler S, Feron O, Boekstegers P: Endothelial nitric oxide synthase overexpression provides a functionally relevant angiogenic switch in hibernating pig myocardium. J Am Coll Cardiol; 2007 Apr 10;49(14):1575-84
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  • [Title] Endothelial nitric oxide synthase overexpression provides a functionally relevant angiogenic switch in hibernating pig myocardium.

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  • (PMID = 17418299.001).
  • [ISSN] 1558-3597
  • [Journal-full-title] Journal of the American College of Cardiology
  • [ISO-abbreviation] J. Am. Coll. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.13.39 / Nitric Oxide Synthase Type III
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42. Ceteci F, Ceteci S, Karreman C, Kramer BW, Asan E, Götz R, Rapp UR: Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer. Cancer Cell; 2007 Aug;12(2):145-59
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer.


43. Aubry K, Barriere G, Chable-Rabinovitch H, Dutour A, Paraf F, Monteil J, Rigaud M: Molecular mechanisms regulating the angiogenic phenotype in tumors: clinical impact in the future. Anticancer Res; 2007 Sep-Oct;27(5A):3111-9
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  • [Title] Molecular mechanisms regulating the angiogenic phenotype in tumors: clinical impact in the future.
  • Tumor progression depends on the angiogenic switch.
  • In this review, we recapitulate the molecular mechanisms involved in this angiogenic switch.

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  • (PMID = 17970051.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Number-of-references] 68
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44. Indraccolo S, Favaro E, Amadori A: Dormant tumors awaken by a short-term angiogenic burst: the spike hypothesis. Cell Cycle; 2006 Aug;5(16):1751-5

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  • [Title] Dormant tumors awaken by a short-term angiogenic burst: the spike hypothesis.
  • Tumor dormancy, a complex and still poorly understood phenomenon observed both in experimental models and in patients, has been associated with insufficient angiogenic capacity.
  • A defined event, termed "angiogenic switch" and characterized by an imbalance between pro- and anti-angiogenic factors, often marks interruption of the dormant state, thus triggering invasive tumor growth.
  • Recently, we demonstrated that co-administration of proliferation-arrested Kaposi's sarcoma cells or recombinant angiogenic factors interrupts dormancy of poorly angiogenic leukemia cells by providing a brief angiogenic burst.
  • These findings indicate that even a transient angiogenic switch can prime progressive tumor growth and suggest that tumor angiogenesis is a process requiring a higher amount of angiogenic factors for its induction than maintenance.
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Angiogenesis Inhibitors / therapeutic use. Angiogenic Proteins / metabolism. Animals. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Apoptosis. Bevacizumab. Cell Communication. Cell Proliferation. Cell Survival. Endothelial Cells / metabolism. Endothelial Cells / pathology. Humans

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  • (PMID = 16861908.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiogenic Proteins; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
  • [Number-of-references] 59
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45. Naumov GN, Folkman J, Straume O: Tumor dormancy due to failure of angiogenesis: role of the microenvironment. Clin Exp Metastasis; 2009;26(1):51-60
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  • Tumor progression is dependent on a number of sequential steps, including initial recruitment of blood vessels (i.e., angiogenic switch).
  • We also review current experimental human tumor dormancy models with special emphasis on the angiogenic switch which closely recapitulates clinically observed delay in tumor recurrence.

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  • (PMID = 18563595.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [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.
  • [Publication-country] Netherlands
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46. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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47. Lin EY, Li JF, Bricard G, Wang W, Deng Y, Sellers R, Porcelli SA, Pollard JW: Vascular endothelial growth factor restores delayed tumor progression in tumors depleted of macrophages. Mol Oncol; 2007 Dec;1(3):288-302
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • Genetic depletion of macrophages in Polyoma Middle T oncoprotein (PyMT)-induced mammary tumors in mice delayed the angiogenic switch and the progression to malignancy.
  • To determine whether vascular endothelial growth factor A (VEGF-A) produced by tumor-associated macrophages regulated the onset of the angiogenic switch, a genetic approach was used to restore expression of VEGF-A into tumors at the benign stages.

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  • (PMID = 18509509.001).
  • [ISSN] 1878-0261
  • [Journal-full-title] Molecular oncology
  • [ISO-abbreviation] Mol Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100324; United States / NCI NIH HHS / CA / P30 CA 13330; United States / NCI NIH HHS / CA / P01 CA100324-010001; United States / NCI NIH HHS / CA / R01 CA094173-05; United States / NCI NIH HHS / CA / R01 CA094173; United States / NCI NIH HHS / CA / P01 CA100324-019003; United States / NCI NIH HHS / CA / CA RO1 94173; United States / NCI NIH HHS / CA / CA PO1 100324; United States / NCI NIH HHS / CA / P30 CA013330
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 147336-22-9 / Green Fluorescent Proteins
  • [Keywords] NOTNLM ; PyMT / VEGF / angiogenesis / macrophages / malignancy / mammary / mouse / progression / transgenic / tumor
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48. Anand S, Majeti BK, Acevedo LM, Murphy EA, Mukthavaram R, Scheppke L, Huang M, Shields DJ, Lindquist JN, Lapinski PE, King PD, Weis SM, Cheresh DA: MicroRNA-132-mediated loss of p120RasGAP activates the endothelium to facilitate pathological angiogenesis. Nat Med; 2010 Aug;16(8):909-14
The Lens. Cited by Patents in .

