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A genomic screen for DNA hypermethyl...

Chen, Wei.

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A genomic screen for DNA hypermethylome in human cancer.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	A genomic screen for DNA hypermethylome in human cancer./
作者:	Chen, Wei.
面頁冊數:	130 p.
附註:	Adviser: Stephen B. Baylin.
Contained By:	Dissertation Abstracts International68-11B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3288439
ISBN:	9780549311744

A genomic screen for DNA hypermethylome in human cancer.
Chen, Wei.

A genomic screen for DNA hypermethylome in human cancer. - 130 p.

Adviser: Stephen B. Baylin.

Thesis (Ph.D.)--The Johns Hopkins University, 2008.

Gene silencing, via transcriptional repression in association with abnormal DNA methylation of CpG islands in gene promoter regions, is a fundamental aspect of neoplasia. Many approaches have been used to discover methylated and silenced genes in cancer cells, including analysis of candidate genes approach, genomic scanning, and gene expression based approaches.

ISBN: 9780549311744Subjects--Topical Terms:

1017730
Biology, Genetics.

A genomic screen for DNA hypermethylome in human cancer.
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245 1 2 $a A genomic screen for DNA hypermethylome in human cancer.
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502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2008.
520 $a Gene silencing, via transcriptional repression in association with abnormal DNA methylation of CpG islands in gene promoter regions, is a fundamental aspect of neoplasia. Many approaches have been used to discover methylated and silenced genes in cancer cells, including analysis of candidate genes approach, genomic scanning, and gene expression based approaches.
520 $a In this study, we combined pharmacological reactivation of silenced genes with microarray expression profiling to discover aberrantly DNA methylated and silenced genes in cancer. We first used combined drug treatment with the DNA demethylating agent, 5-Aza-deoxycytidine (DAC) and the histone deactylase inhibitor, Trichostatin A (TSA), to reactivate methylated and silenced genes in colorectal cancer (CRC) cell lines. RNA samples from the cells before and after drug treatment was amplified by cDNA subtraction and gene expression was studied using radio-active labeling cDNA microarrays. In the CRC cell line RKO, a successful screen was carried out, with the discovery of 12 new hypermethylated and silenced CRC genes.
520 $a We further used combined pharmacological manipulation with an expression microarray approach to the whole human transcriptome employing the Agilent 44K platform. Six colon cancer cell lines were treated with 5muM DAC and compared with treatment with 300 nM TSA. In this paradigm, a positive re-expression reponse to DAC and a negative response to TSA is the discovery filter. Between 1000 to 1500 candidate DNA hypermethylated genes were discovered in the 6 different colorectal cancer cell lines. By screening cell lines and validating tumor specific hypermethylation in a panel of primary human CRC samples, we can now estimate that nearly 5% of all known genes may be promoter DNA hypermethylated in any individual CRC. We have also found that a significant number of genes with a low incidence of mutations in CRC have a much higher incidence of DNA hypermethylation and silencing in these tumors. We, thus, conclude that random screening for DNA hypermethylated and silenced genes in cancer will produce a wealth of information to enhance our knowledge of the biology of tumorigenesis, and a rich source of genes to use as tumor biomarkers and clinically relevant indicators of tumor behavior.
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