• The Korean Journal of Mycology
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• v.30 no.2
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• pp.152-156
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• 2002

Distribution and alteration of mating type of Korean population for Phytophthora capsici were monitored from 1995 to 1998. Total 973 isolates collected from 75 pepper fields throughout the country were divided into A1 mating type 573 isolates and A2 mating type 400 isolates. Both mating types were founded in all provinces examined, but the distribution patterns differed between the fields, The single mating type of A1 or A2 isolates was found in some fields, whereas various combinations of both mating types were in all years and provinces surveyed. Ratios of A1 and A2 were varied with years and fields. However, only single mating type either A1 or A2 was detected in some fields. While, in another field located in Gongju, only A2 isolates were detected in 1995 and 1997, but A1 isolates were appeared in 1998. Varied ratios and alterations of A1 and A2 mating type in fields indicate a potential sexual recombination of the fungus, which may cause genetic diversity.

• Environmental Analysis Health and Toxicology
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• v.14 no.1_2
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• pp.1-12
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• 1999

Recently, several new methods for the detection of genetic damages in vitro and in vivo based on molecular biological techniques were introduced according to the rapid progress in toxicology combined with cellular and molecular biology. Among these methods, mouse lymphoma thymidine kanase (tk) gene forward mutation assay, single cell gel electrophoresis (comet assay) and transgenic animal and cell line model as a target gene of lac I (Big Blue) and lac Z (Muta Mouse) gene mutation are newly introduced based on molecular toxicological approaches. The mouse lymphoma tk$\^$+/-/ gene assay (MOLY) using L5178Y tk$\^$+/-/ mouse lymphoma cell line is one of the mammalian forward mutation assays, and has many advantages and more sensitive than hprt assay. The target gene of MOLY is a heterozygous tk$\^$+/-/ gene located in 11 chromosome, so it is able to detect the wide range of genetic changes like point mutation, deletion, rearrangement, and mitotic recombination within tk gene or deletion of entire chromosome 11. The comet assay is a rapid, simple, visual and sensitive technique for measuring and analysing DNA breakages in mammalian cells, Also, transgenic animal and cell line models, which have exogenous DNA incorporated into their genome, carry recoverable shuttle vector containing reporter genes to assess endogenous effects or alteration in specific genes related to disease process, are powerful tools to study the mechanism of mutation in vivo and in vitro, respectively. Also in vivo acridine orange supravital staining micronucleus assay by using mouse peripheral reticulocytes was introduced as an alternative of bone marrow micronucleus assay. In this respect, there was an International workshop on genotoxicity procedure (IWGTP) supported by OECD and EMS (Environmental Mutagen Society) at Washington D. C. in March 25-26, 1999. The objective of IWGTP is to harmonize the testing procedures internationally, and to extend to finalization of OECD guideline, and to the agreement of new guidelines under the International Conference of Harmonization (ICH) for these methods mentioned above. Therefore, we introduce and review the principle, detailed procedure, and application of MOLY, comet assay, transgenic mutagenesis assay and supravital staining micronucleus assay.

• Preventive Nutrition and Food Science
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• v.6 no.1
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• pp.66-72
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• 2001

Ginseng may have antioxidant and pharmacologic effects similar to those of vitamin E. The interactive effect of ginseng and vitamin E was studied with respect to cholesterol metabolism and the antioxidant status. A ginseng supplement (0.1%, wt/wt) with comparable levels of vitamin E was provided with a high-cholesterol (1%, wt/wt) diet to rats for 5 weeks. The amount of vitamin E included in the ginseng-free and ginseng diets was either a low (low-E) or a normal (normal-E) level. The ginseng supplements significantly (p<0.05) altered the concentrations of plasma triglycerides in both the low-vitamin E group and normal-vitamin E group compared to the each ginseng-free group. The hepatic triglyceride and cholesterol content were not significantly (p>0.05) different between groups regardless of the vitamin E level in the diet. The hepatic HMG-CoA reductase activity was significantly (p<0.05) lowered by the ginseng supplement in both the low-vitamin E and the normal-vitamin E groups compared to the ginseng-free group. The HMG-CoA reductase activity was also significantly (p<0.05) lowered with in increase of the dietary vitamin E in the ginseng-free group. The excretion of fecal neutral sterol was significantly (p<0.05) lower in the normal-E ginseng group than th low-E ginseng-free group. Neither dietary ginseng nor vitamin E significantly changed the hepatic antioxidant enzymes activity. This data indicates that ginseng supplements lower the concentration of plasma triglyceride and hepatic HMG-CoA reductase activity regardless of eh dietary vitamin E level. This information may contribute to understanding the interactive effect of ginseng and vitamin E on cholesterol biosynthesis in high cholesterol-fed rats.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.17
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• pp.7589-7594
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• 2015

