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  1. Article ; Online: Integrins in angiogenesis and lymphangiogenesis.

    Avraamides, Christie J / Garmy-Susini, Barbara / Varner, Judith A

    Nature reviews. Cancer

    2008  Volume 8, Issue 8, Page(s) 604–617

    Abstract: Blood vessels promote tumour growth, and both blood and lymphatic vessels facilitate tumour metastasis by serving as conduits for the transport of tumour cells to new sites. Angiogenesis and lymphangiogenesis are regulated by integrins, which are members ...

    Abstract Blood vessels promote tumour growth, and both blood and lymphatic vessels facilitate tumour metastasis by serving as conduits for the transport of tumour cells to new sites. Angiogenesis and lymphangiogenesis are regulated by integrins, which are members of a family of cell surface receptors whose ligands are extracellular matrix proteins and immunoglobulin superfamily molecules. Select integrins promote endothelial cell migration and survival during angiogenesis and lymphangiogenesis, whereas other integrins promote pro-angiogenic macrophage trafficking to tumours. Several integrin-targeted therapeutic agents are currently in clinical trials for cancer therapy. Here, we review the evidence implicating integrins as a family of fundamental regulators of angiogenesis and lymphangiogenesis.
    MeSH term(s) Angiogenesis Inhibitors/pharmacology ; Animals ; Humans ; Integrins/drug effects ; Integrins/physiology ; Lymphangiogenesis/physiology ; Neoplasms/blood supply ; Neoplasms/pathology ; Neoplasms/therapy ; Neovascularization, Pathologic/etiology
    Chemical Substances Angiogenesis Inhibitors ; Integrins
    Language English
    Publishing date 2008-05-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/nrc2353
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Combined blockade of integrin-α4β1 plus cytokines SDF-1α or IL-1β potently inhibits tumor inflammation and growth.

    Schmid, Michael C / Avraamides, Christie J / Foubert, Philippe / Shaked, Yuval / Kang, Sang Won / Kerbel, Robert S / Varner, Judith A

    Cancer research

    2011  Volume 71, Issue 22, Page(s) 6965–6975

    Abstract: Tumor-associated macrophages promote tumor growth by stimulating angiogenesis and suppressing antitumor immunity. Thus, therapeutics that inhibit macrophage recruitment to tumors may provide new avenues for cancer therapy. In this study, we showed how ... ...

    Abstract Tumor-associated macrophages promote tumor growth by stimulating angiogenesis and suppressing antitumor immunity. Thus, therapeutics that inhibit macrophage recruitment to tumors may provide new avenues for cancer therapy. In this study, we showed how chemoattractants stromal cell-derived growth factor 1 alpha (SDF-1α) and interleukin 1 beta (IL-1β) collaborate with myeloid cell integrin-α4β1 to promote tumor inflammation and growth. We found that SDF-1α and IL-1β are highly expressed in the microenvironments of murine lung, pancreatic, and breast tumors; surprisingly, SDF-1α was expressed only by tumor cells, whereas IL-1β was produced only by tumor-derived granulocytes and macrophages. In vivo, both factors directly recruited proangiogenic macrophages to tissues, whereas antagonists of both factors suppressed tumor inflammation, angiogenesis, and growth. Signals induced by IL-1β and SDF-1α promoted the interaction of talin and paxillin with the cytoplasmic tails of integrin-α4β1, thereby stimulating myeloid cell adhesion to endothelium in vitro and in vivo. Inhibition of integrin-α4β1, SDF-1α, or IL-1β was sufficient to block tumor inflammation and growth, and the combined blockade of these molecules greatly accentuated these effects. Furthermore, antagonists of integrin-α4β1 inhibited chemotherapy-induced tumor inflammation and acted synergistically with chemotherapeutic agents to suppress tumor inflammation and growth. These results show that targeting myeloid cell recruitment mechanisms can be an effective approach to suppress tumor progression.
    MeSH term(s) Animals ; CD11b Antigen/analysis ; Cell Movement ; Chemokine CXCL12/antagonists & inhibitors ; Chemokine CXCL12/physiology ; Inflammation/prevention & control ; Integrin alpha4beta1/antagonists & inhibitors ; Integrin alpha4beta1/physiology ; Interleukin-1beta/antagonists & inhibitors ; Interleukin-1beta/physiology ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/physiology ; Neoplasms/pathology ; Neoplasms/therapy ; Paxillin/physiology ; Talin/physiology
    Chemical Substances CD11b Antigen ; Chemokine CXCL12 ; ITGAM protein, human ; Integrin alpha4beta1 ; Interleukin-1beta ; Paxillin ; Talin
    Language English
    Publishing date 2011-09-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-11-0588
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  3. Article ; Online: PI3Kα activates integrin α4β1 to establish a metastatic niche in lymph nodes.

