Hypermethylation of E-cadherin in endometrial carcinoma / 부인종양

OBJECTIVE: Hypermethylation of CpG island is a common mechanism for the inactivation of tumor suppressor genes. Hypermethylation of the E-cadherin promoter region has been rarely studied in endometrial carcinoma of Korean women. The purpose of this study is to investigate methylation status of E-cadherin promoter region in endometrial carcinomas and endometrial hyperplasias, and analyze the correlation with clinicopathologic variables in endometrial carcinomas. METHODS: We examined the methylation status of the E-cadherin promoter region using methylation specific polymerase chain reaction and immunohistochemical expression (IHC) of E-cadherin in 30 endometrioid endometrial carcinomas and 20 endometrial hyperplasias, and correlated these results with various clinicopathological factors of endometrial carcinomas. RESULTS: Decreased expression of E-cadherin was detected in 13 of 30 (43.3%) endometrial carcinomas and in 1 of 20 (5%) endometrial hyperplasias (p=0.009). Promoter hypermethylation was detected in 12 of 30 (40%) endometrial carcinomas and 2 of 20 (10%) endometrial hyperplasias (p=0.015). Methylation status did not have a significant influence on the tumor grade and lymph node metastasis. However, the hypermethylation rate was significantly higher in stage above Ic (p=0.025). Decreased expression of E-cadherin was associated with tumor grade, tumor stage, and lymph node metastasis in endometrial carcinomas (p=0.01, p=0.02, p=0.03). There was no correlation between DNA hypermethylation and decreased expression of E-cadherin in endometrial carcinomas (p>0.05). CONCLUSION: These results indicate that hypermethylation of E-cadherin promoter region is a frequent event in endometrial carcinoma, which may play an important role in the progression of carcinogenesis. Also, the promoter methylation of E-cadherin in endometrial carcinoma was found to be significantly associated with higher stage above Ic.

Hypermethylation of E-cadherin in endometrial carcinoma / 부인종양

OBJECTIVE: Hypermethylation of CpG island is a common mechanism for the inactivation of tumor suppressor genes. Hypermethylation of the E-cadherin promoter region has been rarely studied in endometrial carcinoma of Korean women. The purpose of this study is to investigate methylation status of E-cadherin promoter region in endometrial carcinomas and endometrial hyperplasias, and analyze the correlation with clinicopathologic variables in endometrial carcinomas. METHODS: We examined the methylation status of the E-cadherin promoter region using methylation specific polymerase chain reaction and immunohistochemical expression (IHC) of E-cadherin in 30 endometrioid endometrial carcinomas and 20 endometrial hyperplasias, and correlated these results with various clinicopathological factors of endometrial carcinomas. RESULTS: Decreased expression of E-cadherin was detected in 13 of 30 (43.3%) endometrial carcinomas and in 1 of 20 (5%) endometrial hyperplasias (p=0.009). Promoter hypermethylation was detected in 12 of 30 (40%) endometrial carcinomas and 2 of 20 (10%) endometrial hyperplasias (p=0.015). Methylation status did not have a significant influence on the tumor grade and lymph node metastasis. However, the hypermethylation rate was significantly higher in stage above Ic (p=0.025). Decreased expression of E-cadherin was associated with tumor grade, tumor stage, and lymph node metastasis in endometrial carcinomas (p=0.01, p=0.02, p=0.03). There was no correlation between DNA hypermethylation and decreased expression of E-cadherin in endometrial carcinomas (p>0.05). CONCLUSION: These results indicate that hypermethylation of E-cadherin promoter region is a frequent event in endometrial carcinoma, which may play an important role in the progression of carcinogenesis. Also, the promoter methylation of E-cadherin in endometrial carcinoma was found to be significantly associated with higher stage above Ic.