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  • Although it is well established that tumors initiate an angiogenic switch, the molecular basis of this process remains incompletely understood.
  • Here we show that the miRNA miR-132 acts as an angiogenic switch by targeting p120RasGAP in the endothelium and thereby inducing neovascularization.
  • We conclude that miR-132 acts as an angiogenic switch by suppressing endothelial p120RasGAP expression, leading to Ras activation and the induction of neovascularization, whereas the application of anti-miR-132 inhibits neovascularization by maintaining vessels in the resting state.

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  • (PMID = 20676106.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL096498; United States / NCI NIH HHS / CA / R37 CA050286; United States / NCI NIH HHS / CA / P01 CA104898-05; United States / NCI NIH HHS / CA / R37 CA050286-23; United States / NCI NIH HHS / CA / P01 CA104898; United States / NHLBI NIH HHS / HL / R01 HL078912; United States / NCI NIH HHS / CA / R01 CA050286; United States / NCI NIH HHS / CA / CA104898; United States / NHLBI NIH HHS / HL / HL096498; United States / NCI NIH HHS / CA / CA104898-05; United States / NHLBI NIH HHS / HL / R01 HL078912-05; United States / NHLBI NIH HHS / HL / HL078912-05; United States / NCI NIH HHS / CA / CA050286; United States / NHLBI NIH HHS / HL / HL078912; United States / NCI NIH HHS / CA / CA050286-23
  • [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 / Antibodies, Monoclonal; 0 / MIRN132 microRNA, human; 0 / MicroRNAs; 0 / RNA, Small Interfering; 0 / p120 GTPase Activating Protein
  • [Other-IDs] NLM/ NIHMS292907; NLM/ PMC3094020
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49. Zhong H, Bowen JP: Antiangiogenesis drug design: multiple pathways targeting tumor vasculature. Curr Med Chem; 2006;13(8):849-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The blood vessel growth in normal tissues is regulated though a delicate and complex balance between the collective action of proangiogenic factors (e.g., vascular endothelial growth factor, VEGF) and the collective action of angiogenic inhibitors (e.g., thrombospondin-1).
  • In pathological angiogenesis, the angiogenic switch is shifted toward the proangiogenic factors, and if the imbalance continues, irregular tumor vessel growth is the result.
  • Despite intense research, the mechanism of the angiogenic switch is not fully understood.
  • Many factors, however, have been shown to be involved in regulating the equilibrium between angiogenic stimulants and inhibitors.
  • VEGFR tyrosine kinase, methionine aminopeptidase-2 (MetAP-2), p53, tubulin, cyclooxygenase-2 (COX-2), and matrix metalloproteinases (MMPs) all directly and/or indirectly influence the angiogenic switch.

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  • (PMID = 16611071.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclooxygenase 2 Inhibitors; 0 / Tubulin; 0 / Vascular Endothelial Growth Factor A; EC 3.4.11.- / Aminopeptidases; EC 3.4.11.18 / Methionyl Aminopeptidases
  • [Number-of-references] 101
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50. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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51. Ribatti D: Endogenous inhibitors of angiogenesis: a historical review. Leuk Res; 2009 May;33(5):638-44
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  • 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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52. 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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53. Rahimi N: A role for protein ubiquitination in VEGFR-2 signalling and angiogenesis. Biochem Soc Trans; 2009 Dec;37(Pt 6):1189-92
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  • Regulation of angiogenesis is often viewed as a balance between pro-angiogenic and anti-angiogenic factors, and when the balance shifts in favour of angiogenesis stimulators, an angiogenic switch turns on the normally inactive endothelial cells to grow new blood vessels.
  • Notably, this observation suggests that c-Cbl-mediated ubiquitination pathway plays a central role in the 'angiogenic switch' employed by the VEGF system.

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  • (PMID = 19909244.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY017955
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Ubiquitin; 0 / Vascular Endothelial Growth Factors; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.1.4.3 / Phospholipase C gamma; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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54. 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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55. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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56. Nyberg P, Xie L, Kalluri R: Endogenous inhibitors of angiogenesis. Cancer Res; 2005 May 15;65(10):3967-79
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  • It is speculated that tumor growth requires disruption of such balance; thus, the angiogenic switch must be turned "on" for cancer progression.
  • If the angiogenic switch needs to be turned on to facilitate the tumor growth, the question remains as to what the physiologic status of this switch is in the adult human body; is it "off," with inhibitors outweighing the stimulators, or maintained at a fine "balance," keeping the proangiogenic properties of many factors at a delicate "activity" balance with endogenous inhibitors of angiogenesis.
  • The physiologic status of this balance is important to understand as it might determine an individual's predisposition to turn the switch on during pathologic events dependent on angiogenesis.
  • Conceivably, if the physiologic angiogenesis balance in human population exists somewhere between off and even balance, an individual's capacity and rate to turn the switch on might reflect their normal physiologic angiogenic status.

