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설편평상피암에 있어서의 고밀도 SNP Genotyping 어레이를 이용한 전게놈북제수와 헤테로접합성 소실의 분석
黑岩 司(Kuroiwa Tsukasa),山本信治(Yamamoto Nobuharu),恩田健志(Onda Takeshi),別所央城(Bessyo Hiroki),藥師寺 孝( Yakushiji Takashi),片倉 朗(Katakura Akira),野伸夫(Takano Nobuo),柴原孝彦(Shibahara Takahiko) 대한구강악안면외과학회 2011 대한구강악안면외과학회지 Vol.37 No.6
Chromosomal loss of heterozygosity (LOH) is a common mechanism for the inactivation of tumor suppressor genes in human epithelial cancers. LOH patterns can be generated through allelotyping using polymorphic microsatellite markers; however, owing to the limited number of available microsatellite markers and the requirement for large amounts of DNA, only a modest number of microsatellite markers can be screened. Hybridization to single nucleotide polymorphism (SNP) arrays using Affymetarix GeneChip Mapping 10 K 2.0 Array is an efficient method to detect genome-wide cancer LOH. We determined the presence of LOH in oral SCCs using these arrays. DNA was extracted from tissue samples obtained from 10 patients with tongue SCCs who presented at the Hospital of Tokyo Dental College. We examined the presence of LOH in 3 of the 10 patients using these arrays. At the locus that had LOH, we examined the presence of LOH using microsatellite markers. LOH analysis using Affymetarix GeneChip Mapping 10K Array showed LOH in all patients at the 1q31.1. The LOH regions were detected and demarcated by the copy number 1 with the series of three SNP probes. LOH analysis of 1q31.1 using microsatellite markers (D1S1189, D1S2151, D1S2595) showed LOH in all 10 patients (100). Our data may suggest that a putative tumor suppressor gene is located at the 1q31.1 region. Inactivation of such a gene may play a role in tongue tumorigenesis.
Nguyen Thi Trang,Takuya Hirai,Tsukasa Yamamoto,Mari Matsuda,Naoko Okumura,Nguyen Thi Huong Giang,Nguyen Thi Lan,Ryoji Yamaguchi 대한수의학회 2014 Journal of Veterinary Science Vol.15 No.3
The objectives of the present study were to evaluate theanatomic localization of porcine reproductive andrespiratory syndrome virus (PRRSV) in naturally infectedpigs and to determine whether oral fluid could be used todetect the virus in infected animals. Two sows, seven2-month-old grower pigs, and 70 6-month-old gilts wereincluded in this study. PRRSV in sera and oral fluid wereidentified by nested reverse transcription PCR (nRT-PCR)while lung, tonsil, and tissue associated with oral cavity weresubjected to nRT-PCR, immunohistochemistry, and in situhybridization. In sows, PRRSV was identified in oral fluidand tonsils. PRRSV was also detected in oral fluid, tonsils,salivary glands, oral mucosa, and lungs of all seven growerpigs. However, viremia was observed in only two growerpigs. Double staining revealed that PRRSV was distributedin macrophages within and adjacent to the tonsillar cryptepithelium. In gilts, the North American type PRRSV fieldstrain was detected 3 to 8 weeks after introducing theseanimals onto the farm. These results confirm previousfindings that PRRSV primarily replicates in tonsils and isthen shed into oral fluid. Therefore, oral fluid sampling maybe effective for the surveillance of PRRSV in breeding herds.