• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.33 no.2
• /
• pp.81-93
• /
• 2007

Purpose: Adenoid cystic carcinoma (ACC) is a relatively rare tumor that arises in glandular tissues of the head and neck region and sometimes has a protracted clinical course with perineural invasion and delayed onset of distant lung metastasis. Treatment failure of salivary ACC is most often associated with perineural and hematogenous tumor spread. However, very little has been known about the cellular and molecular mechanisms of perineural invasion and hematogenous distant metastasis of parotid ACC. This study was designed to develop an orthotopic tumor model of parotid adenoid cystic carcinoma in athymic nude mice. Experimental Design: A melanoma cell line was injected into the parotid gland of athymic mice to determine whether such implantation was technically feasible. A parotid ACC cell line was then injected into the parotid gland or the subcutaneous tissue of athymic mice at various concentrations of tumor cells, and the mice were thereafter followed for development of tumor nodule. The tumors were examined histopathologically for perineural invasion or regional or distant lung metastasis. We used an oral squmous cell carcinoma cell line as control. Results: Implantation of tumor(melanoma) cell suspension into the parotid gland of nude mice was technically feasible and resulted in the formation of parotid tumors. A parotid ACC cell line, ACC3 showed no significantly higher tumorigenicity, but showed significantly higher lung metastatic potential in the parotid gland than in the subcutis. In contrast, mucosal squmous cell carcinoma cell line doesn’t show significantly higher lung metastatic potential in the parotid gland than in the subcutis. The ACC tumor established in the parotid gland seemed to demonstrate perineural invasion of facial nerve, needs further study. Conclusion: An orthotopic tumor model of salivary ACC in athymic nude mice was successfully developed that closely recapitulates the clinical situations of human salivary ACC. This model should facilitate the understanding of the cellular and molecular mechanisms of tumorigenisis and metastasis of salivary ACC and aid in the development of targeted molecular therapies of salivary ACC.

• Asian-Australasian Journal of Animal Sciences
• /
• v.22 no.12
• /
• pp.1633-1639
• /
• 2009

This study investigated the effect of maternal undernutrition during late pregnancy on the growth and development of ovine fetal visceral organs. One hundred Mongolian ewes were mated at a synchronized oestrus and divided into three groups and offered 0.175 MJ ME $kgw^{-0.75}\;d^{-1}$ (Restricted Group1; RG1), 0.33 MJ ME $kgw^{-0.75}\;d^{-1}$ (Restricted Group2; RG2) and ad libitum access to feed (Control Group; CG) during late pregnancy (90 days). Selected animals in each group were slaughtered immediately at d 90 of pregnancy and after parturition (neonatal lambs), and major visceral organs were removed and weighed separately. The results indicated that the weights of lung (p<0.01), spleen (p<0.01), heart (p<0.05), liver (p<0.05) and abomasum (p<0.01) in RG1 were significantly lighter than those of CG. For RG2, only the weights of the lung (p<0.05) and spleen (p<0.01) were significantly lighter than those of CG; when expressed as a percentage of body weight, significance was retained in the spleen (p<0.01) for both restricted groups, but the percentage of brain in RG1 was significantly higher than that in CG (p<0.01). For lung and spleen, the amount of DNA was significantly lower (p<0.01) in both groups of restricted neonatal lambs compared to CG; however, there was a significant difference only between RG1 and CG for protein: DNA ratio (p<0.01). The DNA content of kidney, abomasum and jejunum were decreased (p<0.05) in RG1 neonatal lambs, but protein: DNA ratio in the liver was decreased compared with that of CG (p<0.05). The plane of maternal undernutrition during late pregnancy had a significant effect on the growth and development of fetal visceral organs, which altered ontogeny of fetal organ growth and development. These perturbations in fetal visceral development may have significant implications on postnatal growth and adult health.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.21
• /
• pp.9203-9210
• /
• 2014

