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  1. AU="Gabig, Theodore G"
  2. AU="Nixon, Ian J"
  3. AU="Huang Xiaoting"
  4. AU="Colturato, Virgílio Antônio Rensi"
  5. AU="Mahfouz, Amira Y"
  6. AU="Ayyappan, Sabarish"
  7. AU=Wang Kevin L-C
  8. AU="Lukas T. Hirschwald"
  9. AU="Morley-Davies, A"
  10. AU="Felsberg, Gary J"
  11. AU="Bogen, Oliver"
  12. AU="de Portu, Simona"
  13. AU="Janssens, Rick"

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  1. Artikel: Primary Diffuse Large B-Cell Lymphoma Localized to the Lacrimal Sac: A Case Presentation and Review of the Literature.

    Zarrabi, Kevin / Desai, Ved / Yim, Brandom / Gabig, Theodore G

    Case reports in hematology

    2016  Band 2016, Seite(n) 5612749

    Abstract: We report a rare case of diffuse large B-cell lymphoma (DLBCL) of the lacrimal sac in a 50-year-old male. The incidence of primary ocular lymphoma is low and it is considered a rare disease. Moreover, reports of ocular DLBCL are uncommon and the disease ... ...

    Abstract We report a rare case of diffuse large B-cell lymphoma (DLBCL) of the lacrimal sac in a 50-year-old male. The incidence of primary ocular lymphoma is low and it is considered a rare disease. Moreover, reports of ocular DLBCL are uncommon and the disease remains poorly characterized. Our patient presented for management of osteomyelitis and was incidentally found to have a painless swelling and cyst around his right eye. A PET/CT scan revealed hypermetabolic activity within the lacrimal sac and a subsequent excisional biopsy of the mass yielded histopathology consistent with DLBCL. Consequently, the patient underwent treatment with R-CHOP therapy. The patient responded well to chemotherapy with a substantial shrinkage in tumor burden and the disease remained localized. Herein, we present a rare case of primary ocular lymphoma, highlight the importance of early diagnosis, and review current treatment modalities.
    Sprache Englisch
    Erscheinungsdatum 2016-09-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2627639-2
    ISSN 2090-6579 ; 2090-6560
    ISSN (online) 2090-6579
    ISSN 2090-6560
    DOI 10.1155/2016/5612749
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Clostridium perfringens enterotoxin as a potential drug for intravesical treatment of bladder cancer.

    Gabig, Theodore G / Waltzer, Wayne C / Whyard, Terry / Romanov, Victor

    Biochemical and biophysical research communications

    2016  Band 478, Heft 2, Seite(n) 887–892

    Abstract: The current intravesical treatment of bladder cancer (BC) is limited to a few chemotherapeutics that show imperfect effectiveness and are associated with some serious complications. Thus, there is an urgent need for alternative therapies, especially for ... ...