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  • (PMID = 15899784.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 55001; United States / NIDDK NIH HHS / DK / DK 62987
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 209
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57. Sogno I, Venè R, Sapienza C, Ferrari N, Tosetti F, Albini A: Anti-angiogenic properties of chemopreventive drugs: fenretinide as a prototype. Recent Results Cancer Res; 2009;181:71-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-angiogenic properties of chemopreventive drugs: fenretinide as a prototype.
  • We found that angiogenesis is a common and key target of many chemopreventive molecules, where they most likely suppress the angiogenic switch in premalignant tumors, a concept we termed "angioprevention."

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  • (PMID = 19213559.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 187EJ7QEXL / Fenretinide
  • [Number-of-references] 40
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58. 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.

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  • (PMID = 20203265.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL068033-07; United States / NHLBI NIH HHS / HL / R01 HL068033-08; United States / NHLBI NIH HHS / HL / HL077471-03; United States / NHLBI NIH HHS / HL / HL077471-04; United States / NHLBI NIH HHS / HL / R01 HL068033; United States / NHLBI NIH HHS / HL / R01 HL057516; United States / NIDDK NIH HHS / DK / T32 DK62716; United States / NHLBI NIH HHS / HL / HL068033-08; United States / NHLBI NIH HHS / HL / R01 HL077471-03; United States / NIDDK NIH HHS / DK / T32 DK062716; United States / NHLBI NIH HHS / HL / R01 HL077471; United States / NHLBI NIH HHS / HL / R01 HL068033-06; United States / NHLBI NIH HHS / HL / R01 HL077471-04; United States / NHLBI NIH HHS / HL / HL068033-06; United States / NHLBI NIH HHS / HL / R01 HL68033; United States / NHLBI NIH HHS / HL / R01 HL068033-07; United States / NHLBI NIH HHS / HL / R01HL077471
  • [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 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Cflar protein, mouse; 0 / Eye Proteins; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / NF-kappa B; 0 / NFATC Transcription Factors; 0 / Nerve Growth Factors; 0 / Nfatc2 protein, mouse; 0 / Serpins; 0 / Thrombospondin 1; 0 / pigment epithelium-derived factor; EC 3.5.1.98 / Hdac1 protein, mouse; EC 3.5.1.98 / Histone Deacetylase 1
  • [Other-IDs] NLM/ PMC2913457
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59. Mangieri D, Nico B, Benagiano V, De Giorgis M, Vacca A, Ribatti D: Angiogenic activity of multiple myeloma endothelial cells in vivo in the chick embryo chorioallantoic membrane assay is associated to a down-regulation in the expression of endogenous endostatin. J Cell Mol Med; 2008 Jun;12(3):1023-8
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  • [Title] Angiogenic activity of multiple myeloma endothelial cells in vivo in the chick embryo chorioallantoic membrane assay is associated to a down-regulation in the expression of endogenous endostatin.
  • We have attempted a fine characterization of the angiogenic response induced by multiple myeloma endothelial cells (MMEC) by using the chick embryo chorioallantoic membrane (CAM) assay and by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • Results showed that in the CAM assay MMEC induced an angiogenic response comparable to that of a well-known angiogenic cytokine, namely fibroblast growth factor-2 (FGF-2), while RT-PCR demonstrated that the expression of endostatin mRNA detected in MM treated CAM was significantly lower respect to control CAM.
  • These data suggest that angiogenic switch in MM may involve loss of an endogenous angiogenesis inhibitor, such as endostatin.

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  • (PMID = 18494942.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Endostatins; 0 / RNA, Messenger; 103107-01-3 / Fibroblast Growth Factor 2
  • [Other-IDs] NLM/ PMC4401142
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60. Zacharoulis S, Chi S, Kadota R, Kieran M: Biological modification strategies following marrow ablative, high-dose chemotherapy (HDCT) with autologous hematopoietic stem cell rescue (AHSCR) for pediatric brain tumors. Pediatr Blood Cancer; 2010 Apr;54(4):654-6
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  • Failure of the HDCT/AHSCR might be due to tumor-immunity dysregulation, reactivation of the angiogenic switch and other mechanisms.
  • The angiogenic factors engaged in this process in childhood brain tumors following HDCT/AHSCR have not been tested in the clinic.

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  • (PMID = 20146216.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 16
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61. Bikfalvi A: [Tumor angiogenesis]. Bull Cancer; 2007;94(7 Suppl):F193-8

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  • Following the work of Folkman, it appears that angiogenesis, which consists in the formation of new blood vessels able to deliver oxygen and nutriments to tumor cells, is a major step in the evolution of tumors, which can only grow after the onset of the angiogenic switch.
  • Numerous factors play a role in angiogenesis stimulation or inhibition : the vascular endothelial growth factor and fibroblastic growth factors as well as angiopoietin are proangiogenic, whereas angiostatin and platelet factor 4 are anti-angiogenic.