Background: MicroRNAs (miRNAs) are small non-coding RNA molecules, implicated in several activities like initiation, progression and prognosis of various cancers. Single nucleotide polymorphisms (SNPs) in miRNA genes can lead to alteration in mRNA expression, resulting in diverse functional consequences. The aim of our study was to investigate the association of miR-149C>T and miR-196a2C>T SNPs with susceptibility to development of oral squamous cell carcinoma (OSCC) in South Indian subjects. Materials and Methods: 100 OSCC patients and 102 healthy controls from the general population were recruited for the study. Genetic analysis was performed by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP) as per a standard protocol. Results: The genotype frequencies in miR-196a2 polymorphism, of TT, CT and CC in the OSCC patients were 69%,10% and 22% respectively while for control group it was 80%, 15% and 5% respectively. The CC genotype of miR196a2 polymorphism was significantly associated with oral squamous cell carcinoma. The genotype frequencies in miR-149 polymorphisms of CC, CT and TT in the oral squamous cell carcinoma (OSCC) patients were 72%, 22% and 6% respectively and for control group 88%, 12% and 0% respectively. CT and TT genotypes of miR149 polymorphism were found to be significantly associated with OSCC (p = 0.05 and 0.07). Conclusions: Our study suggests that miR-196a2C>T and miR-149C>T polymorphisms may play crucial roles in the development of OSCC in South Indian subjects.

• Korean Journal of Head & Neck Oncology
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• v.18 no.1
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• pp.3-10
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• 2002

Background: The molecular pathogenesis of hereditary medullary thyroid carcinoma is well known to be associated with germ-line mutation in the RET proto-oncogene and sporadic medullary thyroid carcinoma has been shown to carry somatic RET mutation especially in exon 13 and 16. The aim of this study is to evaluate the genetic background in the pathogenesis of the sporadic medullary thyroid carcinoma which shows extremely high incidence in Korea. Materials and Methods: Direct DNA sequencing for RET exon 13 and 16, as well as immunohistochemistrical assay for a monoclonal RET antibody were performed from 20 cases of archival tissues of medullary thyroid carcinoma. Results: Monoclonal RET antibody with C-terminal epitope showed comparatively stronger expression in tumor cells than in normal tissues and immunoreactive area in the tumor was $66.0{\pm}40.1%$. Direct sequencing of RET exon 13 revealed 4 cases of mis-sense mutations in Codon 778, Codon 767, and both in Codon 768 and 778. One case showed a silent mutation (ACG-ACT) in RET exon 16 (Codon 926). Conclusions: The strong RET immunoreactivity of medullary thyroid carcinoma may suggest that there could be a genetic alteration in oncoprotein level. RET proto-oncogene mutation may be involved in the evolutional process of medullary thyroid carcinoma in the aspect of molecular basis.

• Clinical and Experimental Reproductive Medicine
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• v.48 no.3
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• pp.245-254
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• 2021

Objective: In humans, polycystic ovary syndrome (PCOS) is an androgen-dependent ovarian disorder. Aberrant gene expression in folliculogenesis can arrest the transition of preantral to antral follicles, leading to PCOS. We explored the possible role of altered gene expression in preantral follicles of estradiol valerate (EV) induced polycystic ovaries (PCO) in a mouse model. Methods: Twenty female balb/c mice (8 weeks, 20.0±1.5 g) were grouped into control and PCO groups. PCO was induced by intramuscular EV injection. After 8 weeks, the animals were killed by cervical dislocation. Blood serum (for hormonal assessments using the enzyme-linked immunosorbent assay technique) was aspirated, and ovaries (the right ovary for histological examinations and the left for quantitative real-time polymerase) were dissected. Results: Compared to the control group, the PCO group showed significantly lower values for the mean body weight, number of preantral and antral follicles, serum levels of estradiol, luteinizing hormone, testosterone, and follicle-stimulating hormone, and gene expression of TGFB1, GDF9 and BMPR2 (p<0.05). Serum progesterone levels were significantly higher in the PCO animals than in the control group (p<0.05). No significant between-group differences (p>0.05) were found in BMP6 or BMP15 expression. Conclusion: In animals with EV-induced PCO, the preantral follicles did not develop into antral follicles. In this mouse model, the gene expression of TGFB1, GDF9, and BMPR2 was lower in preantral follicles, which is probably related to the pathologic conditions of PCO. Hypoandrogenism was also detected in this EV-induced murine PCO model.

• Genomics & Informatics
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• v.19 no.1
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• pp.5.1-5.11
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• 2021

Head and neck squamous cell carcinoma (HNSCC) is the most frequent type of head and neck cancer that usually arises from the mucosal surfaces of several organs including nasal cavity, paranasal sinuses, oral cavity, tongue, pharynx, and larynx. The Wnt signaling pathway is a crucial mechanism for cellular maintenance and development. It regulates cell cycle progression, apoptosis, proliferation, migration, and differentiation. Dysregulation of this pathway correlates with oncogenesis in various tissues including breast, colon, pancreatic as well as head and neck cancers. The present study aims to assess the gene alterations in the Wnt family of genes so as to derive an association with HNSCC. Computational approaches have been utilized for the identification of gene alterations in the Wnt family of genes. Several databases such as cBioportal, STRING, and UALCAN were used for the purpose. The frequency of alteration was high in case of Wnt family member 11 (5%). Gene amplification, deep deletions, missense and truncating mutations were observed in HNSCC patients. There was a marked difference in the gene expression profile of WNT11 between grades as well as normal samples. The survival probability measured using the Kaplan-Meier curve also presented with a significant difference among male and female subjects experiencing a low/medium level expression. The female patients showed less survival probability when compared to the male subjects. This provides the prognostic significance of the WNT11 gene in HNSCC. Taken together, the present study provides clues on the possible association of WNT11 gene alterations with HNSCC, which has to be further validated using experimental approaches.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.11
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• pp.4525-4530
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• 2015

