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  1. Article ; Online: Integrin α3β1 promotes vessel formation of glioblastoma-associated endothelial cells through calcium-mediated macropinocytosis and lysosomal exocytosis.

    Bae, Eunnyung / Huang, Ping / Müller-Greven, Gaёlle / Hambardzumyan, Dolores / Sloan, Andrew Edward / Nowacki, Amy S / Marko, Nicholas / Carlin, Cathleen R / Gladson, Candece L

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 4268

    Abstract: Therapeutic targeting of angiogenesis in glioblastoma has yielded mixed outcomes. Investigation of tumor-associated angiogenesis has focused on the factors that stimulate the sprouting, migration, and hyperproliferation of the endothelial cells. However, ...

    Abstract Therapeutic targeting of angiogenesis in glioblastoma has yielded mixed outcomes. Investigation of tumor-associated angiogenesis has focused on the factors that stimulate the sprouting, migration, and hyperproliferation of the endothelial cells. However, little is known regarding the processes underlying the formation of the tumor-associated vessels. To address this issue, we investigated vessel formation in CD31
    MeSH term(s) Calcium ; Cell Movement ; Endothelial Cells/pathology ; Exocytosis ; Glioblastoma/genetics ; Glioblastoma/pathology ; Humans ; Integrin alpha3beta1 ; Lysosomes/pathology ; Neovascularization, Pathologic/pathology
    Chemical Substances Integrin alpha3beta1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-07-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-31981-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Integrin α3β1 promotes vessel formation of glioblastoma-associated endothelial cells through calcium-mediated macropinocytosis and lysosomal exocytosis

    Eunnyung Bae / Ping Huang / Gaёlle Müller-Greven / Dolores Hambardzumyan / Andrew Edward Sloan / Amy S. Nowacki / Nicholas Marko / Cathleen R. Carlin / Candece L. Gladson

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Volume 15

    Abstract: Tumour-associated angiogenesis facilitates the growth of tumours. Here the authors show that integrin α3β1 promotes blood vessel formation in glioblastoma through calcium-mediated macropinocytosis and lysosomal exocytosis. ...

    Abstract Tumour-associated angiogenesis facilitates the growth of tumours. Here the authors show that integrin α3β1 promotes blood vessel formation in glioblastoma through calcium-mediated macropinocytosis and lysosomal exocytosis.
    Keywords Science ; Q
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Tissue factor is a critical regulator of radiation therapy-induced glioblastoma remodeling.

    Jeon, Hye-Min / Kim, Jeong-Yub / Cho, Hee Jin / Lee, Won Jun / Nguyen, Dayna / Kim, Sung Soo / Oh, Young Taek / Kim, Hee-Jin / Jung, Chan-Woong / Pinero, Gonzalo / Joshi, Tanvi / Hambardzumyan, Dolores / Sakaguchi, Takuya / Hubert, Christopher G / McIntyre, Thomas M / Fine, Howard A / Gladson, Candece L / Wang, Bingcheng / Purow, Benjamin W /
    Park, Jong Bae / Park, Myung Jin / Nam, Do-Hyun / Lee, Jeongwu

    Cancer cell

    2023  Volume 41, Issue 8, Page(s) 1480–1497.e9

    Abstract: Radiation therapy (RT) provides therapeutic benefits for patients with glioblastoma (GBM), but inevitably induces poorly understood global changes in GBM and its microenvironment (TME) that promote radio-resistance and recurrence. Through a cell surface ... ...

    Abstract Radiation therapy (RT) provides therapeutic benefits for patients with glioblastoma (GBM), but inevitably induces poorly understood global changes in GBM and its microenvironment (TME) that promote radio-resistance and recurrence. Through a cell surface marker screen, we identified that CD142 (tissue factor or F3) is robustly induced in the senescence-associated β-galactosidase (SA-βGal)-positive GBM cells after irradiation. F3 promotes clonal expansion of irradiated SA-βGal
    MeSH term(s) Humans ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/radiotherapy ; Thromboplastin ; Cell Line, Tumor ; Neoplasm Recurrence, Local ; Signal Transduction ; Brain Neoplasms/genetics ; Brain Neoplasms/radiotherapy ; Brain Neoplasms/metabolism ; Tumor Microenvironment
    Chemical Substances Thromboplastin (9035-58-9)
    Language English
    Publishing date 2023-07-13
    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.ccell.2023.06.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Progress on antiangiogenic therapy for patients with malignant glioma.

    Ahluwalia, Manmeet S / Gladson, Candece L

    Journal of oncology

    2010  Volume 2010, Page(s) 689018

    Abstract: Glioblastoma (GBM) is the most common primary brain tumor occurring in America. Despite recent advances in therapeutics, the prognosis for patients with newly diagnosed GBM remains dismal. As these tumors characteristically show evidence of angiogenesis ( ...

