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Santa Cruz Biotechnology antibodies to the phosphorylated egfr (tyrosine 1173)
Immunohistochemistry analysis of U87MG.Δ2–7 xenografts treated with AG1478. U87MG.Δ2–7 xenografts were collected 30 min after injection of vehicle (Left) or AG1478 (1,000 μg) (Right) as described in Fig. 1. Frozen sections were cut and stained for expression of total <t>EGFR,</t> <t>phosphorylated</t> EGFR, and phosphorylated Akt.
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Santa Cruz Biotechnology rabbit polyclonal igg against egfr
Figure 1. Immunohistochemical analysis of <t>EGFR</t> protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.
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Figure 1. Immunohistochemical analysis of <t>EGFR</t> protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.
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Figure 1. Immunohistochemical analysis of <t>EGFR</t> protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.
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Figure 1. Immunohistochemical analysis of <t>EGFR</t> protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.
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Figure 1. Immunohistochemical analysis of <t>EGFR</t> protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.
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Santa Cruz Biotechnology polyclonal anti egfr sc03
Figure 1. Immunohistochemical analysis of <t>EGFR</t> protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.
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Image Search Results


Immunohistochemistry analysis of U87MG.Δ2–7 xenografts treated with AG1478. U87MG.Δ2–7 xenografts were collected 30 min after injection of vehicle (Left) or AG1478 (1,000 μg) (Right) as described in Fig. 1. Frozen sections were cut and stained for expression of total EGFR, phosphorylated EGFR, and phosphorylated Akt.

Journal:

Article Title: Antitumor efficacy of cytotoxic drugs and the monoclonal antibody 806 is enhanced by the EGF receptor inhibitor AG1478

doi: 10.1073/pnas.2036503100

Figure Lengend Snippet: Immunohistochemistry analysis of U87MG.Δ2–7 xenografts treated with AG1478. U87MG.Δ2–7 xenografts were collected 30 min after injection of vehicle (Left) or AG1478 (1,000 μg) (Right) as described in Fig. 1. Frozen sections were cut and stained for expression of total EGFR, phosphorylated EGFR, and phosphorylated Akt.

Article Snippet: Sections were cut, fixed in acetone for 10 min, and stained with antibodies to the EGFR (sc-03), phosphorylated EGFR (tyrosine 1173), and phosphorylated Akt (serine 473), all purchased from Santa Cruz Biotechnology.

Techniques: Immunohistochemistry, Injection, Staining, Expressing

In vitro effects of AG1478 and mAb 806. (A) Antiproliferative activity of AG1478 and mAb 806. A431 and U87MG.Δ2–7 cells were treated in vitro with AG1478 (6 μM) or mAb 806 (10 μg/ml) alone or in combination, and the data were expressed as percentage inhibition of cell growth. (Bars = SD.) (B) Effect of AG1478 treatment on antibody reactivity. A431 cells were treated for 10 min with AG1478 at the doses indicated, after which cells were lysed and the amount of EGFR was recognized by mAb 806 or 528 quantified by ELISA. Data are expressed as the percentage increase in antibody reactivity. (Bars = SD.)

Journal:

Article Title: Antitumor efficacy of cytotoxic drugs and the monoclonal antibody 806 is enhanced by the EGF receptor inhibitor AG1478

doi: 10.1073/pnas.2036503100

Figure Lengend Snippet: In vitro effects of AG1478 and mAb 806. (A) Antiproliferative activity of AG1478 and mAb 806. A431 and U87MG.Δ2–7 cells were treated in vitro with AG1478 (6 μM) or mAb 806 (10 μg/ml) alone or in combination, and the data were expressed as percentage inhibition of cell growth. (Bars = SD.) (B) Effect of AG1478 treatment on antibody reactivity. A431 cells were treated for 10 min with AG1478 at the doses indicated, after which cells were lysed and the amount of EGFR was recognized by mAb 806 or 528 quantified by ELISA. Data are expressed as the percentage increase in antibody reactivity. (Bars = SD.)

Article Snippet: Sections were cut, fixed in acetone for 10 min, and stained with antibodies to the EGFR (sc-03), phosphorylated EGFR (tyrosine 1173), and phosphorylated Akt (serine 473), all purchased from Santa Cruz Biotechnology.