Purpose: To explore associations of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region. Materials and Methods: CYP2E1 and NAT2 polymorphisms were detected by PCR-RFLP in 930 lung cancer patients and 1000 controls. Results: (1) Disequilibrium of the distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations (p=0.031). (2) Lung cancer risk was higher in individuals with c1, D allele of CYP2E1 RsaI/PstI, DraI polymorphisms and slow acetylation of NAT2 (c1 compared with c2, OR=1.382, 95%CI: 1.178-1.587, p=0.003; D compared with C, OR=1.241, 95%CI: 1.053-1.419, P<0.001; slow acetylation compared with rapid acetylation, OR=1.359, 95%CI:1.042-1.768, p=0.056) (3) Compared with c2/c2 and rapid acetylation, c1/c1 together with slow acetylation synergetically increased risk of lung cancer 2.83 fold. (4) Smokers with CYP2E1 c1/c1, DD, and NAT2 slow acetylation have 2.365, 1.916, 1.841 fold lung cancer risk than others with c2/c2, CC and NAT2 rapid acetylation, respectively. (5) Han smokers with NAT2 slow acetylation have 1.974 fold lung cancer risk than others with rapid acetylation. Conclusions: Disequilibrium distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations. Besides, Han smokers with NAT2 slow acetylation may have higher lung cancer risk compared with rapid acetylation couterparts. CYP2E1 c1/c1, DD and NAT2 slow acetylation, especially combined with smoking, contributes to the development of lung cancer. CYP2E1 c1/c1 or DD genotype and NAT2 slow acetylation have strong synergistic action in increasing lung cancer risk.

• Asian Pacific Journal of Cancer Prevention
• /
• v.13 no.9
• /
• pp.4689-4693
• /
• 2012

Lung cancer is the most common type of cancer and one of the leading causes of death in the world. Genetic factors play an important role in its development. PDCD6, the encoding gene for programmed cell death protein 6, may function as a tumor suppressor gene. Non-small cell lung cancer (NSCLC) contributes about 80% to newly histologically diagnosed lung cancer patients. To explore the relationship between PDCD6 and NSCLC, we examined two single nucleotide polymorphisms(rs3756712 G/T andrs4957014 G/T, both in the intron region) of the PDCD6gene.A hospital-based case-control study was carried out including 302 unrelated NSCLC patients and 306 healthy unrelated subjects. Significantly increased NSCLC risk was found to be associated with the T allele of rs4957014 (P=0.027, OR=0.760, 95%CI=0.596-0.970). The genotype and allele frequencies of rs3756712 did not shown any significant difference between NSCLC group and controls (P=0.327, OR=0.879, 95%CI=0.679-1.137). In conclusion, we firstly demonstrated the association between the PDCD6 gene and risk of NSCLC in a Chinese Han population.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.6
• /
• pp.3725-3728
• /
• 2013

Background: The mammalian target of rapamycin (mTOR) /RPS6KB1 activation has recently been implicated in tumour development, but its role in lung cancer remains unclear. The aim of this study was to explore the role of mTOR/RPS6KB1 signaling pathway in non-small-cell lung cancer (NSCLC). Methods: Immunohistochemistry was performed to assess the expression of phosphorylated mammalian target of rapamycin (p-mTOR) and its downstream ribosomal phosphorylated RPS6KB1 (p-RPS6KB1) in NSCLC patients. We also analyzed p-mTOR/p-RPS6KB1 protein expression in 45 fresh NSCLC tissues using Western blotting. Results: The expression level of p-mTOR and p-RPS6KB1 was significantly higher in NSCLC tumor specimens than that in adjacent noncancerous normal lung tissues (P<0.01). p-mTOR expression correlated with p-RPS6KB1. Furthermore, high expression level of p-mTOR or p-RPS6KB1 in NSCLC was associated with a shorter overall survival (both P<0.01). Multivariate analysis indicated high level of p-mTOR expression was an independent prognostic factor (HR=2.642, 95%CI 1.157-4.904, p=0.002). Conclusions: p-mTOR and p-RPS6KB1 could be useful prognostic markers for NSCLC.

• Proceedings of the Korea Information Processing Society Conference
• /
• 2017.04a
• /
• pp.609-610
• /
• 2017

국내 외에서 잘못된 생활습관으로 대사증후군 환자가 급증하고 있다. 최근 대사증후군 환자들을 위한 웨어러블 디바이스를 이용하여 생활습관정보를 수집 분석하여 피드백하는 연구가 진행되고 있다. 생활습관 정보를 수집하는 대표적인 방법은 온라인/오프라인 설문지 또는 웨어러블 디바이스를 활용하여 수집하는 형태로 구분된다. 그러나 기존 설문지 방법은 연속적인 데이터를 얻기 어렵고, 웨어러블 디바이스를 이용하는 방법은 신뢰성 있는 데이터를 수집하기에는 한계가 있다. 따라서 본 논문에서는 대사증후군 환자를 대상으로 생활습관 정보 수집을 위한 병원의 설문지를 앱을 기반으로 개발하여 수집하고 스마트 폰과 밴드와 같은 웨어러블 디바이스를 이용하여 실시간 활동정보를 수집하여 환자 생활 습관에 따른 맞춤 별 예방정보를 제공하는 시스템을 제안하고자 한다.