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  • (PMID = 17964996.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiopoietins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 62031-54-3 / Fibroblast Growth Factors
  • [Number-of-references] 50
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62. Bhuvaneswari R, Gan YY, Soo KC, Olivo M: The effect of photodynamic therapy on tumor angiogenesis. Cell Mol Life Sci; 2009 Jul;66(14):2275-83
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  • Though therapeutic responses are encouraging, PDT-mediated oxidative stress can act as an angiogenic switch that ultimately leads to neovascularization and tumor recurrence.

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  • [CommentIn] Cell Mol Life Sci. 2010 May;67(9):1559-60; author reply 1561 [20155480.001]
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  • (PMID = 19333552.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 70
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63. 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 / / TI/ 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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64. Yoder MC, Ingram DA: The definition of EPCs and other bone marrow cells contributing to neoangiogenesis and tumor growth: is there common ground for understanding the roles of numerous marrow-derived cells in the neoangiogenic process? Biochim Biophys Acta; 2009 Aug;1796(1):50-4
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  • We will briefly review some recently published high profile papers that appear to derive polar interpretations for the role of EPCs in the angiogenic switch and discuss possible reasons for the disparate views in work conducted in both mouse and man.

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  • (PMID = 19393290.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL085036-03; United States / NHLBI NIH HHS / HL / P50 HL085036; United States / NHLBI NIH HHS / HL / P50 HL085036-03
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 58
  • [Other-IDs] NLM/ NIHMS143747; NLM/ PMC2756602
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65. Schipani E: Hypoxia and HIF-1 alpha in chondrogenesis. Semin Cell Dev Biol; 2005 Aug-Oct;16(4-5):539-46

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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66. Crivellato E, Nico B, Ribatti D: Mast cells and tumour angiogenesis: new insight from experimental carcinogenesis. Cancer Lett; 2008 Sep 28;269(1):1-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Data suggest indeed that tumour-infiltrating mast cells may exert a prominent function in the angiogenic "switch", which is essential for the progression of early tumours.

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  • (PMID = 18450371.001).
  • [ISSN] 1872-7980
  • [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 / Neurofibromin 1; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 32
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67. 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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68. 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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69. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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70. Bluff JE, Menakuru SR, Cross SS, Higham SE, Balasubramanian SP, Brown NJ, Reed MW, Staton CA: Angiogenesis is associated with the onset of hyperplasia in human ductal breast disease. Br J Cancer; 2009 Aug 18;101(4):666-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The precise timing of the angiogenic switch and the role of angiogenesis in the development of breast malignancy is currently unknown.
  • CONCLUSIONS: These findings are the first to suggest that the angiogenic switch, associated with increases in HIF-1alpha, VEGF and TF expression, occurs at the onset of hyperplasia in the mammary duct, although the greatest increase in angiogenesis occurs with the development of invasion.

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  • (PMID = 19623180.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 9035-58-9 / Thromboplastin
  • [Other-IDs] NLM/ PMC2736809
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71. Castellino RC, Muh CR, Durden DL: PI-3 kinase-PTEN signaling node: an intercept point for the control of angiogenesis. Curr Pharm Des; 2009;15(4):380-8
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  • Angiogenesis is tightly regulated by opposing mechanisms in mammalian cells and is controlled by the angiogenic switch.
  • In this review, we focus on literature that supports the PTEN/PI-3 kinase/AKT signaling node as a major control point for the angiogenic switch in both the on and off positions.
  • Our hypothesis is that, instead of inhibiting one cell surface receptor, such as VEGFR2 with bevacizumab (Avastin), thereby leaving a significant number of receptors free to pulse angiogenic signals, a more effective strategy may be to regulate signaling through an intercept node where redundant cell surface receptor signals converge to transmit important signaling events within the cell.

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  • (PMID = 19199965.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 87
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72. Persano L, Crescenzi M, Indraccolo S: Anti-angiogenic gene therapy of cancer: current status and future prospects. Mol Aspects Med; 2007 Feb;28(1):87-114

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-angiogenic gene therapy of cancer: current status and future prospects.
  • The discovery of endogenous inhibitors of angiogenesis has made it possible to test the hypothesis that blocking the angiogenic switch may keep tumor growth in check, and has added a new investigational arm to the field of cancer gene therapy.
  • The experimental approaches attempted to date, reviewed herein, indicate overall that anti-angiogenic gene therapy has efficacy mainly as an early intervention strategy and that a better understanding of the biological mechanisms underlying resistance to angiogenesis inhibition, as well as appropriate combined treatments, are required to generate a conceptual advancement which could drive the field towards successful management of established tumors.

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  • (PMID = 17306361.001).
  • [ISSN] 0098-2997
  • [Journal-full-title] Molecular aspects of medicine
  • [ISO-abbreviation] Mol. Aspects Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 175
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73. Indraccolo S, Stievano L, Minuzzo S, Tosello V, Esposito G, Piovan E, Zamarchi R, Chieco-Bianchi L, Amadori A: Interruption of tumor dormancy by a transient angiogenic burst within the tumor microenvironment. Proc Natl Acad Sci U S A; 2006 Mar 14;103(11):4216-21
MedlinePlus Health Information. consumer health - Kaposi's Sarcoma.

