• Journal of Pathology and Translational Medicine
• /
• v.52 no.6
• /
• pp.386-395
• /
• 2018

Background: Previous studies on synchronous colorectal carcinoma (SCRC) have reported inconsistent results about its clinicopathologic and molecular features and prognostic significance. Methods: Forty-six patients with multiple advanced tumors (T2 or higher category) who did not receive neoadjuvant chemotherapy and/or radiotherapy and who are not associated with familial adenomatous polyposis were selected and 99 tumors from them were subjected to clinicopathologic and molecular analysis. Ninety-two cases of solitary colorectal carcinoma (CRC) were selected as a control considering the distributions of types of surgeries performed on patients with SCRC and T categories of individual tumors from SCRC. Results: SCRC with multiple advanced tumors was significantly associated with more frequent nodal metastasis (p=.003) and distant metastasis (p=.001) than solitary CRC. KRAS mutation, microsatellite instability, and CpG island methylator phenotype statuses were not different between SCRC and solitary CRC groups. In univariate survival analysis, overall and recurrence-free survival were significantly lower in patients with SCRC than in patients with solitary CRC, even after adjusting for the extensiveness of surgical procedure, adjuvant chemotherapy, or staging. Multivariate Cox regression analysis revealed that tumor multiplicity was an independent prognostic factor for overall survival (hazard ratio, 4.618; 95% confidence interval, 2.126 to 10.030; p<.001), but not for recurrence-free survival (p=.151). Conclusions: Findings suggested that multiplicity of advanced T category-tumors might be associated with an increased risk of nodal metastasis and a risk factor for poor survival, which raises a concern about the guideline of American Joint Committee on Cancer's tumor-node-metastasis staging that T staging of an index tumor determines T staging of SCRC.

• Clinical and Experimental Pediatrics
• /
• v.45 no.9
• /
• pp.1126-1133
• /
• 2002

Purpose : Prader-Willi syndrome(PWS) is a complex disorder affecting multisystems with characteristic clinical features. Its genetic basis is an expression defect in the paternally derived chromosome 15q11-q13. We analyzed the clinical features and genetic basis of PWS patients for early detection and treatment. Methods : We retrospectively studied 24 patients with PWS in Department of Pediatrics, Samsung Medical Center, from September 1997 to September 2001. We performed cytogenetic and molecular genetic techniques using high resolution GTG banding techniques, fluorescent in situ hybridization and methylation-specific PCR for CpG island of SNRPN gene region. Results : The average birth weight of PWS patients was $2.67{\pm}0.47kg$ and median age at diagnosis was 1.3 years. The average height and weight of PWS patients under one year at diagnostic time were located in a 3-10 percentile relatively, and a rapid weight gain was seen between two and six years. Feeding problems in infancy and neonatal hypotonia were the two most consistently positive major criteria in over 95% of the patients. In 18 of the 24 cases(75%), deletion of chromosome 15q11-q13 was demonstrated and one case among 18 had an unbalanced 14;15 translocation. In four cases without any cytogenetic abnormality, it may be considered as maternal uniparental disomy and the rest showed another findings. Conclusion : We suggest diagnostic testing for PWS in all infants/neonates with unexplained feeding problems and hypotonia. It is necessary for clinically suspicious patients to undergo an early genetic test. As the genetic basis of PWS was heterogenous and complex, further study is required.

• Journal of The Korean Society of Grassland and Forage Science
• /
• v.41 no.4
• /
• pp.223-233
• /
• 2021