Relationship between spontaneous preterm birth and polymorphisms of Interleukin-1beta and Interleukin-1 receptor antagonist in Korean women / 대한산부인과학회지

OBJECTIVE: Preterm birth is an important cause of infant death and morbidity but its pathophysiology still remains to be clear. The associations between preterm birth and the polymorphism of interleukin-1beta gene and interleukin-1 receptor antagonist gene have been suspected. And ethnic variations in the polymorphism of the genes were also reported. We decided to study polymorphisms of interleukin-1beta+3953 and interleukin-1 receptor antagonist in Korean pregnant women. METHODS: Patients were divided into 2 groups. Group 1 is the control group of 33 subjects with uncomplicated term delivery : group 2 is the case group of patients who had spontaneous preterm delivery. Polymorphisms were determined by polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: There were significant differences in gestational age and birth weight between two groups (P<0.001). No significant differences were found in genotypic frequencies and allelic frequencies in interleukin-1beta+3953 between two groups. Interleukin-1 receptor antagonist gene had 5 alleles and the most frequent allele was IL1RN*1 (410bp), 66.7% in control group and 77.8% in case group. And significant differences were not found in genotypic frequencies and allelic frequencies between two groups, too. CONCLUSION: There were no significant differences in polymorphisms in interleukin-1beta +3953 and interleukin-1 receptor antagonist between term delivery group and preterm birth group.

Clinical and histopathological studies on ovarian tumors / 대한산부인과학회지

OBJECTIVE: To know the clinical and histopathologic profiles of ovarian tumors. METHODS: 822 women undergone operations for their ovarian tumors were enrolled in this study from July of 1996 to June of 2004 at Inha University Hospital in S. Korea. Incidence, age, laterality and size were analyzed according to their histopathologic results. RESULTS: Among 822 women, there were 2.1% of non-neoplastic ovarian cysts, 81.0% of benign tumors, 4.4% of borderline tumors, and 12.5% of malignant tumors. Among benign tumors, 48.2 were cystic teratomas, 22.5% were mucinous, and 19.4% were serous tumors. Among borderline tumors, 52.8% were mucinous and 42.2% were serous. Among malignant tumors, 25.2% were serous and metastatic, respectively, and 18.4% were mucinous. The average and median age of non-neoplastic cysts were 39.1 +/- 12.7, 41 years old, those of benign tumors were 38.2 +/- 18.4, those of borderline tumors were 33.4 +/- 16.7, 28, and those of malignant tumors were 47.8 +/- 15.4, 49. The bilaterality of benign tumors was 10.7%, that of borderline were 16.7%, and that of malignant were 24.2%. The average and median diameter of non-neoplastic cysts were 3.2 +/- 1.4 cm, 3 cm, those of benign tumors were 8.1 +/- 4.3 cm, 7 cm, those of borderline tumors were 13.5 +/- 7.8 cm, 12 cm, and those of malignant tumors were 10.2 +/- 6.1 cm, 9.3 cm. CONCLUSION: We analyzed clinical and histopathologic data of 822 ovarian tumors.

Leptin and growth hormone in the cord blood of healthy neonates: correlation with fetal growth / 대한산부인과학회지

OBJECTIVE: To understand the correlation between leptin in cord blood and parameters indicating fetal growth and to investigate the relationship between leptin and growth hormone. METHODS: We measured leptin and growth hormone levels in the cord blood of 46 healthy neonates by radioimmunoassay (RIA), and analyzed the correlation of leptin with growth hormone, birth weight, gestational age, sex, birth height, body mass index, maternal body mass index (BMI), and Ponderal Index by Pearson correlation coefficients. RESULTS: Leptin concentration of cord blood was 5.16 g/l in median value; concentration in female cord blood was significantly higher than in male's (P=0.005). Growth hormone concentration was 28.60 g/l; there was no significant difference between female and male (P=0.584). There were significant correlations between leptin and birth weight, birth height, and BMI at birth, with correlation coefficients 0.56 (P=0.0001), 0.35 (P=0.017), and 0.35 (P=0.017), respectively. Growth hormone was correlated with leptin but statistically insignificant (P=0.085). And growth hormone was not correlated with gestational age, Ponderal Index or maternal BMI. CONCLUSION: Leptin is significantly correlated with fetal growth, and growth hormone is potentially correlated with fetal growth.