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  • [Title] Interruption of tumor dormancy by a transient angiogenic burst within the tumor microenvironment.
  • Tumor growth is currently viewed as a phenomenon associated with neovascularization and sustained production of angiogenic factors, but whether a transient angiogenic switch may trigger tumor growth remains unclear.
  • Here, we report that leukemia cells (MOLT-3) were poorly angiogenic and remained dormant when injected s.c. into immunodeficient mice.
  • However, progressive growth of lymphoid tumors was invariably recorded when irradiated angiogenic cells from Kaposi's sarcoma (KS-IMM) were locally coinjected with MOLT-3 cells or administered later.
  • Moreover, short-term treatment with angiogenic factors, including basic FGF or VEGF, either given as recombinant factors or delivered by retroviral vectors, also accelerated tumor growth.
  • These findings may emphasize that tumor angiogenesis is a process requiring a higher amount of angiogenic factors for its induction than maintenance.

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  • (PMID = 16537511.001).
  • [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, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
  • [Other-IDs] NLM/ PMC1449673
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74. Fazel S, Cimini M, Chen L, Li S, Angoulvant D, Fedak P, Verma S, Weisel RD, Keating A, Li RK: Cardioprotective c-kit+ cells are from the bone marrow and regulate the myocardial balance of angiogenic cytokines. J Clin Invest; 2006 Jul;116(7):1865-77
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardioprotective c-kit+ cells are from the bone marrow and regulate the myocardial balance of angiogenic cytokines.
  • We conclude that, consistent with their documented role in tumorigenesis, bone marrow c-kit+ cells act as key regulators of the angiogenic switch in infarcted myocardium, thereby driving efficient cardiac repair.

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  • (PMID = 16823487.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Recombinant Fusion Proteins; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC1483161
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75. Perez-Pinera P, Berenson JR, Deuel TF: Pleiotrophin, a multifunctional angiogenic factor: mechanisms and pathways in normal and pathological angiogenesis. Curr Opin Hematol; 2008 May;15(3):210-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pleiotrophin, a multifunctional angiogenic factor: mechanisms and pathways in normal and pathological angiogenesis.
  • RECENT FINDINGS: Pleiotrophin is directly angiogenic; it initiates an angiogenic switch in different cancer models in vivo.
  • It acts as an angiogenic factor through multiple mechanisms that include a unique signaling pathway that activates newly identified downstream tyrosine kinases through a unique mechanism, an interaction with endothelial cells to initiate proliferation, migration, and tube formation, the regulation of basic fibroblast growth factor and vascular endothelial growth factor signaling, the remodeling of the stromal microenvironment, and induction of transdifferentiation of monocytes into endothelial cells.

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  • (PMID = 18391787.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 2 T32 DK007022-26; United States / NCI NIH HHS / CA / CA84400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytokines; 134034-50-7 / pleiotrophin
  • [Number-of-references] 41
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76. Hasina R, Pontier AL, Fekete MJ, Martin LE, Qi XM, Brigaudeau C, Pramanik R, Cline EI, Coignet LJ, Lingen MW: NOL7 is a nucleolar candidate tumor suppressor gene in cervical cancer that modulates the angiogenic phenotype. Oncogene; 2006 Jan 26;25(4):588-98
SciCrunch. HGNC: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOL7 is a nucleolar candidate tumor suppressor gene in cervical cancer that modulates the angiogenic phenotype.
  • The induction of tumor dormancy correlated with an angiogenic switch caused by a decreased production of vascular endothelial growth factor and an increase in the production of the angiogenesis inhibitor thrombospondin-1.
  • These data suggest that NOL7 may function as a TSG in part by modulating the expression of the angiogenic phenotype.


77. Harper J, Moses MA: Molecular regulation of tumor angiogenesis: mechanisms and therapeutic implications. EXS; 2006;(96):223-68

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the last 20 years of angiogenesis research, a variety of angiogenic regulators, both positive and negative, have been identified.
  • The discovery of several anti-angiogenic factors has led to the development of novel cancer therapies based on targeting a tumor's vascular supply.
  • A major advance in the field of anti-angiogenic therapy occurred recently when the FDA approved Avastin (bevacizumab), the first solely anti-angiogenesis therapy approved for treatment of human cancer.
  • While it has long been appreciated that tumor growth and progression are dependent on angiogenesis, it is only recently that progress has been made in elucidating the molecular mechanisms that regulate the earliest stage in the angiogenic program, the angiogenic switch.
  • Anti-angiogenic therapies to date have essentially been designed to suppress the neovasculature in established tumors.
  • However, identifying the mechanisms that cause a tumor to acquire an angiogenic phenotype may lead to the discovery of new therapeutic modalities and complementary diagnostics that could be used to block the angiogenic switch, thereby preventing subsequent tumor progression.
  • In this chapter on the role of angiogenesis in cancer, we (1) provide an overview of the process of angiogenesis with special regard to the molecules and physiological conditions that regulate this process, (2) review recent studies describing the use of anti-angiogenic approaches in the treatment of a variety of human cancers, and (3) discuss the recent literature focused on the study of the molecules and molecular mechanisms that may be regulating the initiation of the angiogenic phenotype in tumors, and the clinical impact that this knowledge may have in the future.