    Abstract The current intravesical treatment of bladder cancer (BC) is limited to a few chemotherapeutics that show imperfect effectiveness and are associated with some serious complications. Thus, there is an urgent need for alternative therapies, especially for patients with high-risk non-muscle invasive (NMIBC). Clostridium perfringens enterotoxin (CPE), cytolytic protein binds to its receptors: claudin 3 and 4 that are expressed in epithelial cells. This binding is followed by rapid cell death. Claudin 4 is present in several epithelial tissue including bladder urothelium and its expression is elevated in some forms of BC. In addition to directly targeting BC cells, binding of CPE to claudins increases urothelium permeability that creates conditions for better accession of the tumor. Therefore, we evaluated CPE as a candidate for intravesical treatment of BC using a cellular model. We examined cytotoxicity of CPE against BC cells lines and 3D cultures of cells derived from surgical samples. To better elucidate cellular mechanisms, activated by CPE and to consider the use of CPE non-toxic fragment (C-CPE) for combination treatment with other drugs we synthesized C-CPE, compared its cytotoxic activity with CPE and examined claudin 4 expression and intracellular localization after C-CPE treatment. CPE induced cell death after 1 h in low aggressive RT4 cells, in moderately aggressive 5637 cells and in the primary 3D cultures of BC cells derived from NMIBC. Conversely, non-transformed urothelial cells and cells derived from highly aggressive tumor (T24) survived this treatment. The reason for this resistance to CPE might be the lower expression of CLDNs or their inaccessibility for CPE in these cells. C-CPE treatment for 48 h did not affect cell viability in tested cells, but declined expression of CLDN4 in RT4 cells. C-CPE increased sensitivity of RT4 cells to Mitommycin C and Dasatinib. To better understand mechanisms of this effect we examined expression and phosphorylation status of EphA2 and Src after C-CPE treatment and found changes in expression and phosphorylated status of these regulatory molecules. These observations show that after additional preclinical studies CPE and C-CPE in combinations with other drugs can be considered as a potential modalities for intravesical treatment of BC because of its ability to effectively destroy BC cells expressing claudin 4 and low toxicity against normal urothelium.
    Mesh-Begriff(e) Administration, Intravesical ; Antineoplastic Agents/isolation & purification ; Antineoplastic Agents/metabolism ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Claudin-4/genetics ; Claudin-4/metabolism ; Clostridium perfringens/chemistry ; Dasatinib/pharmacology ; Drug Evaluation, Preclinical ; Enterotoxins/biosynthesis ; Enterotoxins/isolation & purification ; Enterotoxins/pharmacology ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Mitomycin/pharmacology ; Models, Biological ; Molecular Targeted Therapy ; Protein Binding ; Receptor, EphA2/genetics ; Receptor, EphA2/metabolism ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/pharmacology ; Spheroids, Cellular/drug effects ; Spheroids, Cellular/metabolism ; Spheroids, Cellular/pathology ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/pathology ; Urothelium/drug effects ; Urothelium/metabolism ; Urothelium/pathology ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
    Chemische Substanzen Antineoplastic Agents ; CLDN4 protein, human ; Claudin-4 ; Enterotoxins ; Recombinant Proteins ; enterotoxin, Clostridium ; Mitomycin (50SG953SK6) ; Receptor, EphA2 (EC 2.7.10.1) ; src-Family Kinases (EC 2.7.10.2) ; Dasatinib (RBZ1571X5H)
    Sprache Englisch
    Erscheinungsdatum 2016--16
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2016.08.046
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 116: Hefte anzeigen Standort:
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  3. Artikel: Clostridium perfringens enterotoxin as a potential drug for intravesical treatment of bladder cancer

    Gabig, Theodore G / Terry Whyard / Victor Romanov / Wayne C. Waltzer

    Biochemical and biophysical research communications. 2016 Sept. 16, v. 478, no. 2

    2016  

    Abstract: The current intravesical treatment of bladder cancer (BC) is limited to a few chemotherapeutics that show imperfect effectiveness and are associated with some serious complications. Thus, there is an urgent need for alternative therapies, especially for ... ...

    Abstract The current intravesical treatment of bladder cancer (BC) is limited to a few chemotherapeutics that show imperfect effectiveness and are associated with some serious complications. Thus, there is an urgent need for alternative therapies, especially for patients with high-risk non-muscle invasive (NMIBC).Clostridium perfringens enterotoxin (CPE), cytolytic protein binds to its receptors: claudin 3 and 4 that are expressed in epithelial cells. This binding is followed by rapid cell death. Claudin 4 is present in several epithelial tissue including bladder urothelium and its expression is elevated in some forms of BC. In addition to directly targeting BC cells, binding of CPE to claudins increases urothelium permeability that creates conditions for better accession of the tumor. Therefore, we evaluated CPE as a candidate for intravesical treatment of BC using a cellular model.We examined cytotoxicity of CPE against BC cells lines and 3D cultures of cells derived from surgical samples. To better elucidate cellular mechanisms, activated by CPE and to consider the use of CPE non-toxic fragment (C-CPE) for combination treatment with other drugs we synthesized C-CPE, compared its cytotoxic activity with CPE and examined claudin 4 expression and intracellular localization after C-CPE treatment.CPE induced cell death after 1 h in low aggressive RT4 cells, in moderately aggressive 5637 cells and in the primary 3D cultures of BC cells derived from NMIBC. Conversely, non-transformed urothelial cells and cells derived from highly aggressive tumor (T24) survived this treatment. The reason for this resistance to CPE might be the lower expression of CLDNs or their inaccessibility for CPE in these cells. C-CPE treatment for 48 h did not affect cell viability in tested cells, but declined expression of CLDN4 in RT4 cells.C-CPE increased sensitivity of RT4 cells to Mitommycin C and Dasatinib. To better understand mechanisms of this effect we examined expression and phosphorylation status of EphA2 and Src after C-CPE treatment and found changes in expression and phosphorylated status of these regulatory molecules.These observations show that after additional preclinical studies CPE and C-CPE in combinations with other drugs can be considered as a potential modalities for intravesical treatment of BC because of its ability to effectively destroy BC cells expressing claudin 4 and low toxicity against normal urothelium.
    Schlagwörter alternative medicine ; bladder ; cell death ; cell viability ; Clostridium perfringens ; cytotoxicity ; drug therapy ; drugs ; enterotoxins ; epithelial cells ; epithelium ; patients ; permeability ; phosphorylation ; receptors ; urinary bladder neoplasms
    Sprache Englisch
    Erscheinungsverlauf 2016-0916
    Umfang p. 887-892.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2016.08.046
    Datenquelle NAL Katalog (AGRICOLA)

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    Verfügbar in ZB MED Bonn

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  4. Artikel ; Online: A claudin 3 and claudin 4-targeted Clostridium perfringens protoxin is selectively cytotoxic to PSA-producing prostate cancer cells.