    Abstract Glioblastoma (GBM) is the most common primary brain tumor occurring in America. Despite recent advances in therapeutics, the prognosis for patients with newly diagnosed GBM remains dismal. As these tumors characteristically show evidence of angiogenesis (neovascularization) there has been great interest in developing anti-angiogenic therapeutic strategies for the treatment of patients with this disease and some anti-angiogenic agents have now been used for the treatment of patients with malignant glioma tumors. Although the results of these clinical trials are promising in that they indicate an initial therapeutic response, the anti-angiogenic therapies tested to date have not changed the overall survival of patients with malignant glioma tumors. This is due, in large part, to the development of resistance to these therapies. Ongoing research into key features of the neovasculature in malignant glioma tumors, as well as the general angiogenesis process, is suggesting additional molecules that may be targeted and an improved response when both the neovasculature and the tumor cells are targeted. Prevention of the development of resistance may require the development of anti-angiogenic strategies that induce apoptosis or cell death of the neovasculature, as well as an improved understanding of the potential roles of circulating endothelial progenitor cells and vascular co-option by tumor cells, in the development of resistance.
    Language English
    Publishing date 2010-04-06
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 2461349-6
    ISSN 1687-8469 ; 1687-8450
    ISSN (online) 1687-8469
    ISSN 1687-8450
    DOI 10.1155/2010/689018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: New insights into the role of CXCR4 in prostate cancer metastasis.

    Gladson, Candece L / Welch, Danny R

    Cancer biology & therapy

    2008  Volume 7, Issue 11, Page(s) 1849–1851

    MeSH term(s) Animals ; Cell Line, Tumor ; Chemokine CXCL12/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Ligands ; Male ; Mice ; Models, Biological ; Neoplasm Transplantation ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Receptors, CXCR4/metabolism
    Chemical Substances CXCL12 protein, human ; Chemokine CXCL12 ; Ligands ; Receptors, CXCR4
    Language English
    Publishing date 2008-11-17
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/cbt.7.11.7218
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Progress on Antiangiogenic Therapy for Patients with Malignant Glioma

    Candece L. Gladson / Manmeet S. Ahluwalia

    Journal of Oncology, Vol

    2010  Volume 2010

    Keywords Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2010-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: The pathobiology of glioma tumors.

    Gladson, Candece L / Prayson, Richard A / Liu, Wei Michael

    Annual review of pathology

    2009  Volume 5, Page(s) 33–50

    Abstract: The ongoing characterization of the genetic and epigenetic alterations in the gliomas has already improved the classification of these heterogeneous tumors and enabled the development of rodent models for analysis of the molecular pathways underlying ... ...

    Abstract The ongoing characterization of the genetic and epigenetic alterations in the gliomas has already improved the classification of these heterogeneous tumors and enabled the development of rodent models for analysis of the molecular pathways underlying their proliferative and invasive behavior. Effective application of the targeted therapies that are now in development will depend on pathologists' ability to provide accurate information regarding the genetic alterations and the expression of key receptors and ligands in the tumors. Here we review the mechanisms that have been implicated in the pathogenesis of the gliomas and provide examples of the cooperative nature of the pathways involved, which may influence the initial therapeutic response and the potential for development of resistance.
    MeSH term(s) Animals ; Cell Proliferation ; Disease Models, Animal ; Epigenesis, Genetic ; Glioma/genetics ; Glioma/pathology ; Glioma/therapy ; Humans ; Signal Transduction/genetics
    Language English
    Publishing date 2009-09-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathol-121808-102109
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Selenoprotein P neutralizes lipopolysaccharide and participates in hepatic cell endoplasmic reticulum stress response.

    Zhao, Yongzhong / Banerjee, Shuvojit / Huang, Ping / Wang, Xinning / Gladson, Candece L / Heston, Warren D / Foster, Charles B

    FEBS letters

    2016  Volume 590, Issue 24, Page(s) 4519–4530

    Abstract: Low serum selenium or selenoprotein P (SePP) levels have been repetitively observed in severe sepsis. The role of SePP in sepsis is incompletely characterized. To test the hypothesis that lipopolysaccharide (LPS) interacts with SePP, we investigated the ... ...

