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  1. Article ; Online: Characterization of 7A5: A Human CD137 (4-1BB) Receptor Binding Monoclonal Antibody with Differential Agonist Properties That Promotes Antitumor Immunity.

    Kotanides, Helen / Sattler, Rose Marie / Lebron, Maria B / Carpenito, Carmine / Shen, Juqun / Li, Jingxing / Surguladze, David / Haidar, Jaafar N / Burns, Colleen / Shen, Leyi / Inigo, Ivan / Pennello, Anthony L / Forest, Amelie / Chen, Xinlei / Chin, Darin / Sonyi, Andreas / Topper, Michael / Boucher, Lauren / Sharma, Prachi /
    Zhang, Yiwei / Burtrum, Douglas / Novosiadly, Ruslan D / Ludwig, Dale L / Plowman, Gregory D / Kalos, Michael

    Molecular cancer therapeutics

    2021  Volume 19, Issue 4, Page(s) 988–998

    Abstract: The CD137 receptor plays a key role in mediating immune response by promoting T cell proliferation, survival, and memory. Effective agonism of CD137 has the potential to reinvigorate potent antitumor immunity either alone or in combination with other ... ...

    Abstract The CD137 receptor plays a key role in mediating immune response by promoting T cell proliferation, survival, and memory. Effective agonism of CD137 has the potential to reinvigorate potent antitumor immunity either alone or in combination with other immune-checkpoint therapies. In this study, we describe the discovery and characterization of a unique CD137 agonist, 7A5, a fully human IgG1 Fc effector-null monoclonal antibody. The biological properties of 7A5 were investigated through
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; Apoptosis ; CD8-Positive T-Lymphocytes/immunology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/immunology ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Proliferation ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/immunology ; Lung Neoplasms/pathology ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; NF-kappa B/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tumor Necrosis Factor Receptor Superfamily, Member 9/immunology ; Xenograft Model Antitumor Assays
    Chemical Substances Antibodies, Monoclonal ; NF-kappa B ; TNFRSF9 protein, human ; Tumor Necrosis Factor Receptor Superfamily, Member 9
    Language English
    Publishing date 2021-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-19-0893
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5750: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Bispecific Targeting of PD-1 and PD-L1 Enhances T-cell Activation and Antitumor Immunity.

    Kotanides, Helen / Li, Yiwen / Malabunga, Maria / Carpenito, Carmine / Eastman, Scott W / Shen, Yang / Wang, George / Inigo, Ivan / Surguladze, David / Pennello, Anthony L / Persaud, Krishnadatt / Hindi, Sagit / Topper, Michael / Chen, Xinlei / Zhang, Yiwei / Bulaon, Danielle K / Bailey, Tim / Lao, Yanbin / Han, Bing /
    Torgerson, Stacy / Chin, Darin / Sonyi, Andreas / Haidar, Jaafar N / Novosiadly, Ruslan D / Moxham, Christopher M / Plowman, Gregory D / Ludwig, Dale L / Kalos, Michael

    Cancer immunology research

    2020  Volume 8, Issue 10, Page(s) 1300–1310

    Abstract: The programmed cell death protein 1 receptor (PD-1) and programmed death ligand 1 (PD-L1) coinhibitory pathway suppresses T-cell-mediated immunity. We hypothesized that cotargeting of PD-1 and PD-L1 with a bispecific antibody molecule could provide an ... ...

