Ganglioside GD1a is specifically formed by the addition of sialic acid to ganglioside GM1a by ST3 β- galactoside α -2,3-sialyltransferase 2 (ST3GAL2). Above all, GD1a are known to be related with the functional regulation of several growth factor receptors, including activation and dimerization of epidermal growth factor receptor (EGFR) in tumor cells. The activity of EGF and EGFR is known to be a very important factor for meiotic and cytoplasmic maturation during in vitro maturation (IVM) of mammalian oocytes. However, the role of gangliosides GD1a for EGFR-related signaling pathways in porcine oocyte is not yet clearly understood. Here, we investigated that the effect of ST3GAL2 as synthesizing enzyme GD1a for EGFR activation and phosphorylation during meiotic maturation. To investigate the expression of ST3GAL2 according to the EGF treatment (0, 10 and 50 ng/ml), we observed the patterns of ST3GAL2 genes expression by immunofluorescence staining in denuded oocyte (DO) and cumulus cell-oocyte-complex (COC) during IVM process (22 and 44 h), respectively. Expression levels of ST3GAL2 significantly decreased (p<0.01) in an EGF concentration (10 and 50 ng/ml) dependent manner. And fluorescence expression of ST3GAL2 increased (p<0.01) in the matured COCs for 44 h. Under high EGF concentration (50 ng/ml), ST3GAL2 protein levels was decreased (p<0.01), and their shown opposite expression pattern of phosphorylation-EGFR in COCs of 44 h. Phosphorylation of EGFR significantly increased (p<0.01) in matured COCs treated with GD1a for 44 h. In addition, ST3GAL2 protein levels significantly decreased (p<0.01) in GD1a (10 μM) treated COCs without reference to EGF pre-treatment. These results suggest that treatment of exogenous ganglioside GD1a may play an important role such as EGF in EGFR-related activation and phosphorylation in porcine oocyte maturation of in vitro.

Malignant pleural effusion (MPE) and blood samples can be used as a practical source for detection of epidermal growth factor receptor (EGFR) mutations in patients with advanced non-small cell lung cancer. We compared EGFR mutation status of cell blocks, cell-free fluid of MPE, and plasma from patients with lung adenocarcinoma. We obtained paired samples of MPE and plasma from 14 pathologically-confirmed lung adenocarcinoma patients. Peptide nucleic acid (PNA)-mediated real-time polymerase chain reaction (RT-PCR) clamping was performed for determination of EGFR mutation status. EGFR mutations were detected in five (35.7%) cell blocks of MPE, which showed results identical to those of the corresponding cell-free fluid, whereas mutations were detected in the plasma of only two (40.0%) of the five patients. Of seven patients treated with EGFR tyrosine kinase inhibitors (TKIs), EGFR mutations were detected in cell blocks, cell-free fluid of MPE, and plasma for only one of the four patients who responded to EGFR TKIs, while mutations were detected only in cell blocks of MPE and cell-free fluid of the three remaining patients. Our results suggest that detection of EGFR mutations in cell-free pleural fluid from lung adenocarcinoma patients using highly sensitive methods may be feasible, but that analysis of free plasma may lead to undetected mutations and misdiagnosis.

The central role of tyrosine phosphorylation in cell proliferative signaling mechanisms provides another target for chemotherapy. The aim of this research is to develop new quinazoline derivatives that possess the inhibitory activity for depidermal growth factor receptor (EGFR) tyrosine kinase (TK) as protein kinase inhibitors. In this work, a series of new 4-anilino-6-guanidino-7-methoxyquinazoline derivatives (12a-l) were synthesized by the introduction of guanidine moiety at C-6 of quinazoline nucleus and evaluated for their EGFR TK inhibitory activities.

