Journal: World Journal of Surgical Oncology

Article Title: E-cadherin expression phenotypes associated with molecular subtypes in invasive non-lobular breast cancer: evidence from a retrospective study and meta-analysis

doi: 10.1186/s12957-017-1210-8

Figure Lengend Snippet: Clinic and pathological characteristics and IHC results of 156 early stage IDCs

Article Snippet: Anti-E-cad (clone 4A2C7), anti-ER (clone SP1), anti-progesterone receptor (PR) (clone SP2), anti-human epidermal growth factor receptor 2 (HER2) (clone EP3), and anti-Ki67 (clone MIB-1) mouse monoclonal antibodies (Maxim Biotech, Inc., Fuzhou, China) were used for the IHC detection of E-cad, ER, PR, HER2, and Ki67 expression.

Techniques:

Journal: World Journal of Surgical Oncology

Article Title: E-cadherin expression phenotypes associated with molecular subtypes in invasive non-lobular breast cancer: evidence from a retrospective study and meta-analysis

doi: 10.1186/s12957-017-1210-8

Figure Lengend Snippet: Expression of E-cad, ER, PR, HER2, and Ki67 in early stage IDC. a ER positive expression in nucleus of IDC. b ER negative expression in nucleus of IDC. c PR positive expression in nucleus of IDC. d PR negative expression in nucleus of IDC. e HER2 positive expression in membrane of IDC. f HER2 negative expression in membrane of IDC. g Ki67 positive expression in nucleus of IDC. h Ki67 negative expression in nucleus of IDC. i E-cad positive expression in membrane of IDC. j E-cad negative/low expression in membrane of IDC. Bar = 100 μm

Article Snippet: Anti-E-cad (clone 4A2C7), anti-ER (clone SP1), anti-progesterone receptor (PR) (clone SP2), anti-human epidermal growth factor receptor 2 (HER2) (clone EP3), and anti-Ki67 (clone MIB-1) mouse monoclonal antibodies (Maxim Biotech, Inc., Fuzhou, China) were used for the IHC detection of E-cad, ER, PR, HER2, and Ki67 expression.

Techniques: Expressing, Membrane

Journal: World Journal of Surgical Oncology

Article Title: E-cadherin expression phenotypes associated with molecular subtypes in invasive non-lobular breast cancer: evidence from a retrospective study and meta-analysis

doi: 10.1186/s12957-017-1210-8

Figure Lengend Snippet: E-cadherin expression in early stage IDCs

Article Snippet: Anti-E-cad (clone 4A2C7), anti-ER (clone SP1), anti-progesterone receptor (PR) (clone SP2), anti-human epidermal growth factor receptor 2 (HER2) (clone EP3), and anti-Ki67 (clone MIB-1) mouse monoclonal antibodies (Maxim Biotech, Inc., Fuzhou, China) were used for the IHC detection of E-cad, ER, PR, HER2, and Ki67 expression.

Techniques: Expressing

Journal: World Journal of Surgical Oncology

Article Title: E-cadherin expression phenotypes associated with molecular subtypes in invasive non-lobular breast cancer: evidence from a retrospective study and meta-analysis

doi: 10.1186/s12957-017-1210-8

Figure Lengend Snippet: Characteristics of the included studies in the meta-analysis

Article Snippet: Anti-E-cad (clone 4A2C7), anti-ER (clone SP1), anti-progesterone receptor (PR) (clone SP2), anti-human epidermal growth factor receptor 2 (HER2) (clone EP3), and anti-Ki67 (clone MIB-1) mouse monoclonal antibodies (Maxim Biotech, Inc., Fuzhou, China) were used for the IHC detection of E-cad, ER, PR, HER2, and Ki67 expression.

Techniques: Expressing

Journal: World Journal of Surgical Oncology

Article Title: E-cadherin expression phenotypes associated with molecular subtypes in invasive non-lobular breast cancer: evidence from a retrospective study and meta-analysis

doi: 10.1186/s12957-017-1210-8

Figure Lengend Snippet: Comparison of E-cad expression loss between TNBC and luminal subtype and HER2-enriched tumors. TNBC triple-negative breast cancer

Article Snippet: Anti-E-cad (clone 4A2C7), anti-ER (clone SP1), anti-progesterone receptor (PR) (clone SP2), anti-human epidermal growth factor receptor 2 (HER2) (clone EP3), and anti-Ki67 (clone MIB-1) mouse monoclonal antibodies (Maxim Biotech, Inc., Fuzhou, China) were used for the IHC detection of E-cad, ER, PR, HER2, and Ki67 expression.

Techniques: Comparison, Expressing

Journal: World Journal of Surgical Oncology

Article Title: E-cadherin expression phenotypes associated with molecular subtypes in invasive non-lobular breast cancer: evidence from a retrospective study and meta-analysis

doi: 10.1186/s12957-017-1210-8

Figure Lengend Snippet: Pooled analysis of E-cad expression between molecular subtypes of breast cancer

Article Snippet: Anti-E-cad (clone 4A2C7), anti-ER (clone SP1), anti-progesterone receptor (PR) (clone SP2), anti-human epidermal growth factor receptor 2 (HER2) (clone EP3), and anti-Ki67 (clone MIB-1) mouse monoclonal antibodies (Maxim Biotech, Inc., Fuzhou, China) were used for the IHC detection of E-cad, ER, PR, HER2, and Ki67 expression.