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  • (PMID = 16383021.001).
  • [ISSN] 1023-294X
  • [Journal-full-title] EXS
  • [ISO-abbreviation] EXS
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1P50 DK065298; United States / NCI NIH HHS / CA / 2PO1CA45548; United States / NCCIH NIH HHS / AT / AT00650-01; United States / NCI NIH HHS / CA / CA83106
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 387
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78. Veliceasa D, Ivanovic M, Hoepfner FT, Thumbikat P, Volpert OV, Smith ND: Transient potential receptor channel 4 controls thrombospondin-1 secretion and angiogenesis in renal cell carcinoma. FEBS J; 2007 Dec;274(24):6365-77
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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  • Angiogenic switch in renal cell carcinoma (RCC) is attributed to the inactivation of the von Hippel-Lindau tumor suppressor, stabilization of hypoxia inducible factor-1 transcription factor and increased vascular endothelial growth factor.
  • However, HNK cells secreted high TSP1, which rendered them nonangiogenic, whereas RCC cells secreted little TSP1 and were angiogenic.
  • Our study indicates that TRPC4 loss in RCC leads to impaired Ca(2+) intake, misfolding, retrograde transport and diminished secretion of antiangiogenic TSP1, thus enabling angiogenic switch during RCC progression.

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  • (PMID = 18021253.001).
  • [ISSN] 1742-464X
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL077471
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / TRPC Cation Channels; 0 / TRPC4 ion channel; 0 / Thrombospondin 1; 139890-68-9 / 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; 526U7A2651 / Egtazic Acid; SY7Q814VUP / Calcium
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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. 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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81. 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
The Lens. Cited by Patents in .

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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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82. Hamano Y, Kalluri R: Tumstatin, the NC1 domain of alpha3 chain of type IV collagen, is an endogenous inhibitor of pathological angiogenesis and suppresses tumor growth. Biochem Biophys Res Commun; 2005 Jul 29;333(2):292-8
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  • During tumor growth, angiogenesis is supported by up-regulation of angiogenic stimulators (pro-angiogenic) and down-regulation of angiogenic inhibitors (anti-angiogenic).
  • The switch to the angiogenic phenotype (angiogenic switch) allows the tumors to grow and facilitate metastasis.

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  • [CommentIn] Biochem Biophys Res Commun. 2005 Jul 29;333(2):289-91 [15953588.001]
  • (PMID = 15979458.001).
  • [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 / DK 55001; United States / NIDDK NIH HHS / DK / DK 62987
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Autoantigens; 0 / Collagen Type IV; 0 / type IV collagen alpha3 chain
  • [Number-of-references] 98
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83. Fischer C, Jonckx B, Mazzone M, Zacchigna S, Loges S, Pattarini L, Chorianopoulos E, Liesenborghs L, Koch M, De Mol M, Autiero M, Wyns S, Plaisance S, Moons L, van Rooijen N, Giacca M, Stassen JM, Dewerchin M, Collen D, Carmeliet P: Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels. Cell; 2007 Nov 2;131(3):463-75
The Lens. Cited by Patents in .

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  • We explored the therapeutic potential and mechanisms of alphaPlGF, an antibody against placental growth factor (PlGF), a VEGF homolog, which regulates the angiogenic switch in disease, but not in health. alphaPlGF inhibited growth and metastasis of various tumors, including those resistant to VEGF(R) inhibitors (VEGF(R)Is), and enhanced the efficacy of chemotherapy and VEGF(R)Is. alphaPlGF inhibited angiogenesis, lymphangiogenesis, and tumor cell motility.
  • Distinct from VEGF(R)Is, alphaPlGF prevented infiltration of angiogenic macrophages and severe tumor hypoxia, and thus, did not switch on the angiogenic rescue program responsible for resistance to VEGF(R)Is.
  • The efficacy and safety of alphaPlGF, its pleiotropic and complementary mechanism to VEGF(R)Is, and the negligible induction of an angiogenic rescue program suggest that alphaPlGF may constitute a novel approach for cancer treatment.


84. Berger M, Bergers G, Arnold B, Hämmerling GJ, Ganss R: Regulator of G-protein signaling-5 induction in pericytes coincides with active vessel remodeling during neovascularization. Blood; 2005 Feb 1;105(3):1094-101
The Lens. Cited by Patents in .

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  • We identified regulator of G-protein signaling-5 (RGS-5) as an angiogenic pericyte marker at sites of physiologic and pathologic angiogenesis.
  • In a mouse model of pancreatic islet cell carcinogenesis, RGS-5 is specifically induced in the vasculature of premalignant lesions during the "angiogenic switch" and further elevated in tumor vessels.
  • Similarly, RGS-5 is overexpressed in highly angiogenic astrocytomas but not in hypoxia-inducible factor-1alpha (HIF-1alpha)-deficient tumors, which grow along preexisting brain capillaries without inducing neovessels.

