CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Autoantibodies against muscarinic acetylcholine receptors in breast cancer. Its role in tumor angiogenesis.
Autor/es:
LOMBARDI G,; DE LA TORRE EULALIA; FISZMAN G,; NEGRONI MARIA PÍA; AZAR ME,; CRESTA MORGADO C,; SALES ME
Lugar:
Buenos Aires
Reunión:
Congreso; 1st French-Argentine Immunology Congress; 2010
Institución organizadora:
Sociedad Argentina de Inmunología-Sociedad Francesa de Inmunologia
Resumen:
We had demonstrated that autoantibodies from the IgG subtype, present in the sera of breast cancer patients activate muscarinic acetylcholine receptors (mAChR). These receptors are expressed in human breast tumors and in the line, MCF-7, derived from a human mammary adenocarcinoma. Both, the muscarinic agonist carbachol (CARB) and the IgG from patients at T1N0Mx stage (tumor size <2cm, without lymph node metastases) stimulate the proliferation and migration in tumor cells but not in normal in human breast cells, MCF-10A. Angiogenesis is a central step in tumor progression because it promotes tumor growth and metastatic spread, so we investigate the role of CARB and T1N0Mx-IgG in the angiogenic response induced by MCF-7 cells. By western blot, we demonstrated that MCF-7 cells but not MCF- 10A cells express vascular endothelial growth factor A (VEGF-A) (1.01E}0.01 relative O.D; n=3). Treatment with CARB (10-9M) for 1 h increased VEGF-A expression (2.64E}0.26; p<0.001 vs. cell without treatment) and preincubation with the nonselective antagonist atropine (AT) (10-6M) reverted this effect (1.67E}0.17; n=3). In an vivo angiogenesis assay in nude female mice, we found that MCF-7 cells stimulated neovascularization (vessels N‹/mm2) (control: 1.12E}0.2; n=3; MCF-7: 1.86E}0.30; n=15 p<0.05 vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. N‹/mm2) (control: 1.12E}0.2; n=3; MCF-7: 1.86E}0.30; n=15 p<0.05 vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. N‹/mm2) (control: 1.12E}0.2; n=3; MCF-7: 1.86E}0.30; n=15 p<0.05 vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. n=3). In an vivo angiogenesis assay in nude female mice, we found that MCF-7 cells stimulated neovascularization (vessels N‹/mm2) (control: 1.12E}0.2; n=3; MCF-7: 1.86E}0.30; n=15 p<0.05 vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. N‹/mm2) (control: 1.12E}0.2; n=3; MCF-7: 1.86E}0.30; n=15 p<0.05 vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. N‹/mm2) (control: 1.12E}0.2; n=3; MCF-7: 1.86E}0.30; n=15 p<0.05 vs. control), whereas MCF-10A were not angiogenic (1.46E}0.38; n=10). When MCF-7 cells were previously treated with CARB (10- 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. 9M or 10-10M) an increase in the neovascular response was observed (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the neovascular response in patients with breast cancer. (2.82E}0.55; n=14 p<0.001 vs. control or 3.50E}0.74; n=10 p<0.001 vs. control). AT reduced these effects (1.42E}0.3; p<0.05). We also observed that pretreatment of cells with T1N0Mx-IgG produced and angiogenic effect that was stronger than that of CARB (3.24E}0.24; p<0.01 vs. CARB) and was also decreased in the presence of AT (2.06E}0.42; p<0.001 vs. IgG-T1N0Mx). We conclude that mAChR activation either by CARB or by auto-Abs may promote the ne