    Abstract The programmed cell death protein 1 receptor (PD-1) and programmed death ligand 1 (PD-L1) coinhibitory pathway suppresses T-cell-mediated immunity. We hypothesized that cotargeting of PD-1 and PD-L1 with a bispecific antibody molecule could provide an alternative therapeutic approach, with enhanced antitumor activity, compared with monospecific PD-1 and PD-L1 antibodies. Here, we describe LY3434172, a bispecific IgG1 mAb with ablated Fc immune effector function that targets both human PD-1 and PD-L1. LY3434172 fully inhibited the major inhibitory receptor-ligand interactions in the PD-1 pathway. LY3434172 enhanced functional activation of T cells
    MeSH term(s) Animals ; Antibodies, Bispecific/immunology ; Antibodies, Bispecific/pharmacology ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/immunology ; CHO Cells ; Cricetulus ; Female ; Humans ; Immunotherapy/methods ; Lymphocyte Activation ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Molecular Targeted Therapy ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology ; T-Lymphocytes/immunology ; Xenograft Model Antitumor Assays
    Chemical Substances Antibodies, Bispecific ; B7-H1 Antigen ; CD274 protein, human ; PDCD1 protein, human ; Programmed Cell Death 1 Receptor
    Language English
    Publishing date 2020-07-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2732489-8
    ISSN 2326-6074 ; 2326-6066
    ISSN (online) 2326-6074
    ISSN 2326-6066
    DOI 10.1158/2326-6066.CIR-20-0304
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7022: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Novel therapeutic approach for neurogenic erectile dysfunction: effect of neurotrophic tyrosine kinase receptor type 1 monoclonal antibody.

    Lin, Guiting / Li, Huixi / Zhang, Xiaoyu / Wang, Jianwen / Zaid, Uwais / Sanford, Melissa T / Tu, Victor / Wu, Alex / Wang, Lin / Tian, Fei / Kotanides, Helen / Krishnan, Venkatesh / Wang, Guifang / Ning, Hongxiu / Banie, Lia / Lin, Ching-Shwun / Deng, Gary G / Lue, Tom F

    European urology

    2015  Volume 67, Issue 4, Page(s) 716–726

    Abstract: Background: Erectile dysfunction (ED) is a major health issue in aged populations, and neurogenic ED is particularly difficult to treat. Novel therapeutic approaches are needed for treatment of neurogenic ED of peripheral origin.: Objective: To ... ...

    Abstract Background: Erectile dysfunction (ED) is a major health issue in aged populations, and neurogenic ED is particularly difficult to treat. Novel therapeutic approaches are needed for treatment of neurogenic ED of peripheral origin.
    Objective: To investigate the therapeutic effects of a neurotrophic tyrosine kinase receptor type 1 monoclonal antibody (TrkA-mAb) on erectile function and sexual behavior in a rat model of cavernous nerve injury (CNI).
    Design, setting, and participants: In one experiment, 84 male rats were randomly assigned to seven groups. The groups underwent either CNI or sham surgery, subsequent injection into the major pelvic ganglion (IMPG) of phosphate-buffered saline (PBS), an immunoglobulin G (IgG) control, or TrkA-mAb, and then intracavernosal (IC) injection of either PBS or varying TrkA-mAb concentrations immediately after surgery and then 1 wk later. Erectile function was assessed and histologic/molecular analyses were performed at 6 wk after surgery. In a second experiment, 36 male rats were randomly divided into three groups. The groups underwent CNI or sham surgery and then IC injection of PBS, IgG, or TrkA-mAb immediately after surgery and for 5 wk thereafter. At 6 wk after surgery, the performance of the rats in sexual behavior tests was videotaped.
    Intervention: CNI or sham surgery; IMPG of PBS, IgG, or TrkA-mAb; IC injection of PBS or TrkA-mAb.
    Outcome measurements and statistical analysis: The intracavernous pressure response to cavernous nerve electrostimulation was measured and midpenile cross-sections were histologically examined. Western blotting (WB) of cavernous tissue protein was performed. Rats were assessed for chasing, mounting, intromission, and ejaculation behaviors during sexual behavior tests. The data were analyzed using one-way analysis of variance followed by the Tukey-Kramer t test.
    Results and limitations: Recovery of erectile function of varying degrees was observed in the TrkA-mAb groups. TrkA-mAb treatment significantly suppressed tyrosine hydroxylase-positive nerve fibers in the corpus cavernosum and enhanced neuronal nitric oxide synthase-positive fibers in the dorsal nerve. The ratio of smooth muscle to collagen in the corpus cavernosum was significantly improved in TrkA-mAb treatment groups compared to PBS vehicle and IgG control groups. WB confirmed these biological changes. There was a nonsignificant increase in the average number of intromissions and ejaculations in the TrkA-mAb group. The study limitations include small sample size, variability in sexual behavior, lack of data on the neuromuscular mechanism involved, and lack of information of the role of neurotrophins or cytokines in regeneration.
    Conclusions: TrkA-mAb successfully inhibits sympathetic nerve regeneration, leads to parasympathetic nerve regeneration, and has therapeutic effects on ED and sexual behavior disorder in a rat model of CNI.
    Patient summary: This report provides strong evidence that a neurotrophic tyrosine kinase receptor type 1 monoclonal antibody (TrkA-mAb) inhibits sympathetic nerve regeneration, leads to parasympathetic nerve regeneration, and has therapeutic effects on erectile dysfunction and sexual behavior disorder in a rat model of cavernous nerve injury. The results raise the possibility that human patients with neurogenic erectile dysfunction may respond to TrkA-mAb in a manner that parallels the response seen in our rodent study.
    MeSH term(s) Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/pharmacology ; Disease Models, Animal ; Erectile Dysfunction/drug therapy ; Erectile Dysfunction/physiopathology ; Humans ; Male ; Nerve Regeneration/drug effects ; Penile Erection/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptor, trkA/immunology ; Sexual Behavior, Animal/drug effects ; Treatment Outcome
    Chemical Substances Antibodies, Monoclonal ; Receptor, trkA (EC 2.7.10.1)
    Language English
    Publishing date 2015-04
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 193790-x
    ISSN 1873-7560 ; 1421-993X ; 0302-2838
    ISSN (online) 1873-7560 ; 1421-993X
    ISSN 0302-2838
    DOI 10.1016/j.eururo.2014.10.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1247: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 294: Show issues