Background: The MTHFR C677T polymorphism is a genetic alteration affecting an enzyme involved in folate metabolism, but its relationship to host susceptibility to prostate cancer remains uncertain. The aim of this study was to investigate the association between MTHFR C677T polymorphism and prostate cancer by performing a meta-analysis. Materials and Methods: Pubmed and Web of Science databases were searched for case-control studies investigating the association between MTHFR C677T polymorphism and prostate cancer. Odds ratios (OR) and 95% confidence intervals (95%CI) were used to assess any link. Results: A total of 22 independent studies were identified, including 10,832 cases and 11,993 controls. Meta-analysis showed that there was no obvious association between MTHFR C677T polymorphism and risk of prostate cancer under all five genetic models. There was also no obvious association between MTHFR C677T polymorphism and risk of prostate cancer in the subgroup analyses of Caucasians. In contrast, MTHFR C677T polymorphism was associated with increased risk for prostate cancer in Asians with the allele model (C vs G: OR=1.299, 95 %CI =1.121-1.506, P=0.001, $P_{heterogeneity}=0.120$, $I^2=45%$), additive genetic model (CC vs TT: OR =1.925, 95 % CI= 1.340-2.265, P=0.00, $P_{heterogeneity}=0.587$, $I^2=0.00%$), recessive model (CC vs TT+TC: OR= 1.708, 95 % CI=1.233-2.367, P=0.001, $P_{heterogeneity}=0.716$, $I^2=0.00%$), and heterozygote genetic model (CT vs TT: OR=2.193, 95 % CI =1.510-3.186, P=0.000, $P_{heterogeneity}=0.462$, $I^2=0.00%$). Conclusions: These results suggest that the MTHFR C677T polymorphism does not contribute to the risk of prostate cancer from currently available evidence in populations overall and Caucasians. However, the meta analysis indicates that it may play a role in prostate cancer development in Asians.

• Economic and Environmental Geology
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• v.21 no.1
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• pp.57-67
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• 1988

K-Ar age determinations were carried out on muscovite and other gangue and wallrock alteration minerals from seventeen mineral deposits in the Taebaeg mountain district. Tin deposits give the ages of 1792 Ma and 158-127 Ma, whereas tungsten-molybdenum deposits give the ages of 1520-1480 Ma. 173-168 Ma and 84-81 Ma. Polymetallic mineral deposits. gold-silver deposits and sericite deposits yield the ages of 98-52 Ma. 93-75 Ma, and 202 Ma, respectively. Mineralization ages for each genetic type of deposits in this district can be summarized as follows; pegmatite deposits. 1792 Ma ; pegmatite-hydrothermal deposits. 1526-1480 Ma ; greisen deposits. 157-127 Ma ; skarn deposits, 98-73 Ma and 52 Ma ; hydrothermal deposits, 202-168 Ma and 93-76 Ma. Present results together with data available in the literature reveal that five distinct mineralization ages can be recognized in this district ; (1) 1792 Ma, (2) 1526-1480 Ma, (3) 202-127 Ma. (4) 98-73 Ma, (5) 52 Ma, These age data are similar to the reported radiometric age data of igneous rocks in this district except for two ages such as 2154-2084 Ma and 880-738 Ma.

• Biomolecules & Therapeutics
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• v.26 no.1
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• pp.45-56
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• 2018

Cancer is the leading cause of human deaths worldwide. Understanding the biology underlying the evolution of cancer is important for reducing the economic and social burden of cancer. In addition to genetic aberrations, recent studies demonstrate metabolic rewiring, such as aerobic glycolysis, glutamine dependency, accumulation of intermediates of glycolysis, and upregulation of lipid and amino acid synthesis, in several types of cancer to support their high demands on nutrients for building blocks and energy production. Moreover, oncogenic mutations are known to be associated with metabolic reprogramming in cancer, and these overall changes collectively influence tumor-microenvironment interactions and cancer progression. Accordingly, several agents targeting metabolic alterations in cancer have been extensively evaluated in preclinical and clinical settings. Additionally, metabolic reprogramming is considered a novel target to control cancers harboring un-targetable oncogenic alterations such as KRAS. Focusing on lung cancer, here, we highlight recent findings regarding metabolic rewiring in cancer, its association with oncogenic alterations, and therapeutic strategies to control deregulated metabolism in cancer.