    Garmy-Susini, Barbara / Avraamides, Christie J / Desgrosellier, Jay S / Schmid, Michael C / Foubert, Philippe / Ellies, Lesley G / Lowy, Andrew M / Blair, Sarah L / Vandenberg, Scott R / Datnow, Brian / Wang, Huan-You / Cheresh, David A / Varner, Judith

    Proceedings of the National Academy of Sciences of the United States of America

    2013  Volume 110, Issue 22, Page(s) 9042–9047

    Abstract: Lymph nodes are initial sites of tumor metastasis, yet whether the lymph node microenvironment actively promotes tumor metastasis remains unknown. We show here that VEGF-C/PI3Kα-driven remodeling of lymph nodes promotes tumor metastasis by activating ... ...

    Abstract Lymph nodes are initial sites of tumor metastasis, yet whether the lymph node microenvironment actively promotes tumor metastasis remains unknown. We show here that VEGF-C/PI3Kα-driven remodeling of lymph nodes promotes tumor metastasis by activating integrin α4β1 on lymph node lymphatic endothelium. Activated integrin α4β1 promotes expansion of the lymphatic endothelium in lymph nodes and serves as an adhesive ligand that captures vascular cell adhesion molecule 1 (VCAM-1)(+) metastatic tumor cells, thereby promoting lymph node metastasis. Experimental induction of α4β1 expression in lymph nodes is sufficient to promote tumor cell adhesion to lymphatic endothelium and lymph node metastasis in vivo, whereas genetic or pharmacological blockade of integrin α4β1 or VCAM-1 inhibits it. As lymph node metastases accurately predict poor disease outcome, and integrin α4β1 is a biomarker of lymphatic endothelium in tumor-draining lymph nodes from animals and patients, these results indicate that targeting integrin α4β1 or VCAM to inhibit the interactions of tumor cells with the lymph node microenvironment may be an effective strategy to suppress tumor metastasis.
    MeSH term(s) Analysis of Variance ; Animals ; Carcinoma, Ductal, Breast/pathology ; Cell Adhesion/physiology ; Endothelium, Lymphatic/metabolism ; Female ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Immunohistochemistry ; Integrin alpha4beta1/metabolism ; Lymph Nodes/metabolism ; Lymphangiogenesis/physiology ; Mice ; Neoplasm Metastasis/physiopathology ; Neoplasm Metastasis/prevention & control ; Phosphatidylinositol 3-Kinases/metabolism ; Vascular Cell Adhesion Molecule-1/metabolism ; Vascular Cell Adhesion Molecule-1/physiology
    Chemical Substances Integrin alpha4beta1 ; Vascular Cell Adhesion Molecule-1 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
    Language English
    Publishing date 2013-05-13
    Publishing country United States
    Document 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.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1219603110
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  4. Article ; Online: A PKA-Csk-pp60Src signaling pathway regulates the switch between endothelial cell invasion and cell-cell adhesion during vascular sprouting.

    Jin, Hui / Garmy-Susini, Barbara / Avraamides, Christie J / Stoletov, Konstantin / Klemke, Richard L / Varner, Judith A

    Blood

    2010  Volume 116, Issue 25, Page(s) 5773–5783

    Abstract: Angiogenesis is controlled by signals that stimulate motility in endothelial cells at the tips of vascular sprouts while maintaining cell-cell adhesion in the stalks of angiogenic sprouts. We show here that Gs-linked G protein-coupled receptor activation ...

    Abstract Angiogenesis is controlled by signals that stimulate motility in endothelial cells at the tips of vascular sprouts while maintaining cell-cell adhesion in the stalks of angiogenic sprouts. We show here that Gs-linked G protein-coupled receptor activation of cAMP-dependent protein kinase (PKA) plays an important role in regulating the switch between endothelial cell adhesion and migration by activating C-terminal Src kinase, leading to inhibition of pp60Src. Activated PKA blocks pp60Src-dependent vascular endot helial-cadherin phosphorylation, thereby stimulating cell-cell adhesion while suppressing endothelial cell polarization, motility, angiogenesis, and vascular permeability. Similar to the actions of Notch and Dll4, PKA activation blocks sprouting in newly forming embryonic blood vessels, while PKA inhibition promotes excessive sprouting in these vessels. These findings demonstrate that G protein-coupled receptors and PKA regulate vascular sprouting during angiogenesis by controlling endothelial cell migration and cell-cell adhesion through their actions on pp60Src.
    MeSH term(s) Blotting, Western ; CSK Tyrosine-Protein Kinase ; Cell Adhesion/physiology ; Cell Movement/physiology ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases/genetics ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Humans ; Immunoprecipitation ; Neovascularization, Physiologic ; Phosphorylation ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins pp60(c-src)/antagonists & inhibitors ; Proto-Oncogene Proteins pp60(c-src)/genetics ; Proto-Oncogene Proteins pp60(c-src)/metabolism ; Signal Transduction ; Umbilical Veins/cytology ; Umbilical Veins/metabolism ; src-Family Kinases
    Chemical Substances Protein-Tyrosine Kinases (EC 2.7.10.1) ; CSK Tyrosine-Protein Kinase (EC 2.7.10.2) ; Proto-Oncogene Proteins pp60(c-src) (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; CSK protein, human (EC 2.7.10.23) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2010-09-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2010-07-296210
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    Zs.MO 364: Show issues