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  • (PMID = 15459006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RGS Proteins; 0 / RGS5 protein, human
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85. Gao D, Nolan DJ, Mellick AS, Bambino K, McDonnell K, Mittal V: Endothelial progenitor cells control the angiogenic switch in mouse lung metastasis. Science; 2008 Jan 11;319(5860):195-8
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  • [Title] Endothelial progenitor cells control the angiogenic switch in mouse lung metastasis.
  • Here, using mouse models of pulmonary metastasis, we identify bone marrow (BM)-derived endothelial progenitor cells (EPCs) as critical regulators of this angiogenic switch.


86. Drogat B, Auguste P, Nguyen DT, Bouchecareilh M, Pineau R, Nalbantoglu J, Kaufman RJ, Chevet E, Bikfalvi A, Moenner M: IRE1 signaling is essential for ischemia-induced vascular endothelial growth factor-A expression and contributes to angiogenesis and tumor growth in vivo. Cancer Res; 2007 Jul 15;67(14):6700-7
Hazardous Substances Data Bank. OXYGEN .

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  • In solid tumors, cancer cells subjected to ischemic conditions trigger distinct signaling pathways contributing to angiogenic stimulation and tumor development.
  • Our results therefore suggest an essential role for IRE1-dependent signaling pathways in response to ischemia and identify this protein as a potential therapeutic target to control both the angiogenic switch and tumor development.

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  • (PMID = 17638880.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 42394; United States / NHLBI NIH HHS / HL / HL 052173
  • [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 / Membrane Proteins; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.- / ERN2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.- / Endoribonucleases; S88TT14065 / Oxygen
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87. Lee HO, Choe H, Seo K, Lee H, Lee J, Kim J: Fgfbp1 is essential for the cellular survival during zebrafish embryogenesis. Mol Cells; 2010 May;29(5):501-7
ZFIN. ZFIN .

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  • Previous studies suggested FGFBP1 functions as an angiogenic switch molecule by regulating the activity of FGF2, and it was later found to associate with a broad spectrum of FGFs.

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  • (PMID = 20396962.001).
  • [ISSN] 0219-1032
  • [Journal-full-title] Molecules and cells
  • [ISO-abbreviation] Mol. Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / FGFBP1 protein, zebrafish; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Zebrafish Proteins; 103107-01-3 / Fibroblast Growth Factor 2; 139946-12-6 / FGFBP1 protein, human
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88. Siegel L, Miternique-Grosse A, Griffon C, Klein-Soyer C, Lobstein A, Raul F, Stephan D: Antiangiogenic properties of lupulone, a bitter acid of hop cones. Anticancer Res; 2008 Jan-Feb;28(1A):289-94

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  • Disturbance of this balance leads to an 'angiogenic' switch critical for tumor development.
  • MATERIALS AND METHODS: Using human umbilical vein endothelial cells (HUVEC) the effects of lupulone were analyzed on proliferation induced by angiogenic growth factors, transmembrane cell migration toward fibronectin and formation of a network of tubular-like structures on Matrigel.

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  • (PMID = 18383859.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / Terpenes; 119978-18-6 / matrigel; 9007-34-5 / Collagen; B7425USG94 / lupulon
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89. Götz R: Inter-cellular adhesion disruption and the RAS/RAF and beta-catenin signalling in lung cancer progression. Cancer Cell Int; 2008;8:7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • Conditional genetic abrogation of epithelial tumour cell adhesion in mice with benign lung tumours induced by oncogenic RAF kinase has been demonstrated to induce intratumourous vascularization (angiogenic switch), progression to invasive adenocarcinoma and micrometastasis.

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  • (PMID = 18492263.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2427011
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90. Harfouche R, Basu S, Soni S, Hentschel DM, Mashelkar RA, Sengupta S: Nanoparticle-mediated targeting of phosphatidylinositol-3-kinase signaling inhibits angiogenesis. Angiogenesis; 2009;12(4):325-38
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  • Activation of this pathway is critical for transformation and also for the angiogenic switch, which is a key step for tumor progression.

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  • (PMID = 19685150.001).
  • [ISSN] 1573-7209
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromones; 0 / Drug Carriers; 0 / Morpholines; 0 / Nanocapsules; 0 / Neoplasm Proteins; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Akt1 protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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91. Kubota Y, Kaneko K, Konishi K, Ito H, Yamamoto T, Katagiri A, Muramoto T, Yano Y, Kobayashi Y, Oyama T, Kushima M, Imawari M: The onset of angiogenesis in a multistep process of esophageal squamous cell carcinoma. Front Biosci (Landmark Ed); 2009;14:3872-8
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  • Our results suggest that CD105 is an efficient marker protein to determine MVD, suggesting that the angiogenic switch occurs at the earliest stage of dysplastic transformation in ESCC.

