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

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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.
Brian H Kushner, Irene Y Cheung, Kim Kramer, Shakeel Modak, Nai-Kong V Cheung

1398 related Products with: High-dose cyclophosphamide inhibition of humoral immune response to murine monoclonal antibody 3F8 in neuroblastoma patients: broad implications for immunotherapy.

100ul0.2 mg100ug100ug200 ug0.25 mg100ug Lyophilized1 ml100 50 UG100ug Lyophilized1 mg

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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.
Masato Ikeda, Akiko Ikeda, Richard Longnecker

1322 related Products with: Lysine-independent ubiquitination of Epstein-Barr virus LMP2A.

96/kit96/kit5ug2ug96/kit2100 100100ug Lyophilized100 6 ml Ready-to-use 100 ml

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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.
S Mesiano, N Ferrara, R B Jaffe

2254 related Products with: Role of vascular endothelial growth factor in ovarian cancer: inhibition of ascites formation by immunoneutralization.

5ug2ug2ug2ug96T2ug x 202ug2ug2 Pieces/Box10ug100.00 ug

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Expression of hybrid Ia molecules on the cell surface of reticulum cell sarcomas that are undetectable on host SJL/J lymphocytes.

SJL/J (H-2 (8)) lymphocytes, primed in vitro against primary, cultured, and transplantable syngeneic reticulum cell sarcomas (RCS) were found to recognize and bind to the tumor without subsequent cytolysis. Additional data showed that the recognition was also directed against Ia molecules of the H-2(d), but not H-2(k), haplotype. Normal spleen cells of DBA/2, B 10.D2, and B 10.OL mice were bound, whereas those of CBA, B 10.BR, B 10.A, B 10.GD, and D2.GD were not. Furthermore, the Ia molecules were in the form of a hybrid, because spleen cells from F(1) progeny of a B10.A and a B10.GD parent were recognized and bound as effectively as the RCS. Recognition was not restricted solely to the H-2(d) haplotype. Spleen cells from B10.S(9R) mice were also significantly bound. This result suggested that the RCS expresses a hybrid Ia molecule containing a beta-chain of the H-2(8) haplotype. Recognition of this hybrid Ia molecule by the host resulted in a cross- reactive recognition of H-2(d) specificities. Further analysis revealed that the RCS express on their cell surface an alpha-chain of the hybrid Ia molecule which is involved in host anti-tumor recognition. Preincubation of the RCS with monoclonal antibody directed against the Ia.7 specificity on the alpha-chain could block lymphocyte-to-tumor cell binding. The blocking activity could be removed by preabsorption of the antibody on the RCS, as well as normal Ia.7-bearing lymphocytes, but not on lymphocytes that do not express Ia.7, such as SJL/J. The data suggest that the hybrid Ia molecules expressed on the RCS, and recognized by tumor-primed syngeneic lymphocytes, are composed of both a syngeneic and an alien chain. The component alien to the SJL/J host is the Ia.7-bearing alpha-chain. Normal SJL/J cells synthesize but do not express the beta-chain. In the RCS, however, alien alpha-chain synthesis permits expression of the syngeneic beta-chain in the form of a hybrid Ia molecule.
S M Wilbur, B Bonavida

1051 related Products with: Expression of hybrid Ia molecules on the cell surface of reticulum cell sarcomas that are undetectable on host SJL/J lymphocytes.

100 ug0.25 mL400 ug0.1ml (1mg/ml)0.2 mL100 ug1 mg1.5 x 10^6 cells400 ug

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