    Abstract Low serum selenium or selenoprotein P (SePP) levels have been repetitively observed in severe sepsis. The role of SePP in sepsis is incompletely characterized. To test the hypothesis that lipopolysaccharide (LPS) interacts with SePP, we investigated the interaction between LPS and the histidine-rich (His-rich) regions of SePP. We demonstrate that both purified SePP and synthetic peptides corresponding to the His-rich motifs neutralized LPS. In addition, we used a hepatocyte model to study the fate of SePP in response to LPS or endoplasmic reticulum (ER) stress. Our findings indicate that ER stress increases the cellular level of SePP and promotes its nuclear localization.
    MeSH term(s) Amino Acid Sequence ; Animals ; Conserved Sequence ; Endoplasmic Reticulum/drug effects ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress/drug effects ; Enzyme Inhibitors/pharmacology ; Gene Expression ; Glycosylation/drug effects ; HEK293 Cells ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Hep G2 Cells ; Humans ; Lipopolysaccharides/pharmacology ; Liver/cytology ; Liver/drug effects ; Liver/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Protein Binding ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Selenoprotein P/agonists ; Selenoprotein P/antagonists & inhibitors ; Selenoprotein P/genetics ; Selenoprotein P/metabolism ; Selenoproteins/genetics ; Selenoproteins/metabolism ; Sequence Alignment ; Thapsigargin/pharmacology ; Tunicamycin/pharmacology ; alpha 1-Antitrypsin/genetics ; alpha 1-Antitrypsin/metabolism
    Chemical Substances Enzyme Inhibitors ; Heat-Shock Proteins ; Lipopolysaccharides ; Membrane Proteins ; RNA, Small Interfering ; SELENOS protein, human ; SERPINA1 protein, human ; Selenoprotein P ; Selenoproteins ; alpha 1-Antitrypsin ; Tunicamycin (11089-65-9) ; Thapsigargin (67526-95-8) ; molecular chaperone GRP78 (YCYIS6GADR)
    Language English
    Publishing date 2016-11-28
    Publishing country England
    Document type Letter
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1002/1873-3468.12494
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Focal adhesion kinase in cancer.

    Hecker, Timothy P / Gladson, Candece L

    Frontiers in bioscience : a journal and virtual library

    2003  Volume 8, Page(s) s705–14

    Abstract: Focal adhesion kinase (FAK) is a non-receptor cytoplasmic tyrosine kinase that transmits signals important in modulating several cell functions, including proliferation, migration, and survival. Several different types of malignant tumors have been ... ...

    Abstract Focal adhesion kinase (FAK) is a non-receptor cytoplasmic tyrosine kinase that transmits signals important in modulating several cell functions, including proliferation, migration, and survival. Several different types of malignant tumors have been reported to express elevated levels of FAK protein in vivo, potentially pointing to a role for FAK in either the progression of tumor cells to malignancy or the pathogenesis of cancer. Considerable knowledge has been gained regarding FAK signaling in non-neoplastic cells, such as fibroblasts, while much less is known regarding FAK signaling in malignant cells. Several studies to date suggest that the regulation of FAK activity and signaling may be different in malignant cells. In this review, we summarize what is known regarding the function and signaling of FAK in cancer cells, and highlight areas that need further study. Evidence is emerging that aberrant FAK expression, activity, and signaling can potentially promote the progression of several types of tumors in vivo through its effects on cell function.
    MeSH term(s) Animals ; Focal Adhesions/enzymology ; Focal Adhesions/physiology ; Humans ; Neoplasms/enzymology ; Neoplasms/physiopathology ; Protein-Tyrosine Kinases/physiology
    Chemical Substances Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2003-05-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2141320-4
    ISSN 1093-9946
    ISSN 1093-9946
    DOI 10.2741/1115
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Therapeutic targeting of VEGF in the treatment of glioblastoma.

    Robles Irizarry, Lizbeth / Hambardzumyan, Dolores / Nakano, Ichiro / Gladson, Candece L / Ahluwalia, Manmeet S

    Expert opinion on therapeutic targets

    2012  Volume 16, Issue 10, Page(s) 973–984

    Abstract: Introduction: Glioblastoma (GBM) is the most common and aggressive type of primary malignant brain tumor in adults. Despite therapy with maximal safe surgical resection, radiation and temozolomide, prognosis remains poor at 14.6 months. Hence, there is ... ...

    Abstract Introduction: Glioblastoma (GBM) is the most common and aggressive type of primary malignant brain tumor in adults. Despite therapy with maximal safe surgical resection, radiation and temozolomide, prognosis remains poor at 14.6 months. Hence, there is an urgent need for developing novel therapeutic agents. In GBMs, the balance of angiogenic growth factors is skewed toward pro-angiogenesis and VEGF is identified as the key growth factor responsible for neovasculature. Targeting angiogenesis is hypothesized to arrest tumor growth and hence VEGF is an attractive therapeutic target.
    Areas covered: The purpose of this review is to discuss VEGF pathway inhibitors, their efficacy as monotherapy or in combination with other drugs, the effects on the radiographic response/assessment for GBMs, mechanisms of resistance and associated biomarkers. A short summary of angiogenesis and of the biological characteristics of angiogenesis will also be provided to enhance the understanding of VEGF pathway inhibitors.
    Expert opinion: Therapeutic targeting of VEGF has lead to improvements in progression-free survival in GBM patients without any change in the overall survival. VEGF-targeted therapy remains a promising therapeutic opportunity if improvements in biomarkers, imaging techniques and rational combination therapy are used to help advance the clinical efficacy of this approach.
    MeSH term(s) Angiogenesis Inhibitors/therapeutic use ; Animals ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Drug Resistance, Neoplasm ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Neovascularization, Pathologic ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Angiogenesis Inhibitors ; Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2012-08-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1517/14728222.2012.711817
    Database MEDical Literature Analysis and Retrieval System OnLINE

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