No abstract available.
Cell Cycle*

Angiogenesis is an essential requirement for development, progression, and metastasis of malignant tumors. Vascular endothelial growth factor (VEGF) is one of the important angiogenic factors. Recently the role of angiogenesis has been known in premalignant lesions. This study was performed to determine whether the angiogenesis and VEGF expression were increased in association with histological grade of cervical intraepithelial neoplasia (CIN) and to see the relationship between the angiogenesis and VEGF. Immunostainings for factor VIII and VEGF were performed on 52 cases of cervical neoplasia (12 cases of CIN I, 11 cases of CIN II, 15 cases of CIN III, 7 cases of microinvasive squamous cell carcinoma, and 7 cases of invasive carcinoma) and 5 cases of normal cervix. The results showed a significant increase of microvessel count from normal cervix through CIN grades to invasive squamous cell cacinoma. VEGF expression was increased in proportion to the CIN grades. There was no significant correlation between microvessel count and VEGF expression. In conclusion, the tumor angiogenesis is an early event in tumorigenesis of uterine cervix. In addition, no significant relationship between the microvessel count and VEGF expression in CIN suggests the possibility of other growth factors affecting mainly angiogenesis of premalignant lesion of uterine cervix.
Angiogenesis Inducing Agents ; Carcinogenesis ; Carcinoma, Squamous Cell ; Cervical Intraepithelial Neoplasia* ; Cervix Uteri ; Factor VIII ; Female ; Intercellular Signaling Peptides and Proteins ; Microvessels ; Neoplasm Metastasis ; Vascular Endothelial Growth Factor A*

OBJECTIVES: Cadherin/catenin adhesion complex is fundamentally involved in epithelial cancer invasion and metastasis. E-cadherin and EGFR colocalize on the basolateral membrane of epithelial cell and EGF down-regulate E-cadherin expression. In the invasion and metastasis of cancer, E-cadherin expression is decreased and growth factors receptor is overexpressed. The present study was aimed to find the role of E-cadherin, beta-and gamma-catenin, growth factors and its receptors in cervical cancer cell lines. METHODS: The cervical cancer cell cultures were treated with different time duration of EGF 30 ng/ml and TGF-a 10 ng/ml(0, 10 min, 20 min, 30 min, 1 hr, 2 hr, 4 hr, 8 hr, 24 hr). The change in cancer cell morphology and the changes in E-cadherin, beta- and gamma-catenin, EGFR and activated EGFR expression were studied with a western blot analysis and an immunoprecipitation. RESULTS: Through a western blot analysis, E-cadherin 120 kDa band and EGFR 170 kDa band were expressed in CaSki, HT-3 and ME-180 cell line, which showed epithelial contact growth. 1n these 3 cell lines, expression of E-cadherin did not decrease with time dependent manner. after the treatment of EGF and TGF- alpha. The expression of EGFR decreased and activated EGFR expression increased in 30 minutes to 1 hour but decreased subsequently. When the cells treated with EGF, there were no change in beta-and gamma-catenin expression with there dependent manner. The tyrosine phosphorylation of beta-and gamma-catenin increased in 30 minutes to 1 hour but decreased subsequently with activated EGFR. CONCLUSION: This study showed that an activated EGFR which has involved with tyrosine phosphorylation of beta- and gamma-catenin influenced by growth factors rather than expression of E-cadherin, has a role in the invasion and metastasis of the cervical cancer.
Blotting, Western ; Cadherins* ; Cell Culture Techniques ; Cell Line* ; Epidermal Growth Factor* ; Epithelial Cells ; gamma Catenin* ; Immunoprecipitation ; Intercellular Signaling Peptides and Proteins ; Membranes ; Neoplasm Metastasis ; Phosphorylation* ; Transforming Growth Factor alpha* ; Tyrosine* ; Uterine Cervical Neoplasms*

OBJECTIVE: Some growth factors may promote tumor growth by affecting tumor angiogenesis. Midkine(MK) are polypeptides that belong to a new family of heparin-binding growth/differentiation factor and has also been reported to be angiogenic. In various tumor tissues, MK was highly expressed between tumor and normal tissues; however, the pattern of MK expression in normal cervix and cervical cancer has not been established. The aim of this study was to determine the MK mRNA expression in cervical cancer. And we questioned whether its expression is related to cancer stages and prognostic factors. METHODS: The cervical and cervical cancer tissues were taken from patients; healthy women(n=15), and the patients with cervical cancer(n=29). The MK mRNA expression was examined by quantative competitive PCR after polymerase chain reaction amplification of reverse transcriptase copies of RNA transcripts(RT-PCR). RESULTS: The cervical cancer expressed higher levels of MK mRNA than normal cervix(p<0.05). The MK mRNA expression was not correlated with the cervical cancer stage and histopathologic type(p>0.05). CONCLUSION: These results suggested that increased MK mRNA expression is associated with the development of cervical cancer.
Cervix Uteri ; Female ; Humans ; Intercellular Signaling Peptides and Proteins ; Peptides ; Polymerase Chain Reaction ; RNA ; RNA, Messenger* ; RNA-Directed DNA Polymerase ; Uterine Cervical Neoplasms*

The Fig. 5A was given incorrectly.

