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Copy number changes of target genes in chromosome 3q25.3-qter of esophageal squamous cell carcinoma: TP63is amplified in early carcinogenesis but down-regulated as disease progressed

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World Journal of Gastroenterology 2005年第9期11卷 1267-1272页

作者： Chueh-ChuanYen Yann-JangChen Chin-ChenPan Kai-HsiLu PaulChih-HsuehChen Jiun-YiHsia Jung-TaChen Yu-ChungWu Wen-HuHsu Liang-ShunWang Min-HsiungHuang biing-shiunghuang Cheng-PoHu Po-MinChen Chi-HungLin DivisionofMedicalOncology DepartmentofMedicineTaipeiVeteransGeneralHospitalandNationalYang-MingUniversitySchoolofMedicineTaipeiTaiwanChina FacultyofLifeScience NationalYang-MingUniversityTaipeiTaiwanChina DepartmentofPathology NationalYang-MingUniversityandTaipeiVeteransGeneralHospitalTaiwanChina InstituteofMicrobiologyandImmunology NationalYang-MingUniversityTaipeiTaiwanChina DivisionofThoracicSurgery DepartmentofSurgeryTaichungVeteransGeneralHospitalTaichungTaiwanChina DepartmentofPathology.TaichungVeteransGeneralHospital andDepartmentofPathologyChung-ShanMedicalUniversityTaichungTaiwanChina DivisionofThoracicSurgery DepartmentofSurgeryTaipeiVeteransGeneralHospitalandNationalYang-MingUniversityTaipeiTaiwanChina InstituteofMicrobiologyandImmunology NationalYang-MingUniversityandDepartmentofMedicalResearchandEducationTaipeiVeteransGeneralHospitalTaipeiTaiwanChina InstituteofMicrobiologyandImmunology andInstituteofBiophotonicsNationalYang-MingUniversityTaipeiTaiwanChina

AIM: By using comparative genomic hybridization, gain of 3q was found in 45-86% cases of esophageal squamous cell carcinoma (EC-SCC). Chromosome 3q25.3-qter is the minimal common region with several oncogenes found within this region. However, amplification patterns of these genes in EC-SCC have never been reported. The possible association of copy number changes of these genes with pathologic characteristics is still not clear. METHODS: Real-time quantitative PCR (Q-PCR) was performed to analyze the copy number changes of 13 candidate genes within this region in 60 primary tumors of EC-SCC, and possible association of copy number changes with pathologic characteristics was analyzed by statistics. Immunohistochemistry (IHC) study was also performed on another set of 111 primary tumors of EC-SCC to verify the association between TP63 expression change and lymph node metastasis status. RESULTS: The average copy numbers (±SE) per haploid genome of individual genes in 60 samples were (from centromere to telomere): SSR3: 4.19 (±0.69); CCNL1: 5.24 (±0.67); SMC4L1: 2.01 (±0.16); EVI1: 2.02 (±0.12); hTERC. 5.28 (±0.54); SKIL 2.71 (±0.14); EIF5A2. 1.95 (±0.12); ECT2: 9.18 (±1.68); PIK3CA: 8.13 (±1.17); EIF4G1: 1.07 (±0.05); 557: 3.07 (±0.25); TP63: 2.51 (±0.22); TFRC. 2.42 (±0.19). Four clusters of amplification were found: SSR3 and CCLN1 at 3q25.31; hTERC and SKIL at 3q26.2; ECT2 and PIK3CA at 3q26.31-q26.32; and 55T, TP63 and TFRC at 3q27.3-q29. Patients with lymph node metastasis had significantly lower copy number of TP63 in the primary tumor than those without lymph node metastasis. IHC study on tissue arrays also showed that patients with lymph node metastasis have significantly lower TP63 staining score in the primary tumor than those without lymph node metastasis. CONCLUSION: This study showed that different amplification patterns were seen among different genes within 3q25.3-qter in EC-SCC, and several novel candidate oncogenes (SSR3, SMC4L1, ECT2, and SST) were ide

关键词： Chromosomal aberration Comparative genomic hybridization Esophageal neoplasm Immunohistochemistry Quantitative real-time PCR Tissue array Tumor protein 63

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