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           Search results for: Mouse Anti-Human EGF Antibodies    

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#17082181   2006/12/25 Save this To Up

Epidermal growth factor receptor (EGFR) antibody down-regulates mutant receptors and inhibits tumors expressing EGFR mutations.

Activating mutations in the kinase domain of the EGF receptor have been reported in non-small cell lung cancer. The majority of tumors expressing these mutants are sensitive to ATP mimetics that inhibit the EGFR tyrosine kinase. The effect of antibodies that bind to the ectodomain of the receptor is less clear. We report herein the effects and mechanisms of action of the antibody cetuximab in lung cancer cells that naturally express receptor mutations and in ErbB-null 32D hematopoietic cells transfected with mutant EGFR. Treatment with cetuximab down-regulated EGFR levels and inhibited cell growth both in vitro and in vivo. This was associated with inhibition of ligand-independent EGFR signaling. These effects were seen in 32D cells arguing the growth inhibitory action was not because of the blockade of autocrine ligand action. Both antibody-induced EGFR down-regulation and inhibition of growth required receptor dimerization as monovalent Fab fragments only eliminated receptor levels or reduced cell proliferation in the presence of antihuman IgG. Finally, cetuximab inhibited growth of H1975 lung cancer cells and xenografts, which expressed L858R/T790M EGFR and were resistant to EGFR tyrosine kinase inhibitors. These data suggest that cetuximab is an effective therapy against mutant EGFR-expressing cancer cells and thus can be considered in combination with other anti-EGFR molecules.

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Epidermal Growth Factor ( Epidermal Growth Factor ( Epidermal Growth Factor ( Epidermal Growth Factor ( Human Epidermal Growth Fa EGFR (Phospho Ser1070) An EGFR (Phospho Tyr1092) An Androgen Receptor (Phosph Androgen Receptor (Phosph EGFR (Phospho Thr678) Ant EGFR (Phospho Thr693) Ant EGFR(Phospho Tyr1172) Ant

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#16420580   2006/01/19 Save this To Up

Function-blocking antithrombospondin-1 monoclonal antibodies.

Thrombospondin-1 (TSP-1) has been implicated in many different processes based in part on inhibitory activities of anti-TSP-1 monoclonal antibodies (mAbs).

1057 related Products with: Function-blocking antithrombospondin-1 monoclonal antibodies.

VEGF (Mouse, Monoclonal, VEGF-C (Rat, Polyclonal, Anti AGO2 Human, Monoclon Anti PIWIL1, Monoclonal A Anti AGO2 Mouse, Monoclon Anti Ago1, Monoclonal Ant Anti Human AGO3, Monoclon Viral antibodies, anti-R Signal Transduction Anti Signal Transduction Anti MONOBODIES (Monoclonal An MONOBODIES (Monoclonal An

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#8814698   1996/10/10 Save this To Up

Anti-idiotypic response to antigrowth factor receptor monoclonal antibodies.

The immunogenicity of the idiotypic portions of two antigrowth factor receptor monoclonal antibodies (MAbs) was studied. Immunisation of allogeneic but not syngeneic mice with antihuman epidermal growth factor receptor (EGF-R) MAb MINT5 or anti-HER-2/neu MGR6 MAb elicited a detectable titre of circulating antibodies, particularly when the MAb was coupled with the keyhole limpet haemocyanin and administered together with Freund's adjuvant. The anti-Ab1 response to MAb MINT5 was slightly delayed as compared with the response obtained with MAb MGR6 and was mainly directed to the variable regions. In both cases, all anti-Ab1-positive sera specifically competed with the binding of homologous radiolabelled Ab1 to the relevant EGF-R+ or HER-2/neu+ target cells. Fusion of splenocytes from MINT5-immunised animals failed to produce MAb, whereas cell fusion was successful in generating a paratope-related MAb in the case of MGR6. The anti-MGR6 MAb-produced IdM6.4 inhibited the binding of MAb MGR6 on breast carcinoma cells, suggesting that it recognises an idiotope in or near the antigen combining site, and can be considered useful in the identification and purification of the Ab1 or its derivatives. We analysed whether a possible recognition of murine EGF-R by MAb MINT5 or a mimicry of EGF by the MAb idiotype prevented or delayed the development of an idiotypic cascade in mice. MINT5 inhibited human and murine EGF binding to the human EGF-R, whereas the anti-Ab1 response competed with MINT5 but not with murine EGF binding to A431 human epidermoid carcinoma cells. Moreover, MINT5 did not recognise the murine EGF-R. In a phase I clinical study, no detectable levels of human antimouse antibody response were observed in 5 of the 6 treated cancer patients. The ability of MAb MINT5 to block human EGF-R function, together with its low immunogenicity in patients, raise the possibility of its application in carcinoma immunotherapy.

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Rat monoclonal anti mouse Goat Anti-Human TEM8 Anth Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse

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