The one event on signaling mechanism is the cleavage by adenyl cyclase of ATP into second messenger, cyclic AMP. The other transfer system of inositol metabolism, it is widely recognized that hydrolysis of the minor membrane lipid phosphoinositide bisphosphate (PIP₂) initiated by occupation of certain receptors and catalyzed by phospholipase C, lead to toe generation of the two intracellular messengers, inositol triphosphate (IP₃) and diacylglycerol (DG). IP₃ is converted to inositol tetrakisphosphate (IP₄) by IP₃ kinase. In the present study, it is that purification of calmodulin is used by phenyl-Sepharose CL-4B chromatography, it's molecular weigh, 17,000 in SDS-polyacrylamide gel electrophoresis. In order to observe the affinity between calmodulin (CaM)-Affigel 15 and IP₃ kinase, and isolated IP₃ kinase, was applied in CaM-Affigel with Ca²⁺ equilibrium buffer and EGTA equilibrium buffer. We compared with binding and elution effect of IP₃ kinase in several condition of buffer. In affinity of binding, Ca²⁺ equilibrium buffer was in the most proper condition, and elution, CaM/Ca²⁺buffer (CE 1 10.36, CE2 12.76pM/min/mg of protein) was effected much more than EGTA buffer (E2 1.48, E 2.43pM/min/mg of protein), but CaM/Ca²⁺stimulate the activity of IP₃ kinase. And then, several detergents such as sodium deoxycholate, tween 20, cholic acid, polyethylene glycol, chaps were applied. The 0.2% chaps buffer (E2 23.19, E3 8.05pnM/min/mg of protein) was the most effective in elution of IP3 kinase.
Adenosine Triphosphate ; Adenylyl Cyclases ; Brain* ; Calmodulin ; Cholic Acid ; Chromatography ; Cyclic AMP ; Deoxycholic Acid ; Detergents ; Egtazic Acid ; Electrophoresis ; Hydrolysis ; Inositol* ; Membranes ; Metabolism ; Occupations ; Phosphotransferases* ; Polyethylene Glycols ; Polysorbates ; Second Messenger Systems ; Toes ; Type C Phospholipases

Because early embryonic development of the tracheobronchial tree and foregut are closely associated, there is a wide spectrum of congenital anomalies involving either one or both organ systems. We analysed a total of 89 surgical and autopsy cases that are assumed to belong to congenital bronchopulmonary foregut malformation from the files of Seoul National University Hospital and Children's Hospital during the periord of 1961~1990. We also reviewed the serial sections of the embryos and fetuses from 3 weeks to fifteen weeks fertilization age for the observation of tracheobronchial and esophageal trees. Intralobar sequestrations(25 cases) and extralobar pulmonary sequestrations(4 cases) with patent, involuted-partial or complete-communication with the alimentary tract, tracheoesophageal fistula(30 cases) with or without esophageal atresia, esophageal atresia, esophageal stenosis due to tracheobroncheal remnant(4 cases), foregut duplication cysts(3 cases), esophageal or gastric diverticulum(1 cases), and bronchogenic cysts(22 cases) are included in this analysis(Table 1). Through this study, we confirmed the unifying concept of "bronchopulmonary forgut malformations". We believe a common embryologic pathogenesis leads to the formation of a previously described spectrum of malformations.

OBJECTIVES: The TGF-Beta1 (transforming growth factor-Beta1 ), which has been shown to inhibit cellular proliferation in vitro as a growth regulator, has been demonstrated to enhance tumori-genicity in vivo. The proteolytic processes of cancer are thought to be the crucial point in tumor invasion and metastasis, mainly by matrix metalloproteinases.(MMPs) We investigated the serum TGF-Beta1 and MMP-2 levels in patients with cervical cancer in contrast to those of normal, patients with benign myoma, and cervical intraepithelial neoplasia (CIN). And we questioned whether these serum levels are different according to the therapy of cancer or not. METHODS: We measured serum TGF-Beta1, MMP-2 concentrations by ELISA in 34 patients with cervical cancer, as well as 5 normal volunteers, 14 patients with benign myoma and 23 patients with CIN. Especially in 7 patients with cervical cancer, we measured serum TGF-Beta1, MMP-2 levels before and after therapy. RESULTS: The serum TGF-Beta1 levels in patients with cervical lancer(37.8 +/-15.4pg/ml) were significantly lower than those of the patients with CIN(46.2+/-9.2pg/ml)(p<0.05). But there is no differences among the serum MMP-2 levels in the patients with cervical cancers(680.30+/-116.6pg/ml), CIN(715.2+/-150.0pg/ml), and benign myoma(682.4+/-112.5pg/ml)(p>0.05). Patients undergoing cancer therapy did not have different values of serum TCF-Beta1 and MMP-2 levels as those without cancer therapy.(p>0.05) CONCLUSION: So we suggest that serum TGF-Beta1 may be helpful in differential diagnosing cervical cancers from CIN.
Cell Proliferation ; Cervical Intraepithelial Neoplasia* ; Enzyme-Linked Immunosorbent Assay ; Healthy Volunteers ; Humans ; Myoma ; Neoplasm Metastasis ; Transforming Growth Factor beta1* ; Uterine Cervical Neoplasms*