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  4. Article: DEGA/AMIGO-2, a leucine-rich repeat family member, differentially expressed in human gastric adenocarcinoma: effects on ploidy, chromosomal stability, cell adhesion/migration and tumorigenicity.

    Rabenau, Karen E / O'Toole, Jennifer M / Bassi, Rajiv / Kotanides, Helen / Witte, Larry / Ludwig, Dale L / Pereira, Daniel S

    Oncogene

    2004  Volume 23, Issue 29, Page(s) 5056–5067

    Abstract: We have discovered DEGA, a novel cDNA differentially expressed in human gastric adenocarcinomas. The DEGA gene product contains a signal peptide, five leucine-rich repeat motifs and a single IgG, and transmembrane domain, suggesting its residence on the ... ...

    Abstract We have discovered DEGA, a novel cDNA differentially expressed in human gastric adenocarcinomas. The DEGA gene product contains a signal peptide, five leucine-rich repeat motifs and a single IgG, and transmembrane domain, suggesting its residence on the plasma membrane. Transfection of 293 cells with a DEGA-GFP fusion construct confirmed its cell surface localization. Although the cytosolic portion of the DEGA gene product does not contain known protein domains, approximately one-fifth of these residues are either a serine or a threonine, suggesting that DEGA may play a role in signal transduction. BLAST searches revealed DEGA to be an exact match to AMIGO-2, a recently identified, but functionally uncharacterized protein related to AMIGO, a leucine-rich repeat containing cell adhesion molecule implicated in axon tract development. In this report, we show that DEGA/AMIGO-2 mRNA is differentially expressed in approximately 45% of tumor versus normal tissue from gastric adenocarcinoma patients. Stable expression of a DEGA/AMIGO-2 antisense construct in the gastric adenocarcinoma cell line, AGS, led to altered morphology, increased ploidy, chromosomal instability, decreased cell adhesion/migration, and a nearly complete abrogation of tumorigenicity in nude mice. These findings suggest a potential etiologic role for DEGA/AMIGO-2 in gastric adenocarcinoma.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Amino Acid Sequence ; Animals ; Base Sequence ; Benzamides/metabolism ; Cell Adhesion ; Cell Movement ; Chromosomal Instability ; Cloning, Molecular ; DNA, Complementary ; Humans ; Leucine ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasms, Experimental/etiology ; Ploidies ; Sequence Homology, Nucleic Acid ; Stomach Neoplasms/genetics ; Stomach Neoplasms/pathology
    Chemical Substances Benzamides ; DNA, Complementary ; N-(2,6-dimethylphenyl)-4-(((diethylamino)acetyl)amino)benzamide (107634-14-0) ; Leucine (GMW67QNF9C)
    Language English
    Publishing date 2004-06-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/sj.onc.1207681
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2218: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: A human monoclonal antibody targeting the stem cell factor receptor (c-Kit) blocks tumor cell signaling and inhibits tumor growth.