Techniques: Expressing

Journal: The Journal of Experimental Medicine

Article Title: Lipid mediators in innate immunity against tuberculosis: opposing roles of PGE 2 and LXA 4 in the induction of macrophage death

doi: 10.1084/jem.20080767

Figure Lengend Snippet: EP2 mediates PGE 2 -dependent protection against cationic mitochondrial dye release. Data are presented as means ± SE. (A) EP1, EP2, EP3, and EP4 are constitutively expressed in human Mφ. Their expression is not increased by either H37Ra or H37Rv infection. (B) EP2 −/− Mφ fail to respond to PGE 2 by down-regulating DiCO 6 (3) release from the mitochondria infected with H37Rv (top) or with H37Ra (bottom), indicating that EP2 mediates the protective function of PGE 2 . Mφ from EP1, EP3, and EP4 −/− mice were equally responsive to 1 μM PGE 2 (*, statistically significant; P < 0.01; n = 5). (C) The cAMP-dependent PKA inhibitor KT5720 abrogates inhibition of mitochondrial cationic dye release by PGE 2 (black columns; P < 0.01; n = 3). Addition of KT5720 to H37Ra-infected (MOI 10:1) Mφ enhanced Mφ necrosis (gray columns; *, P < 0.01; n = 3). (D) The PI3K inhibitor LY294002 does not abrogate inhibition of mitochondrial cationic dye release by PGE 2 (not significant; n = 3). In all studies, n represents the number of independent experiments.

Article Snippet: Rabbit anti-EP1, -EP2, -EP3, and -EP4 receptor antibodies (1:200; Cayman Chemical) were used to detect EP1, EP2, EP3, and EP4 receptor protein.

Techniques: Expressing, Infection, Inhibition

Journal: Allergy, Asthma & Immunology Research

Article Title: Effect of Prostaglandin E2 on Vascular Endothelial Growth Factor Production in Nasal Polyp Fibroblasts

doi: 10.4168/aair.2013.5.4.224

Figure Lengend Snippet: (A) Effect of EP receptor agonists on VEGF production by NPDFs. CAY10580 increased VEGF production significantly; however, no other EP receptor agonist showed an increase in VEGF production. (B) The effect of EP receptor antagonists on VEGF production. AH23848 decreased VEGF production markedly, but no other EP receptor antagonist elicited a decrease in VEGF production. (C) The effect of PGE2 combined with an EP4 receptor agonist or antagonist on VEGF production by immunofluorescence staining. Strong immunoreactivity for VEGF was observed in NPDF cells treated with PGE2 and CAY10580 by confocal laser scanning microscopy. NPDFs treated with PGE2 and EP4 receptor agonists showed blue-stained nuclei with a greenish cytoplasm (representative of four independent experiments; original magnification, ×200). The means±SE of data from six experiments are shown. * P <0.05 vs. control and † P <0.05 vs. PGE2. PGE2, prostaglandin E2; EP, E-prostanoid; Sulprostone, EP1/3 receptor agonist; Butaprost, EP2 receptor agonist; CAY10580, EP4 receptor agonist; SC51322, EP1 receptor antagonist; AH6809, EP2 receptor antagonist; L-798106, EP3 receptor antagonist; AH23848, EP4 receptor antagonist; VEGF, vascular endothelial growth factor; NPDFs, nasal polyp-derived fibroblasts; SE, standard error.

Article Snippet: PGE2, the protein kinase A (PKA) inhibitor KT5720, the EP1/3 receptor agonist sulprostone, the EP2 receptor agonist butaprost, the EP4 receptor agonist CAY 10580, the EP1 receptor antagonist SC51322, the EP2 receptor antagonist AH6809, the EP3 receptor antagonist L798106, and the EP4 receptor antagonist AH23848 were obtained from Cayman Chemical (Ann Arbor, MI, USA).

Techniques: Immunofluorescence, Staining, Confocal Laser Scanning Microscopy, Control, Derivative Assay

Journal: Allergy, Asthma & Immunology Research

Article Title: Effect of Prostaglandin E2 on Vascular Endothelial Growth Factor Production in Nasal Polyp Fibroblasts

doi: 10.4168/aair.2013.5.4.224

Figure Lengend Snippet: (A) Effect of EP receptor agonists on VEGF production by NPDFs. CAY10580 increased VEGF production significantly; however, no other EP receptor agonist showed an increase in VEGF production. (B) The effect of EP receptor antagonists on VEGF production. AH23848 decreased VEGF production markedly, but no other EP receptor antagonist elicited a decrease in VEGF production. (C) The effect of PGE2 combined with an EP4 receptor agonist or antagonist on VEGF production by immunofluorescence staining. Strong immunoreactivity for VEGF was observed in NPDF cells treated with PGE2 and CAY10580 by confocal laser scanning microscopy. NPDFs treated with PGE2 and EP4 receptor agonists showed blue-stained nuclei with a greenish cytoplasm (representative of four independent experiments; original magnification, ×200). The means±SE of data from six experiments are shown. * P <0.05 vs. control and † P <0.05 vs. PGE2. PGE2, prostaglandin E2; EP, E-prostanoid; Sulprostone, EP1/3 receptor agonist; Butaprost, EP2 receptor agonist; CAY10580, EP4 receptor agonist; SC51322, EP1 receptor antagonist; AH6809, EP2 receptor antagonist; L-798106, EP3 receptor antagonist; AH23848, EP4 receptor antagonist; VEGF, vascular endothelial growth factor; NPDFs, nasal polyp-derived fibroblasts; SE, standard error.

Article Snippet: PGE2, the protein kinase A (PKA) inhibitor KT5720, the EP1/3 receptor agonist sulprostone, the EP2 receptor agonist butaprost, the EP4 receptor agonist CAY 10580, the EP1 receptor antagonist SC51322, the EP2 receptor antagonist AH6809, the EP3 receptor antagonist L798106, and the EP4 receptor antagonist AH23848 were obtained from Cayman Chemical (Ann Arbor, MI, USA).

Techniques: Immunofluorescence, Staining, Confocal Laser Scanning Microscopy, Control, Derivative Assay