The puφose of this study was to evaluate the role of EGF(Epidermal Growth Factor), EGFR(Epidermal Growth Factor Receptor), aFGF(acidic Fibroblast Growth Factor or FGF-1), bFGF(basic Fibroblast Growth Factor or FGF-2), FGFR(Fibroblast Growth Faαor Receptor), and VEGF(Vascular Endothelial Growth Factor) in the development of the human ameloblastomas For this study 9 subjects, diagnosed as ameloblastomas referred to the Dept. of Oral Path. College of Dentistry, Kyung Hee University, 2 subjeαs of normal oral mucosa with any inflammatory changes were used as experimental, control groups respectively. All the tissues ; experimental and control group were fixed in 10% neutral formalin solution and embedded in paraffm, serial tissue section were made 하1m in thickness and processed in the standard way for immunohistochemical method, using primary and secondary antibodies, for EGF(Antirabbit Ig G, rabbit kit at }:1oo dilution), EGFR(Antimouse Ig G, mouse kit at 1:100 dilution), aFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), bFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), FGFR(Antimouse Ig G, mouse kit at 1:100 dilution) , and VEGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), all BioGenex U.S. A. made, followed by the Streptavidin - Horse Radish Peroxidase(InnoGenex, Human-avidin kit) appli때on ， counter stained with Mayer’s hematoxylin stain method. And examined under the biologic microscope, graded -(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective 따sue component in ameloblastomas and in normal mucosal epithelium on each. Attained results as follows ; 1. EGF, EGFR, aFGF, bFGF, FGFR, and VEGF showed more intense stainability on experimental group compare t，。 that on the control group. 2. EGF, EGFR, aFGF, bFGF, FGFR, and VEGF showed more intense stainability in epithelial component and more intensely stained on the peripheral ce11s of the ameloblastomas. 3. EGF, EGFR, aFGF, bFGF, FGFR, and VEGF showed positive stainability on the stromal tissues but its level is lower compare to that on the epithelial components. Those results suggested that those growth factors take a role in development and progression on the amelob비las와tomas

Matrix metalloproteinases(MMPs) are involved in the degradation of extracellular matrix, which is re lated to infiltrative growth and metastasis of tumor and are regulated by tisslle inhibitor of metalloproteinases(TIMPs) or cell adhesion molecllles such as E-cadherin and epidermal growth factor receptor (EGFR). The aim of this study is to evaluate the relationship between MMP-2, MMP-9 expressions and clinico-pathologic factors, 끼MP-1 ， TIMP-2, EGFR and E-cadherin expressions. lmmunohistochemical stains were perfom1ed on 55 cases of squamous cell carcinoma of the ordl cavity and the results were as follows. MMP-2 and MMP-9 expressions were noted in 30(54.5%) and 22(40.0%) of 55 cases, TIMP-1 and πMP-2 in 21(38.2%) and 33(60.0%), and E-cadherin and EGFR expressions in 35(63.6%) and 26(47.3%) of 55 cases, respectively. MMP-2 expression rdte was slightly higher 띠 cases without recurrence, and 끼MP- 2 expression rate was slightly higher in cases showing more inftltrative growth pattem. 까1e expression rate of EGFR was higher in cases with well differentiation(p=0.OO47), but no posi디ve relationship between the expression rate of Ecadherin and histologic grade was found. Cases with positive reaction for MMP-9 showed an increasing tendency of nega디ve reaction for TIMP-1. π1e expression rate of MMP-2 was higher in cases with positive reaction for E-cadherin and EGFR with no statistical significance. 까1e expression rate of MMP-9 was significantly higher in cases with positive reaction for E-cadherin(p=0.022l). These results suggest that MMP-2, MMP-9, TIMP-1 and TIMP-2 expressions are involved in the development of oral squamous cell carcinomas, but MMP-2, MMP-9, 끼MP-1 ， and 끼MP-2 expressions might not seem to be a useful prognostic factors because there were no significant relationship between clinicopathologic parameters. EGFR expression showed positive correlation with low histologic grade, so EGFR expression could be regarded as a good prognostic factor. In the progression of sqllamous cell

