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【Cancer research】前列腺癌基因组的系统性分析有

Cancer Res. 2007 Sep 1;67(17):8229-39.

Integrative analysis of genomic aberrations associated with prostate cancer progression.
Kim JH, Dhanasekaran SM, Mehra R, Tomlins SA, Gu W, Yu J, Kumar-Sinha C, Cao X, Dash A, Wang L, Ghosh D, Shedden K, Montie JE, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM.

Integrative analysis of genomic aberrations in the context of trancriptomic alterations will lead to a more comprehensive perspective on prostate cancer progression. Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate cancer samples spanning stages of prostate cancer progression, including precursor lesions, clinically localized disease, and metastatic disease. A total of 62 specific cell populations from 38 patients were profiled. Minimal common regions (MCR) of alterations were defined for each sample type, and metastatic samples displayed the most number of alterations. Clinically localized prostate cancer samples with high Gleason grade resembled metastatic samples with respect to the size of altered regions and number of affected genes. A total of 9 out of 13 MCRs in the putative precursor lesion, high-grade prostatic intraepithelial neoplasia (PIN), showed an overlap with prostate cancer cases (amplifications in 3q29, 5q31.3-q32, 6q27, and 8q24.3 and deletions in 6q22.31, 16p12.2, 17q21.2, and 17q21.31), whereas postatrophic hyperplasia (PAH) did not exhibit this overlap. Interestingly, prostate cancers that do not overexpress ETS family members (i.e., gene fusion-negative prostate cancers) harbor differential aberrations in 1q23, 6q16, 6q21, 10q23, and 10q24. Integrative analysis with matched mRNA profiles identified genetic alterations in several proposed candidate genes implicated in prostate cancer progression. 本人已认领该文编译,48小时后若未提交译文,请其他战友自由认领。 Integrative analysis of genomic aberrations associated with prostate cancer progression.
Kim JH, Dhanasekaran SM, Mehra R, Tomlins SA, Gu W, Yu J, Kumar-Sinha C, Cao X, Dash A, Wang L, Ghosh D, Shedden K, Montie JE, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM.
前列腺癌基因组的系统性分析有助发现演进过程中的关键基因
Integrative analysis of genomic aberrations in the context of trancriptomic alterations will lead to a more comprehensive perspective on prostate cancer progression. Genome-wide copy number changes were monitored using array comparative genomic hybridization of laser-capture microdissected prostate cancer samples spanning stages of prostate cancer progression, including precursor lesions, clinically localized disease, and metastatic disease. A total of 62 specific cell populations from 38 patients were profiled. Minimal common regions (MCR) of alterations were defined for each sample type, and metastatic samples displayed the most number of alterations. Clinically localized prostate cancer samples with high Gleason grade resembled metastatic samples with respect to the size of altered regions and number of affected genes. A total of 9 out of 13 MCRs in the putative precursor lesion, high-grade prostatic intraepithelial neoplasia (PIN), showed an overlap with prostate cancer cases (amplifications in 3q29, 5q31.3-q32, 6q27, and 8q24.3 and deletions in 6q22.31, 16p12.2, 17q21.2, and 17q21.31), whereas postatrophic hyperplasia (PAH) did not exhibit this overlap. Interestingly, prostate cancers that do not overexpress ETS family members (i.e., gene fusion-negative prostate cancers) harbor differential aberrations in 1q23, 6q16, 6q21, 10q23, and 10q24. Integrative analysis with matched mRNA profiles identified genetic alterations in several proposed candidate genes implicated in prostate cancer progression.
在trancriptomic改变的背景下基因组畸变的整合性分析将导致对前列腺癌进展更加广泛认识。通过对各个时期前列腺癌包括癌前病变、临床局限性疾病和转移性疾病,采用激光捕获微切割的前列腺癌样本,应用阵列比较基因组杂交方法检测全基因组拷贝数的改变。总共有来自于38例病人的62种特异性细胞进行了检测。对每个样本类型确定了最小常见区(MCR),转移性样本表现为大多数改变,伴有高Gleason分级的临床上局限性前列腺癌样本在变异区的大小和受累基因的数量上类似于转移性样本。13个MCR中有9个为潜在的癌前病变、高度PIN,与前列腺癌有重叠(3q29, 5q31.3-q32, 6q27和8q24.3的扩增,6q22.31, 16p12.2, 17q21.2和 17q21.31的缺失),而萎缩后增生则没有这种重叠。令人高兴的是,不过表达ETS家族成员(如基因融合阴性的前列腺癌)的前列腺癌在1q23, 6q16, 6q21, 10q23,和10q24有差异的畸变。采用配对的mRNA谱的整合性分析可鉴定参与前列腺癌进展的几种候选基因的遗传学改变。. 前列腺癌基因组的系统性分析有助发现演进过程中的关键基因
在trancriptomic改变的背景下基因组畸变的整合性分析将导致对前列腺癌进展更加广泛认识。通过对各个时期前列腺癌包括癌前病变、临床局限性疾病和转移性疾病,采用激光捕获微切割的前列腺癌样本,应用阵列比较基因组杂交方法检测全基因组拷贝数的改变。总共有来自于38例病人的62种特异性细胞进行了检测。对每个样本类型确定了最小常见区(MCR),转移性样本表现为大多数改变,伴有高Gleason分级的临床上局限性前列腺癌样本在变异区的大小和受累基因的数量上类似于转移性样本。13个MCR中有9个为潜在的癌前病变、高度PIN,与前列腺癌有重叠(3q29, 5q31.3-q32, 6q27和8q24.3的扩增,6q22.31, 16p12.2, 17q21.2和 17q21.31的缺失),而萎缩后增生则没有这种重叠。令人高兴的是,不过表达ETS家族成员(如基因融合阴性的前列腺癌)的前列腺癌在1q23, 6q16, 6q21, 10q23,和10q24有差异的畸变。采用配对的mRNA谱的整合性分析可鉴定参与前列腺癌进展的几种候选基因的遗传学改变。.

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作者:admin@医学,生命科学    2011-03-05 17:14
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