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  5. Article ; Online: Integrin alpha4beta1 signaling is required for lymphangiogenesis and tumor metastasis.

    Garmy-Susini, Barbara / Avraamides, Christie J / Schmid, Michael C / Foubert, Philippe / Ellies, Lesley G / Barnes, Leo / Feral, Chloe / Papayannopoulou, Thalia / Lowy, Andrew / Blair, Sarah L / Cheresh, David / Ginsberg, Mark / Varner, Judith A

    Cancer research

    2010  Volume 70, Issue 8, Page(s) 3042–3051

    Abstract: Recent studies have shown that lymphangiogenesis or the growth of lymphatic vessels at the periphery of tumors promotes tumor metastasis to lymph nodes. We show here that the fibronectin-binding integrin alpha4beta1 and its ligand fibronectin are novel ... ...

    Abstract Recent studies have shown that lymphangiogenesis or the growth of lymphatic vessels at the periphery of tumors promotes tumor metastasis to lymph nodes. We show here that the fibronectin-binding integrin alpha4beta1 and its ligand fibronectin are novel functional markers of proliferative lymphatic endothelium. Tumors and lymphangiogenic growth factors, such as vascular endothelial growth factor-C (VEGF-C) and VEGF-A, induce lymphatic vessel expression of integrin alpha4beta1. Integrin alpha4beta1 then promotes growth factor and tumor-induced lymphangiogenesis, as genetic loss of integrin alpha4beta1 expression in Tie2Cre+ alpha4(loxp/loxp) mice or genetic loss of alpha4 signaling in alpha4Y991A knock-in mice blocks growth factor and tumor-induced lymphangiogenesis, as well as tumor metastasis to lymph nodes. In addition, antagonists of integrin alpha4beta1 suppress lymphangiogenesis and tumor metastasis. Our studies show that integrin alpha4beta1 and the signals it transduces regulate the adhesion, migration, invasion, and survival of proliferating lymphatic endothelial cells. As suppression of alpha4beta1 expression, signal transduction, or function in tumor lymphatic endothelium not only inhibits tumor lymphangiogenesis but also prevents metastatic disease, these results show that integrin alpha4beta1-mediated tumor lymphangiogenesis promotes metastasis and is a useful target for the suppression of metastatic disease.
    MeSH term(s) Animals ; Cell Adhesion ; Cell Movement ; Cell Proliferation ; Endothelial Cells/cytology ; Female ; Humans ; Integrin alpha4beta1/biosynthesis ; Ligands ; Lymphangiogenesis ; Melanoma, Experimental ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction
    Chemical Substances Integrin alpha4beta1 ; Ligands
    Language English
    Publishing date 2010-04-13
    Publishing country United States
    Document 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.
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-09-3761
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  6. Article ; Online: Receptor tyrosine kinases and TLR/IL1Rs unexpectedly activate myeloid cell PI3kγ, a single convergent point promoting tumor inflammation and progression.

    Schmid, Michael C / Avraamides, Christie J / Dippold, Holly C / Franco, Irene / Foubert, Philippe / Ellies, Lesley G / Acevedo, Lissette M / Manglicmot, Joan R E / Song, Xiaodan / Wrasidlo, Wolfgang / Blair, Sara L / Ginsberg, Mark H / Cheresh, David A / Hirsch, Emilio / Field, Seth J / Varner, Judith A

    Cancer cell

    2011  Volume 19, Issue 6, Page(s) 715–727

    Abstract: Tumor inflammation promotes angiogenesis, immunosuppression, and tumor growth, but the mechanisms controlling inflammatory cell recruitment to tumors are not well understood. We found that a range of chemoattractants activating G protein-coupled ... ...