Techniques: In Vitro, Activity Assay, Inhibition, Enzyme-linked Immunosorbent Assay

Figure 1. Immunohistochemical analysis of EGFR protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.

Journal: Oncology letters

Article Title: Epidermal growth factor receptor expression and gene copy number analysis in gastric carcinoma samples from Chinese patients.

doi: 10.3892/ol.2015.3875

Figure Lengend Snippet: Figure 1. Immunohistochemical analysis of EGFR protein expression in GC. (A) GC exhibiting weak EGFR expression. (B) GC exhibiting EGFR overexpres sion (magnification, x200). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.

Article Snippet: Immunohistochemical staining of samples was performed using rabbit polyclonal IgG against EGFR (anti‐EGFR; 1:50; sc03; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) and avidin-biotin-peroxidase techniques (VECTASTAIN® Elite ABC kit; Vector Laboratories, Inc., Burlingame, CA, USA).

Techniques: Immunohistochemical staining, Expressing

Figure 2. Fluorescence in situ hybridization analysis of EGFR gene copy number in GC. EGFR produced a red signal and chromosome 7 centromere produced a green signal; nuclei were stained by DAPI which appeared as a blue signal. (A) GC cells exhibiting gene amplification demonstrated a formation of clusters with numerous signals for EGFR. (B) GC cells exhibiting increased EGFR copy number due to chromosome 7 polysomy (magnification, x100). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.

Journal: Oncology letters

Article Title: Epidermal growth factor receptor expression and gene copy number analysis in gastric carcinoma samples from Chinese patients.

doi: 10.3892/ol.2015.3875

Figure Lengend Snippet: Figure 2. Fluorescence in situ hybridization analysis of EGFR gene copy number in GC. EGFR produced a red signal and chromosome 7 centromere produced a green signal; nuclei were stained by DAPI which appeared as a blue signal. (A) GC cells exhibiting gene amplification demonstrated a formation of clusters with numerous signals for EGFR. (B) GC cells exhibiting increased EGFR copy number due to chromosome 7 polysomy (magnification, x100). EGFR, epidermal growth factor receptor; GC, gastric carcinoma.

Article Snippet: Immunohistochemical staining of samples was performed using rabbit polyclonal IgG against EGFR (anti‐EGFR; 1:50; sc03; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) and avidin-biotin-peroxidase techniques (VECTASTAIN® Elite ABC kit; Vector Laboratories, Inc., Burlingame, CA, USA).

Techniques: Fluorescence, In Situ Hybridization, Produced, Staining, Amplification

Figure 3. Survival curves constructed using the Kaplan‑Meier method and log‑rank test. (A) Survival curves revealed that GC patients exhibiting weak EGFR expression (1+) and EGFR overexpression (2+) possessed an unfavorable prognosis compared with EGFR‑negative GC patients (0). (B) Survival curves revealed that GC patients demonstrating increased EGFR gene copy numbers, as detected by FISH, possessed an unfavorable prognosis. GC, gastric carcinoma; EGFR, epidermal growth factor receptor; FISH, fluorescence in situ hybridization; Cum, cumulative.

Journal: Oncology letters

Article Title: Epidermal growth factor receptor expression and gene copy number analysis in gastric carcinoma samples from Chinese patients.

doi: 10.3892/ol.2015.3875

Figure Lengend Snippet: Figure 3. Survival curves constructed using the Kaplan‑Meier method and log‑rank test. (A) Survival curves revealed that GC patients exhibiting weak EGFR expression (1+) and EGFR overexpression (2+) possessed an unfavorable prognosis compared with EGFR‑negative GC patients (0). (B) Survival curves revealed that GC patients demonstrating increased EGFR gene copy numbers, as detected by FISH, possessed an unfavorable prognosis. GC, gastric carcinoma; EGFR, epidermal growth factor receptor; FISH, fluorescence in situ hybridization; Cum, cumulative.

Article Snippet: Immunohistochemical staining of samples was performed using rabbit polyclonal IgG against EGFR (anti‐EGFR; 1:50; sc03; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) and avidin-biotin-peroxidase techniques (VECTASTAIN® Elite ABC kit; Vector Laboratories, Inc., Burlingame, CA, USA).

Techniques: Construct, Expressing, Over Expression, Fluorescence, In Situ Hybridization