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           Search results for: CA 15-3 antibody, Monoclonal Antibodies, Host Mouse   

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#16421906   2007/02/27 Save this To Up

High-dose cyclophosphamide inhibition of humoral immune response to murine monoclonal antibody 3F8 in neuroblastoma patients: broad implications for immunotherapy.

The murine monoclonal antibody 3F8 mediates lysis of neuroblastoma (NB) by complement and leukocytes (including neutrophils) but is neutralized if human anti-mouse antibody (HAMA) forms. We assessed the impact on rapid HAMA formation of prior chemotherapy in NB patients.

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MOUSE ANTI BOVINE ROTAVIR Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon HIV1 integrase antibody, Shiga Toxin 1 antibody, M Shiga Toxin 2 antibody, M Cholera toxin antibody, M Clostridium botulinum D T Clostridum difficile toxi Clostridum difficile toxi

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#12202215   2002/08/30 Save this To Up

Lysine-independent ubiquitination of Epstein-Barr virus LMP2A.

Latent membrane protein 2A (LMP2A) of latent Epstein-Barr virus (EBV) specifically associates with HECT domain-containing Nedd4-family ubiquitin-protein ligases (E3s). Here we demonstrate that LMP2A is specifically ubiquitinated by the HECT domains of AIP4 and WWP2. Deletion and site-specific mutation of LMP2A indicates that LMP2A is ubiquitinated at its amino-terminus and is not ubiquitinated on lysine residues. LMP2A and LMP1, also encoded by EBV, are two of only four proteins that have been identified that are ubiquitinated at the amino-terminus, indicating that EBV may specifically target and utilize this host cell protein modification.

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Human Epstein-Barr Virus Mouse Epstein-Barr Virus Epstein Barr Virus VCA Ig Epstein Barr Virus VCA Ig Epstein Barr Virus VCA Ig HbcAg - Hepatitis B Viru HbcAg - Hepatitis B Viru HbcAg - Hepatitis B Viru Gag Polymerase (Retro Vir Recombinant Viral Antige Tick born encephalitis vi Rubella virus E1 mosaic r

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#9777956   1998/10/28 Save this To Up

Role of vascular endothelial growth factor in ovarian cancer: inhibition of ascites formation by immunoneutralization.

Ovarian cancer is characterized by the rapid growth of solid intraperitoneal tumors and large volumes of ascitic fluid. Vascular endothelial growth factor (VEGF) augments tumor growth by inducing neovascularization and may stimulate ascites formation by increasing vascular permeability. We examined the role of VEGF in ovarian carcinoma using in vivo models in which intraperitoneal or subcutaneous tumors were induced in immunodeficient mice using the human ovarian carcinoma cell line SKOV-3. After tumor engraftment (7 to 10 days), some mice were treated with a function-blocking VEGF antibody (A4.6.1) specific for human VEGF. A4.6.1 significantly (P < 0.05) inhibited subcutaneous SKOV-3 tumor growth compared with controls. However, tumor growth resumed when A4.6.1 treatment was discontinued. In mice bearing intraperitoneal tumors (IP mice), ascites production and intraperitoneal carcinomatosis were detected 3 to 7 weeks after SKOV-3 inoculation. Importantly, A4.6.1 completely inhibited ascites production in IP mice, although it only partially inhibited intraperitoneal tumor growth. Tumor burden was variable in A4.6.1-treated IP mice; some had minimal tumor, whereas in others tumor burden was similar to that of controls. When A4.6.1 treatment was stopped, IP mice rapidly (within 2 weeks) developed ascites and became cachectic. These data suggest that in ovarian cancer, tumor-derived VEGF is obligatory for ascites formation but not for intraperitoneal tumor growth. Neutralization of VEGF activity may have clinical application in inhibiting malignant ascites formation in ovarian cancer.

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Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Mouse Vascular Endothelia Recombinant Human Vascula Epidermal Growth Factor ( Epidermal Growth Factor ( Human Insulin-like Growth Human Insulin-like Growth

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