    Abstract Tumor inflammation promotes angiogenesis, immunosuppression, and tumor growth, but the mechanisms controlling inflammatory cell recruitment to tumors are not well understood. We found that a range of chemoattractants activating G protein-coupled receptors (GPCRs), receptor tyrosine kinases (RTKs) and Toll-like/IL-1 receptors (TLR/IL1Rs) unexpectedly initiate tumor inflammation by activating the PI3-kinase isoform p110γ in Gr1+CD11b+ myeloid cells. Whereas GPCRs activate p110γ in a Ras/p101-dependent manner, RTKs and TLR/IL1Rs directly activate p110γ in a Ras/p87-dependent manner. Once activated, p110γ promotes inside-out activation of a single integrin, α4β1, causing myeloid cell invasion into tumors. Pharmacological or genetic blockade of p110γ suppressed inflammation, growth, and metastasis of implanted and spontaneous tumors, revealing an important therapeutic target in oncology.
    MeSH term(s) Animals ; Cell Adhesion ; Cell Movement ; Class Ib Phosphatidylinositol 3-Kinase/physiology ; Disease Progression ; Humans ; Inflammation/etiology ; Integrin alpha4beta1/physiology ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Neoplasms/pathology ; Neoplasms/prevention & control ; Receptor Protein-Tyrosine Kinases/physiology ; Receptors, Interleukin-1/physiology ; Toll-Like Receptors/physiology ; ras Proteins/physiology
    Chemical Substances Integrin alpha4beta1 ; Receptors, Interleukin-1 ; Toll-Like Receptors ; Class Ib Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; PIK3CG protein, human (EC 2.7.1.137) ; Pik3cg protein, mouse (EC 2.7.1.153) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; ras Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2011-04-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccr.2011.04.016
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    Zs.A 5650: Show issues Location:
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    Zs.MG 104: Show issues

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  7. Article ; Online: ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC.

    McMurray, John J V / Adamopoulos, Stamatis / Anker, Stefan D / Auricchio, Angelo / Böhm, Michael / Dickstein, Kenneth / Falk, Volkmar / Filippatos, Gerasimos / Fonseca, Cândida / Gomez-Sanchez, Miguel Angel / Jaarsma, Tiny / Køber, Lars / Lip, Gregory Y H / Maggioni, Aldo Pietro / Parkhomenko, Alexander / Pieske, Burkert M / Popescu, Bogdan A / Rønnevik, Per K / Rutten, Frans H /
    Schwitter, Juerg / Seferovic, Petar / Stepinska, Janina / Trindade, Pedro T / Voors, Adriaan A / Zannad, Faiez / Zeiher, Andreas / Bax, Jeroen J / Baumgartner, Helmut / Ceconi, Claudio / Dean, Veronica / Deaton, Christi / Fagard, Robert / Funck-Brentano, Christian / Hasdai, David / Hoes, Arno / Kirchhof, Paulus / Knuuti, Juhani / Kolh, Philippe / McDonagh, Theresa / Moulin, Cyril / Reiner, Zeljko / Sechtem, Udo / Sirnes, Per Anton / Tendera, Michal / Torbicki, Adam / Vahanian, Alec / Windecker, Stephan / Bonet, Luis Almenar / Avraamides, Panayiotis / Ben Lamin, Hisham A / Brignole, Michele / Coca, Antonio / Cowburn, Peter / Dargie, Henry / Elliott, Perry / Flachskampf, Frank Arnold / Guida, Guido Francesco / Hardman, Suzanna / Iung, Bernard / Merkely, Bela / Mueller, Christian / Nanas, John N / Nielsen, Olav Wendelboe / Orn, Stein / Parissis, John T / Ponikowski, Piotr

    European journal of heart failure

    2012  Volume 14, Issue 8, Page(s) 803–869

    MeSH term(s) Algorithms ; Antihypertensive Agents/therapeutic use ; Cardiotonic Agents/therapeutic use ; Europe ; Heart Failure/diagnosis ; Heart Failure/drug therapy ; Humans ; Natriuretic Peptides ; Renin-Angiotensin System ; Societies, Medical ; Stroke Volume ; Ventricular Function, Left
    Chemical Substances Antihypertensive Agents ; Cardiotonic Agents ; Natriuretic Peptides
    Language English
    Publishing date 2012-08
    Publishing country England
    Document type Journal Article ; Practice Guideline
    ZDB-ID 1483672-5
    ISSN 1879-0844 ; 1388-9842
    ISSN (online) 1879-0844
    ISSN 1388-9842
    DOI 10.1093/eurjhf/hfs105
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