    Romanov, Victor / Whyard, Terry C / Waltzer, Wayne C / Gabig, Theodore G

    Cancer letters

    2014  Band 351, Heft 2, Seite(n) 260–264

    Abstract: Prostate cancer is the second leading cause of non-cutaneous cancer-related death in males, and effective strategies for treatment of metastatic disease are currently limited. The tight junction proteins, claudin 3 and claudin 4, serve as cell-surface ... ...

    Abstract Prostate cancer is the second leading cause of non-cutaneous cancer-related death in males, and effective strategies for treatment of metastatic disease are currently limited. The tight junction proteins, claudin 3 and claudin 4, serve as cell-surface receptors for the pore-forming Clostridium perfringens enterotoxin [CPE]. Most prostate cancer cells overexpress claudin 3 and claudin 4, and claudins are aberrantly distributed over the plasma membrane, making these cells particularly sensitive to cytolysis by CPE. Prostate cancer cells secrete PSA locally that is proteolytically active; however, circulating PSA is inactivated via binding to protease inhibitors. To overcome systemic toxicity of CPE, a modified protoxin was constructed with a tethered ligand attached to the C-terminus connected by a flexible linker containing a PSA-specific protease cleavage site. This engineered protoxin selectively and efficiently lyses PSA-producing prostate cancer cells whereas CLDN3 and CLDN4 positive cells that do not express PSA are resistant to cytolysis.
    Mesh-Begriff(e) Amino Acid Sequence ; Cell Line, Tumor ; Claudin-3/genetics ; Claudin-3/metabolism ; Claudin-4/genetics ; Claudin-4/metabolism ; Cloning, Molecular ; Clostridium perfringens/metabolism ; Enterotoxins/genetics ; Enterotoxins/pharmacokinetics ; Enterotoxins/pharmacology ; Humans ; Kallikreins/biosynthesis ; Male ; Molecular Sequence Data ; Molecular Targeted Therapy ; Prostate-Specific Antigen/biosynthesis ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/pharmacokinetics ; Recombinant Fusion Proteins/pharmacology ; Transfection
    Chemische Substanzen CLDN3 protein, human ; CLDN4 protein, human ; Claudin-3 ; Claudin-4 ; Enterotoxins ; Recombinant Fusion Proteins ; enterotoxin, Clostridium ; KLK3 protein, human (EC 3.4.21.-) ; Kallikreins (EC 3.4.21.-) ; Prostate-Specific Antigen (EC 3.4.21.77)
    Sprache Englisch
    Erscheinungsdatum 2014-06-18
    Erscheinungsland Ireland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2014.06.009
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1177: Hefte anzeigen Standort:
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  5. Artikel: Clostridium perfringens enterotoxin elicits rapid and specific cytolysis of breast carcinoma cells mediated through tight junction proteins claudin 3 and 4.

    Kominsky, Scott L / Vali, Mustafa / Korz, Dorian / Gabig, Theodore G / Weitzman, Sigmund A / Argani, Pedram / Sukumar, Saraswati

    The American journal of pathology

    2004  Band 164, Heft 5, Seite(n) 1627–1633

    Abstract: Clostridium perfringens enterotoxin (CPE) induces cytolysis very rapidly through binding to its receptors, the tight junction proteins CLDN 3 and 4. In this study, we investigated CLDN 3 and 4 expression in breast cancer and tested the potential of CPE- ... ...