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  • (PMID = 19273317.001).
  • [ISSN] 1093-4715
  • [Journal-full-title] Frontiers in bioscience (Landmark edition)
  • [ISO-abbreviation] Front Biosci (Landmark Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD31; 0 / ENG protein, human; 0 / Receptors, Cell Surface; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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92. Abuharbeid S, Czubayko F, Aigner A: The fibroblast growth factor-binding protein FGF-BP. Int J Biochem Cell Biol; 2006;38(9):1463-8
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  • This indicates that FGF-BP can be rate-limiting for tumor growth and serves as an angiogenic switch molecule, and that it represents an increasingly promising target molecule in anti-tumor therapy.

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  • (PMID = 16324873.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Intercellular Signaling Peptides and Proteins; 103107-01-3 / Fibroblast Growth Factor 2; 139946-12-6 / FGFBP1 protein, human; 9005-49-6 / Heparin
  • [Number-of-references] 30
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93. 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.


94. 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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95. Qin J, Chen X, Yu-Lee LY, Tsai MJ, Tsai SY: Nuclear receptor COUP-TFII controls pancreatic islet tumor angiogenesis by regulating vascular endothelial growth factor/vascular endothelial growth factor receptor-2 signaling. Cancer Res; 2010 Nov 1;70(21):8812-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, we used the prototypical RIP-Tag model of multistage pancreatic islet tumorigenesis to show that the nuclear receptor COUP-TFII is essential to regulate the balance between pro- and anti-angiogenic molecules that influence the angiogenic switch in cancer.
  • Mechanistic investigations revealed that COUP-TFII suppressed vascular endothelial growth factor (VEGF)/VEGF receptor-2 (VEGFR-2) signaling by transcriptionally repressing the expression of VEGFR-1, thereby curtailing a central angiogenic driver of vascular growth.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20978203.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R37 HD017379; United States / NICHD NIH HHS / HD / HD17379; United States / NHLBI NIH HHS / HL / HL076448; United States / NIDDK NIH HHS / DK / DK45641; United States / NIDDK NIH HHS / DK / DK059820; United States / NIDDK NIH HHS / DK / P01 DK059820; United States / NIDDK NIH HHS / DK / R01 DK045641; United States / NHLBI NIH HHS / HL / R01 HL076448; United States / NICHD NIH HHS / HD / R01 HD017379; United States / NIDDK NIH HHS / DK / R37 DK045641
  • [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 / COUP Transcription Factor II; 0 / GTPase-Activating Proteins; 0 / Gt(ROSA)26Sor non-coding RNA, mouse; 0 / Nr2f2 protein, mouse; 0 / Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / RNA, Untranslated; 0 / Ralbp1 protein, mouse; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ NIHMS237839; NLM/ PMC2970665
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96. Nyberg P, Salo T, Kalluri R: Tumor microenvironment and angiogenesis. Front Biosci; 2008 May 01;13:6537-53
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  • The tumor microenvironment contributes to this pathological angiogenic process.
  • On the other hand, many extracellular matrix molecules can promote angiogenesis by stabilizing blood vessels and sequestering pro-angiogenic growth factors.
  • Taken together, the tumor microenvironment is a complex unorganized tissue of various cell types and extracellular matrix that can regulate the pathological angiogenic switch.

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  • (PMID = 18508679.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK61688; United States / NIDDK NIH HHS / DK / DK55001; United States / NIDDK NIH HHS / DK / R01 DK061688; United States / NIDDK NIH HHS / DK / R01 DK055001; 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 / Integrins
  • [Number-of-references] 183
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97. Essafi-Benkhadir K, Onesto C, Stebe E, Moroni C, Pagès G: Tristetraprolin inhibits Ras-dependent tumor vascularization by inducing vascular endothelial growth factor mRNA degradation. Mol Biol Cell; 2007 Nov;18(11):4648-58
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  • However, ERKs reduce the VEGF mRNA-destabilizing effect of TTP, leading to an increase in VEGF expression that favors the angiogenic switch.
  • Determination of TTP and ERKs status would provide useful information for the evaluation of the angiogenic potential in human tumors.

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  • (PMID = 17855506.001).
  • [ISSN] 1059-1524
  • [Journal-full-title] Molecular biology of the cell
  • [ISO-abbreviation] Mol. Biol. Cell
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Tristetraprolin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC2043565
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98. 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
Hazardous Substances Data Bank. MAGNESIUM, ELEMENTAL .

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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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  • (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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99. Alison MR, Lim S, Houghton JM: Bone marrow-derived cells and epithelial tumours: more than just an inflammatory relationship. Curr Opin Oncol; 2009 Jan;21(1):77-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The contribution of bone marrow-derived cells (BMDCs) to tumour neovascularization is controversial, but BMD--endothelial progenitor cells (EPCs)--are strongly implicated in the angiogenic switch in a mouse model.

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  • (PMID = 19125022.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA119061
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 46
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100. Roskoski R Jr: Vascular endothelial growth factor (VEGF) signaling in tumor progression. Crit Rev Oncol Hematol; 2007 Jun;62(3):179-213
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  • There are about 30 endogenous pro-angiogenic factors and about 30 endogenous anti-angiogenic factors.
  • In order to increase in size, tumors undergo an angiogenic switch where the action of pro-angiogenic factors predominates, resulting in angiogenesis and tumor progression.

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  • (PMID = 17324579.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Neuropilins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 286
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