Zobrazeno 1 - 10
of 48
pro vyhledávání: '"H. Terry Wepsic"'
Autor:
H. Terry Wepsic, Neil Hoa
Publikováno v:
International Immunopharmacology. 114:109491
Paraptosis is the programmed cell death pathway that leads to cellular necrosis. Manystudies have shown that prolonged paraptosis activation improves tumorimmunogenicity; this treatment reproduces the vaccinating effects of mM-CSFtransduced cells. In
Autor:
Neil Hoa, H. Terry Wepsic, Christina Delgado, Gerald Vandeusen, Patric M. Schiltz, Martin R. Jadus, Michael P. Myers, Linda L. Callahan, Jian Gang Zhang
Publikováno v:
Laboratory Investigation. 87:115-129
In this study, human monocytes/macrophages were observed to kill human U251 glioma cells expressing membrane macrophage colony-stimulating factor (mM-CSF) via a swelling and vacuolization process called paraptosis. Human monocytes responded to the mM
Autor:
Neil Hoa, H. Terry Wepsic, Hideho Okada, Martin R. Jadus, Boris Minev, Junichi Eguchi, Wenxue Ma, Carol A. Kruse, Stephanie Schroter, Habib Fakhrai, Christina Delgado, Jian Gang Zhang, German G. Gomez
Publikováno v:
Clinical Cancer Research. 13:566-575
Purpose: Allogeneic glioma cell lines that are partially matched to the patient at class I human leukocyte antigen (HLA) loci and that display tumor-associated antigens (TAA) or antigenic precursors [tumor antigen precursor proteins (TAPP)] could be
Autor:
Samuel Chong, Tetyana Khomenko, Animesh Petkar, Chirag Shah, Neil Hoa, Jing-Li Zhuang, Christina Delgado, Seema Vohra, Jian Gang Zhang, Reza Alipanah, H. Terry Wepsic, Andre Obenaus, Edward W. B. Jeffes, Jessie Liu, Martin R. Jadus, Tuong-Vi Nguyen, Brandon A. Knight, Ramon Sanchez, Sakineh Khalaghizadeh
Publikováno v:
The Journal of Immunology. 174:2533-2543
Combining a T9/9L glioma vaccine, expressing the membrane form of M-CSF, with a systemic antiangiogenic drug-based therapy theoretically targeted toward growth factor receptors within the tumor’s vasculature successfully treated >90% of the rats be
Autor:
Ramon Sanchez, Christina Delgado, Martin R. Jadus, H. Terry Wepsic, Christopher C. Williams, Ronald C. Kim, Yijun Chen, Qingcheng Xu, Michael T. Kleinman, Edward W. B. Jeffes, Thomas Douglass, Neary Arpajirakul, Qinghong Dan
Publikováno v:
Blood. 100:1373-1380
Cloned T9-C2 glioma cells transfected with membrane macrophage colony-stimulating factor (mM-CSF) never formed subcutaneous tumors when implanted into Fischer rats, whereas control T9 cells did. The T9-C2 cells were completely killed within 1 day thr
Publikováno v:
The Journal of Immunology. 163:5544-5551
We investigated the ability of Fischer rat T9 glioblastoma cells transduced with cDNA genes for the secreted (s) or membrane-associated (m) isoform of M-CSF to elicit an antitumor response when implanted into syngeneic animals. Intracranial (i.c.) im
Autor:
Maria D. Avina, Martin R. Jadus, H. Terry Wepsic, Christopher C. Williams, N.Sarena Zeineddine
Publikováno v:
Immunology Letters. 70:63-68
Malignant rat T9 glioma cells retrovirally transduced with the membrane form of macrophage colony stimulating factor (mM-CSF) were killed by bone marrow derived macrophages in 24 h cytotoxicity assays. Prostaglandin E2 (PGE) and interleukin-10 (IL10)
Autor:
Martin R. Jadus, Christopher C. Williams, Maria D. Avina, Mann Ly, Suzanna Kim, Ying Liu, Ryan Narasaki, Clifford A. Lowell, H. Terry Wepsic
Publikováno v:
The Journal of Immunology. 160:361-368
Rat T9 glioma cells transfected with the gene for the membrane isoform of macrophage-CSF (mM-CSF) but not for the secreted isoform of M-CSF were directly killed by bone marrow-derived macrophages. Macrophage-mediated cytolysis of the mM-CSF-transfect
Publikováno v:
Developmental & Comparative Immunology. 19:261-277
The neonatal spleen:myeloma hybridoma cell, NBXFO, with immunosuppressive properties supported rodent hematopoietic colony formation. We identified this hybridoma to be an undifferentiated fibroblast that produced macrophage colony-stimulating factor
Publikováno v:
Immunology Letters. 45:143-148
Cultured murine bone marrow macrophages specifically bound 125I-labeled beta-endorphin. Binding was displaceable by 100 times molar excess of full-length beta-endorphin but was insensitive to the opioid receptor antagonist, naloxone. Binding was inhi