The objective of this study was to investigate the effect of gypsum on the dry matter yield and the chemical composition of alfalfa in reclaimed tideland with soil dressing. The experimental site was Sukmoon reclaimed tideland. The tideland was reclaimed approximately 17 to 33 years ago and the 70 cm of soil was top-dressed. The soil that covers the reclaimed tideland brought from the island did not treat di-salinized. Treatments were consisted of three groups; control group where no gypsum (G0) was applied and two experimental groups where 2 ton/ha (G2) and 4 ton/ha (G4) of gypsum were applied, respectively. The first harvest was conducted when the alfalfa reached early flowering (open the flower 10%), and after that subsequent harvest was conducted at approximately 35 days intervals. The dry matter yield of the alfalfa showed that G2 was significantly higher in the first year than G0 and G4, and G2 tended to be higher in the second year than G0 and G4, although there were no significant differences between treatments. The reason for the high dry matter yield in G2 was that the soil pH and EC of the soil were at marginal and ideal levels and the coverage and alfalfa botanical composition were also high. In both years, there were no differences in the crude protein, neutral detergent fiber and acid detergent fiber contents and relative feed value between gypsum treatments. Meanwhile, the results in the first and second years showed that the alfalfa dry matter yield were negatively affected by droughts stress in spring and concentrated precipitation in summer. Therefore, this study suggests gypsum treatment in reclaimed tidal land could increase the dry matter yield of alfalfa, and 2 ton/ha of gypsum was the optimum rate.

• Tuberculosis and Respiratory Diseases
• /
• v.65 no.6
• /
• pp.495-503
• /
• 2008

Background: Epigenetic alterations in certain genes are now known as at least important as genetic mutation in pathogenesis of cancer. Especially abnormal hypermethylation in or near promoter region of tumor suppressor genes (TSGs) are known to result in gene silencing and loss of gene function eventually. The authors tried to search for new lung cancer-specific TSGs which have CpG islands and HpaII sites, and are thought to be involved in carcinogenesis by epigenetic mechanism. Methods: Tumor tissue and corresponding adjacent normal tissue were obtained from 10 patients who diagnosed with non small cell lung cancer (NSCLC) and underwent surgery in Konyang university hospital in 2005. Methylation profiles of promoter region of 21 genes in tumor tissue & non-tumor tissue were examined with HpaII-MspI methylation microarray (Methyl-Scan DNA chip$^{(R)}$, Genomic tree, Inc, South Korea). The rates of hypermethylation were compared in tumor and non-tumor group, and as a normal control, we obtained lung tissue from two young patients with pneumothorax during bullectomies, methylation profiles were examined in the same way. Results: Among the 21 genes, 10 genes were commonly methylated in tumor, non-tumor, and control group. The 6 genes of APC, AR, RAR-b, HTR1B, EPHA3, and CFTR, among the rest of 11 genes were not methylated in control, and more frequently hypermethylated in tumor tissue than non-tumor tissue. Conclusion: In the present study, HTR1B, EPHA3, and CFTR are suggested as possible novel TSGs of NSCLC by epigenetic mechanism.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.8
• /
• pp.3495-3501
• /
• 2014

Melanoma-associated antigen (MAGE) family genes have been considered as potentially promising targets for anticancer immunotherapy. MAGED4 was originally identified as a glioma-specific antigen. Current knowledge about MAGED4 expression in glioma is only based on mRNA analysis and MAGED4 protein expression has not been elucidated. In the present study, we investigated this point and found that MAGED4 mRNA and protein were absent or very lowly expressed in various normal tissues and glioma cell line SHG44, but overexpressed in glioma cell lines A172,U251,U87-MG as well as glioma tissues, with significant heterogeneity. Furthermore, MAGED4 protein expression was positively correlated with the glioma type and grade. We also found that the expression of MAGED4 inversely correlated with the overall methylation status of the MAGED4 promoter CpG island. Furthermore, when SHG44 and A172 with higher methylation were treated with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-AZA-CdR) reactivation of MAGED4 mRNA was mediated by significant demethylation in SHG44 instead of A172. However, 5-AZA-CdR treatment had no effect on MAGED4 protein in both SHG44 and A172 cells. In conclusion, MAGED4 is frequently and highly expressed in glioma and is partly regulated by DNA methylation. The results suggest that MAGED4 might be a promising target for glioma immunotherapy combined with 5-AZA-CdR to enhance its expression and eliminate intratumor heterogeneity.