    Abstract Clostridium perfringens enterotoxin (CPE) induces cytolysis very rapidly through binding to its receptors, the tight junction proteins CLDN 3 and 4. In this study, we investigated CLDN 3 and 4 expression in breast cancer and tested the potential of CPE-mediated therapy. CLDN 3 and 4 proteins were detected in all primary breast carcinomas tested (n = 21) and, compared to normal mammary epithelium, were overexpressed in approximately 62% and 26%, respectively. Treatment of breast cancer cell lines in culture with CPE resulted in rapid and dose-dependent cytolysis exclusively in cells that expressed CLDN 3 and 4. Intratumoral CPE treatment of xenografts of T47D breast cancer cells in immunodeficient mice resulted in a significant reduction in tumor volume (P = 0.007), with accompanying necrosis. Necrotic reactions were also seen in three freshly resected primary breast carcinoma samples treated with CPE for 12 hours, while isolated primary breast carcinoma cells underwent rapid and complete cytolysis within 1 hour. Thus, expression of CLDN 3 and 4 sensitizes primary breast carcinomas to CPE-mediated cytolysis and emphasizes the potential of CPE in breast cancer therapy.
    Mesh-Begriff(e) Animals ; Blotting, Western ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Claudin-3 ; Claudin-4 ; Dose-Response Relationship, Drug ; Enterotoxins/metabolism ; Female ; Humans ; Immunohistochemistry ; Membrane Proteins/metabolism ; Mice ; Mice, SCID ; Necrosis ; Neoplasm Transplantation ; Tumor Cells, Cultured
    Chemische Substanzen CLDN3 protein, human ; CLDN4 protein, human ; Claudin-3 ; Claudin-4 ; Cldn3 protein, mouse ; Cldn4 protein, mouse ; Enterotoxins ; Membrane Proteins ; enterotoxin, Clostridium
    Sprache Englisch
    Erscheinungsdatum 2004-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/S0002-9440(10)63721-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: MOZ and MOZ-CBP cooperate with NF-kappaB to activate transcription from NF-kappaB-dependent promoters.

    Chan, Edward M / Chan, Rebecca J / Comer, Elisha M / Goulet, Robert J / Crean, Colin D / Brown, Zachary D / Fruehwald, Amy M / Yang, Zhenyun / Boswell, H Scott / Nakshatri, Harikrishna / Gabig, Theodore G

    Experimental hematology

    2007  Band 35, Heft 12, Seite(n) 1782–1792

    Abstract: Objective: Monocytic zinc finger (MOZ) maintains hematopoietic stem cells and, upon fusion to the coactivator CREB-binding protein (CBP), induces acute myeloid leukemia (AML). Leukemic stem cells in AML often exhibit excessive signal-dependent activity ... ...

    Abstract Objective: Monocytic zinc finger (MOZ) maintains hematopoietic stem cells and, upon fusion to the coactivator CREB-binding protein (CBP), induces acute myeloid leukemia (AML). Leukemic stem cells in AML often exhibit excessive signal-dependent activity of the transcription factor nuclear factor (NF)-kappaB. Because aberrant interaction between NF-kappaB and coactivators represents an alternative mechanism for enhancing NF-kappaB activity, we evaluated whether MOZ and MOZ-CBP cooperate with NF-kappaB to activate transcription from NF-kappaB-dependent promoters.
    Methods: The ability of MOZ, MOZ mutants, and MOZ-CBP to enhance expression of NF-kappaB-dependent promoters was tested in reporter studies. The interaction between MOZ and NF-kappaB was evaluated by both coimmunoprecipitation and glutathione S-transferase pulldown assays.
    Results: MOZ activates transcription from the NF-kappaB-dependent interleukin-8 promoter; interestingly, this effect is markedly enhanced by CBP. Although MOZ has less potent transcriptional activity than MOZ-CBP, both proteins cooperate with steroid receptor coactivator-1 to activate transcription. MOZ also induces multiple NF-kappaB-dependent viral promoters. Importantly, MOZ associates in a protein complex with the p65 subunit of NF-kappaB and interacts directly with p65 in vitro. Transcriptional activity of MOZ requires its C-terminal domain, which is absent from MOZ-CBP, indicating that the transcriptional activity of MOZ-CBP derives from its CBP sequence.
    Conclusions: MOZ interacts with the p65 subunit of NF-kappaB and enhances expression of NF-kappaB-dependent promoters. The more potent transcriptional activity of MOZ-CBP derives from its CBP sequence. Thus, interaction between NF-kappaB and MOZ-CBP may play an important role in the pathogenesis of certain acute myeloid leukemias.
    Mesh-Begriff(e) Base Sequence ; Cell Line ; DNA Primers ; Humans ; Immunoprecipitation ; Interleukin-8/genetics ; NF-kappa B/metabolism ; Oncogene Proteins, Fusion/physiology ; Promoter Regions, Genetic ; Transcription, Genetic
    Chemische Substanzen DNA Primers ; Interleukin-8 ; MOZ-CBP fusion protein, human ; NF-kappa B ; Oncogene Proteins, Fusion
    Sprache Englisch
    Erscheinungsdatum 2007-12
    Erscheinungsland Netherlands
    Dokumenttyp 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 185107-x
    ISSN 1873-2399 ; 0301-472X ; 0531-5573
    ISSN (online) 1873-2399
    ISSN 0301-472X ; 0531-5573
    DOI 10.1016/j.exphem.2007.07.015
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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