The central role of sequential accumulation of genetic alterations during the development of cancer has been firmly established since the pioneering cytogenetic studies successfully defined recurrent chromosome change...The central role of sequential accumulation of genetic alterations during the development of cancer has been firmly established since the pioneering cytogenetic studies successfully defined recurrent chromosome changes in spedfic types of tumor. In the course of carcinogenesis, cells experience several genetic alterations that are associated with the transition from a preneoplastic lesion to an invasive tumor and finally to the metastatic state. Tumor progression is characterized by stepwise accumulation of genetic alterations.So does the dominant metastatic clone. Modern molecular genetic analyses have clarified that genomic changes accumulate during the development and progression of cancers. In comparison with the corresponding primary tumor,additional events of chromosomal aberrations (including gains or allelic losses) are frequently found in metastases, and the incidence of combined chromosomal alterations in the primary tumor, plus the occurrence of additional aberrations inthe distant metastases, correlated significantly with decreased postmetastatic survival. The deletions at 3p, 4p, 6q, 8p, 10q,11p, 11q, 12p, 13q, 16q, 17p, 18q, 21q, and 22q, as well as the over-representations at 1q, 8q, 9q, 14q and 15q, have been found to associate preferentially with the metastatic phenotype of human cancers. Among of them, the deletions on chromosomes 8p, 17p, 11p and 13p seem to be more significant, and more detail fine regions of them, including 8p11, 8p21-12, 8p22, 8p23, 17p13.3, 11p15.5, and 13q12-13 have been suggested harboring metastasis-suppressor genes.During the past decade, several human chromosomes have been functionally tested through the use of microcell-mediated chromosome transfer (MMCT), and metastasis-suppressor activities have been reported on chromosomes 1, 6, 7, 8, 10,11, 12, 16, and 17. However, it is not actually known at what stage of the metastatic cascade these alterations have occurred.There is still controversial with the association between the chromosomal aberrations and the metastatic 展开更多
目的探索ZMIZ1-AS1编码区体细胞拷贝数变异在原发肿瘤组织分布及在特定肿瘤预后监测中的作用,为相关肿瘤预防提供特异性标志物线索及依据。方法由The Cancer Genome Atlas(TCGA)数据库下载31类实质肿瘤患者数据,用R 3.4.2进行统计分析,...目的探索ZMIZ1-AS1编码区体细胞拷贝数变异在原发肿瘤组织分布及在特定肿瘤预后监测中的作用,为相关肿瘤预防提供特异性标志物线索及依据。方法由The Cancer Genome Atlas(TCGA)数据库下载31类实质肿瘤患者数据,用R 3.4.2进行统计分析,采用χ^2检验及Fisher精确概率法分析ZMIZ1-AS1编码区体细胞拷贝数变异的分布差异,采用Kruskal-Wallis检验分析其对ZMIZ1-AS1与ZMIZ1表达的影响以及采用COX比例风险回归模型分析其对患者预后的影响。结果10547名患者原发肿瘤组织ZMIZ1-AS1编码区体细胞拷贝数缺失与增加在不同实质肿瘤间的分布差异有统计学意义(χ^2=3218.284,P<0.01);Kruskal-Wallis检验显示,ZMIZ1-AS1编码区拷贝数变异显著影响多数肿瘤中的ZMIZ1-AS1、ZMIZ1表达;COX回归分析结果显示,ZMIZ1-AS1编码区体细胞拷贝数缺失显著增加低分化胶质瘤(HR=11.06,95%CI:7.28~16.80)和间皮瘤(HR=4.04,95%CI:1.56~10.48)患者死亡风险。结论不同实质肿瘤其ZMIZ1-AS1编码区拷贝数变异分布存在差异,ZMIZ1-AS1编码区体细胞拷贝数缺失可作为低分化胶质瘤和间皮瘤预后监测的特异性生物标志物。展开更多
文摘The central role of sequential accumulation of genetic alterations during the development of cancer has been firmly established since the pioneering cytogenetic studies successfully defined recurrent chromosome changes in spedfic types of tumor. In the course of carcinogenesis, cells experience several genetic alterations that are associated with the transition from a preneoplastic lesion to an invasive tumor and finally to the metastatic state. Tumor progression is characterized by stepwise accumulation of genetic alterations.So does the dominant metastatic clone. Modern molecular genetic analyses have clarified that genomic changes accumulate during the development and progression of cancers. In comparison with the corresponding primary tumor,additional events of chromosomal aberrations (including gains or allelic losses) are frequently found in metastases, and the incidence of combined chromosomal alterations in the primary tumor, plus the occurrence of additional aberrations inthe distant metastases, correlated significantly with decreased postmetastatic survival. The deletions at 3p, 4p, 6q, 8p, 10q,11p, 11q, 12p, 13q, 16q, 17p, 18q, 21q, and 22q, as well as the over-representations at 1q, 8q, 9q, 14q and 15q, have been found to associate preferentially with the metastatic phenotype of human cancers. Among of them, the deletions on chromosomes 8p, 17p, 11p and 13p seem to be more significant, and more detail fine regions of them, including 8p11, 8p21-12, 8p22, 8p23, 17p13.3, 11p15.5, and 13q12-13 have been suggested harboring metastasis-suppressor genes.During the past decade, several human chromosomes have been functionally tested through the use of microcell-mediated chromosome transfer (MMCT), and metastasis-suppressor activities have been reported on chromosomes 1, 6, 7, 8, 10,11, 12, 16, and 17. However, it is not actually known at what stage of the metastatic cascade these alterations have occurred.There is still controversial with the association between the chromosomal aberrations and the metastatic
文摘目的探索ZMIZ1-AS1编码区体细胞拷贝数变异在原发肿瘤组织分布及在特定肿瘤预后监测中的作用,为相关肿瘤预防提供特异性标志物线索及依据。方法由The Cancer Genome Atlas(TCGA)数据库下载31类实质肿瘤患者数据,用R 3.4.2进行统计分析,采用χ^2检验及Fisher精确概率法分析ZMIZ1-AS1编码区体细胞拷贝数变异的分布差异,采用Kruskal-Wallis检验分析其对ZMIZ1-AS1与ZMIZ1表达的影响以及采用COX比例风险回归模型分析其对患者预后的影响。结果10547名患者原发肿瘤组织ZMIZ1-AS1编码区体细胞拷贝数缺失与增加在不同实质肿瘤间的分布差异有统计学意义(χ^2=3218.284,P<0.01);Kruskal-Wallis检验显示,ZMIZ1-AS1编码区拷贝数变异显著影响多数肿瘤中的ZMIZ1-AS1、ZMIZ1表达;COX回归分析结果显示,ZMIZ1-AS1编码区体细胞拷贝数缺失显著增加低分化胶质瘤(HR=11.06,95%CI:7.28~16.80)和间皮瘤(HR=4.04,95%CI:1.56~10.48)患者死亡风险。结论不同实质肿瘤其ZMIZ1-AS1编码区拷贝数变异分布存在差异,ZMIZ1-AS1编码区体细胞拷贝数缺失可作为低分化胶质瘤和间皮瘤预后监测的特异性生物标志物。