• Clinical and Experimental Pediatrics
• /
• v.61 no.1
• /
• pp.30-34
• /
• 2018

Congenital pulmonary airway malformation (CPAM), previously known as congenital cystic adenomatoid malformation, is a rare developmental lung abnormality associated with rhabdomyosarcoma, pleuropulmonary blastoma, and mucinous adenocarcinoma of the lung. We report an unusual case of a 10-day-old male newborn with a left lower lobe pulmonary cyst who underwent lobectomy, which revealed type II CPAM complicated by multifocal mucinous adenocarcinoma. KRAS sequencing revealed a somatic mutation in Codon12 ($GGT{\rightarrow}GAT$), suggesting the development of a mucinous adenocarcinoma in the background of mucinous metaplasia. Mucinous adenocarcinoma is the most common lung tumor associated with CPAM, but it generally occurs in older children and adults. Further, all cases in the literature are of type I CPAM. This case in a neonate indicates that malignant transformation can occur very early in type II CPAM.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.8
• /
• pp.4485-4494
• /
• 2013

Epidermal growth factor receptor (EGFR) is considered to be one of the key driver genes in non-small cell lung cancer (NSCLC). Several clinical trials have shown great promise of EGFR tyrosine kinase inhibitors (TKIs) in the first-line treatment of NSCLC. Many advances have been made in the understanding of EGFR signal transduction network and the interaction between EGFR and tumor microenvironment in mediating cancer survival and development. The concomitant targeted therapy and radiation is a new strategy in the treatment of NSCLC. A number of preclinical studies have demonstrated synergistic anti-tumor activity in the combination of EGFR inhibitors and radiotherapy in vitro and in vivo. In the present review, we discuss the rationale of the combination of EGFR inhibitors and radiotherapy in the treatment of NSCLC.

• The Journal of Korean Medicine
• /
• v.26 no.1 s.61
• /
• pp.18-25
• /
• 2005

Objective & Methods: We examined the effects of Platycodi radix on the process of lipopolysaccharide (LPS)-induced nuclear factor $NF-{\kappa}Bp65$ and inhibitory $(I)-{\kappa}B{\alpha}$ alteration in RAW 264.7 cells and acute lung injury in rats. Results: Immunoblot analysis showed that LPS-induced degradation of $I-{\kappa}B{\alpha}$ in RAW 264.7 was inhibited by pretreatment of Platycodi radix. The total cells of bronchoalveolar lavage fluid by LPS challenge markedly decreased in the Platycodi radix pretreatment rats. Platycodi radix pretreatment also caused a decline in neutrophils infiltration into interstitium of the lung. In the alveolar macrophages and neutrophils, decreased $NF-{\kappa}Bp65$ and inducible nitric oxide synthase and increased $I-{\kappa}B{\alpha}$ immunoreaction were detected in Platycodi radix pretreated rats compared with LPS alone treated ones. Conclusion : It may be concluded that Platycodi radix attenuates the development of LPS-induced inflammation by reduction of $NF-{\kappa}Bp65$ activation and neutrophil-mediated acute lung injury. Platycodi radix would be useful as a therapeutic agent for endotoxin-induced lung disease.

• IMMUNE NETWORK
• /
• v.11 no.6
• /
• pp.309-323
• /
• 2011

MicroRNAs (miRNAs) are a class of naturally occurring small non-coding RNAs of about 22 nucleotides that have recently emerged as important regulators of gene expression at the posttranscriptional level. Recent studies provided clear evidence that microRNAs are abundant in the lung, liver and kidney and modulate a diverse spectrum of their functions. Moreover, a large number of studies have reported links between alterations of miRNA homeostasis and pathological conditions such as infectious diseases, sickle cell disease and endometrium diseases as well as lung, liver and kidney diseases. As a consequence of extensive participation of miRNAs in normal functions, alteration and/or abnormalities in miRNAs should have importance in human diseases. Beside their important roles in patterning and development, miRNAs also orchestrated responses to pathogen infections. Particularly, emerging evidence indicates that viruses use their own miRNAs to manipulate both cellular and viral gene expression. Furthermore, viral infection can exert a profound impact on the host cellular miRNA expression profile, and several RNA viruses have been reported to interact directly with cellular miRNAs and/or to use these miRNAs to augment their replication potential. Here I briefly summarize the newly discovered roles of miRNAs in various human diseases including infectious diseases, sickle cell disease and enodmetrium diseases as well as lung, liver and kidney diseases.