까le purpose of this study was to evaluate the role of EGF(Epidermal Growth Factor) , EGFR(Epidemlal Growth Factor Receptor), aFGF(acidic Fibroblast Growth Factor, FGF-1), bFGF(basic Fibroblast Growth Factor, FGF-2), FGFR(Fibroblast Growth Factor Receptor), and VEGF(Vascular Endothelial Growth Factor) 띠 the development of the oral squamous cell carcinoma. For this study 6 subjects, diagnosed as squamous cell carcinoma refelTed to the Dept. of Oral Path. College of Dentistry, Kyung Hee University, 2 subjects of normal 이띠 mucosa with any inflammatolY changes were used as expelimental, control groups respectively. AlI the 디ssu es ; expe디me nta l and control group were fixed in 100;ú neutral fOlmalin solution and embeclded in paraffìn , seIial tissue section were made 511m in thickness ancl processecl in the standard way for immunohistochemical methocl, using primary ancl seconclalY antibodies, for EGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), EGFR(Antimouse Ig G, mouse kit at 1:100 dilution), aFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), bFGF(Antirabbit Ig G, rabbit 써t at 1:100 dilution), FGFR(Antimouse Ig G, mouse kit at 1:100 dilution), ancl VEGF(Antirabbit Ig G, rabbit kit at 1:100 clilution), all BioGenex U.S.A. macle, followed by the Stre ptavidin - Horse Radish Peroxidase(InnoGenex, Human-avidin kit) application, counter stained with Mayer’s hematoxylin stain method. And examined under the biologic microscope, -(no epithelial stain), +(weak or focal epithelial stain), ++(mode rate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective tissue component in squamous cell carcinoma and in nomlal mucosal epithelium on each. Attained results as follows ; 1. It is noted that more intensed reactio n EGF, EGFR, aFGF, bFGF, FGFR, and VEGF on experimental group compare to that on the control group. 2. Increased reaction is noted on the tumor components compare to that in the stromal tissues. 3. Intensed reaction is noted on the basement membrane adjacent to cancer nest to EGF, EGFR, aFGF, bFGF, FGFR, and VEGF 4. It is noted that intensed positive reaction on cancer pearls, cancer components with hyperactivities, in cancer nest. And at the peIiphelY of cancer nest, diffuse moclerate reaction to EGF, EGFR, aFGF, bFGF, FGFR, and VEGF is notecl This results suggest that EGF, EGFR, aFGF, bFGF, FGFR, and VEGF mJy be effectecl to the growth ancl clevelopment of the squamous cell carcinoma.

The purpose of this study was to evaluate the role of EGF(Epidermal Growth Factor), EGFR(Epidermal Growth Factor Receptor), aFGF(acidic Fibroblast Growth Factor, FGF-1), bFGF(basic Fibroblast Growth Factor, FGF-2), FGFR(Fibroblast Growth Factor Receptor) in the development of radicular cyst. For this study 37 subjects, diagnosed as radicular cysts. referred to the Dept. of Oral Path. College of Dentistry, Kyung Hee University, were used as experimental group. And for control group, 2 subjects of normal oral epithelium without any inflammatory changes were used. All the tissues; experimental and control group were neutral formation fixed and paraffin embedded. serial tissue section were made at 5㎛ and processed in the standard way for immunohistochemical method, using primary antibodies against, EGF(Antirabbit Ig G at 1:100 dilution), EGFR(Antimouse Ig G at 1:100 dilution), aFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), bFGF(Antirabbit Ig G, mouse kit at 1:100 dilution), FGFR(Antimouse Ig G mouse kit at 1:100 dilution), all BioGenex U.S.A. made except EGFR(Chemicon U.S.A.) followed by the Streptavidin - Horse Radish Peroxidase (InnoGenex Human-avidin kit) application, counter stained with Meyer's hematoxylin stain method. And examined under microscope, graded 0(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelium, and connective tissue of cyst wall. 1. EGF, EGFR, aFGF, bFGF, FGFR showed more intense staining on radicular cysts compare to that on the normal mucosa. 2. EGF, EGFR, aFGF, bFGF, FGFR stained in mucosa, submucosa of the control group and also stained on the lining epithelium, connective tissues of cyst wall in the experimental group. EGF, EGFR, aFGF, bFGF, FGFR take a part in the development of the radicular cyst.