    Lebron, Maria B / Brennan, Laura / Damoci, Christopher B / Prewett, Marie C / O'Mahony, Marguerita / Duignan, Inga J / Credille, Kelly M / DeLigio, James T / Starodubtseva, Marina / Amatulli, Michael / Zhang, Yiwei / Schwartz, Kaben D / Burtrum, Douglas / Balderes, Paul / Persaud, Kris / Surguladze, David / Loizos, Nick / Paz, Keren / Kotanides, Helen

    Cancer biology & therapy

    2014  Volume 15, Issue 9, Page(s) 1208–1218

    Abstract: Stem cell factor receptor (c-Kit) exerts multiple biological effects on target cells upon binding its ligand stem cell factor (SCF). Aberrant activation of c-Kit results in dysregulated signaling and is implicated in the pathogenesis of numerous cancers. ...

    Abstract Stem cell factor receptor (c-Kit) exerts multiple biological effects on target cells upon binding its ligand stem cell factor (SCF). Aberrant activation of c-Kit results in dysregulated signaling and is implicated in the pathogenesis of numerous cancers. The development of more specific and effective c-Kit therapies is warranted given its essential role in tumorigenesis. In this study, we describe the biological properties of CK6, a fully human IgG1 monoclonal antibody against the extracellular region of human c-Kit. CK6 specifically binds c-Kit receptor with high affinity (EC 50 = 0.06 nM) and strongly blocks its interaction with SCF (IC 50 = 0.41 nM) in solid phase assays. Flow cytometry shows CK6 binding to c-Kit on the cell surface of human small cell lung carcinoma (SCLC), melanoma, and leukemia tumor cell lines. Furthermore, exposure to CK6 inhibits SCF stimulation of c-Kit tyrosine kinase activity and downstream signaling pathways such as mitogen-activated protein kinase (MAPK) and protein kinase B (AKT), in addition to reducing tumor cell line growth in vitro. CK6 treatment significantly decreases human xenograft tumor growth in NCI-H526 SCLC (T/C% = 57) and Malme-3M melanoma (T/C% = 58) models in vivo. The combination of CK6 with standard of care chemotherapy agents, cisplatin and etoposide for SCLC or dacarbazine for melanoma, more potently reduces tumor growth (SCLC T/C% = 24, melanoma T/C% = 38) compared with CK6 or chemotherapy alone. In summary, our results demonstrate that CK6 is a c-Kit antagonist antibody with tumor growth neutralizing properties and are highly suggestive of potential therapeutic application in treating human malignancies harboring c-Kit receptor.
    MeSH term(s) Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cisplatin/administration & dosage ; Dacarbazine/administration & dosage ; Etoposide/administration & dosage ; Female ; Heterografts ; Humans ; Immunoglobulin G/administration & dosage ; Immunoglobulin G/pharmacology ; Immunoglobulin G/therapeutic use ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/metabolism ; Melanoma, Experimental/pathology ; Mice, Nude ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/immunology ; Proto-Oncogene Proteins c-kit/metabolism ; Signal Transduction ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/metabolism ; Small Cell Lung Carcinoma/pathology
    Chemical Substances Antibodies, Monoclonal ; Immunoglobulin G ; Etoposide (6PLQ3CP4P3) ; Dacarbazine (7GR28W0FJI) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2014-06-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/cbt.29523
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5887: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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