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Full genomic sequencing of prostate cancer tumors may lead to better therapeutic interventions
Berger MF. Nature. 2011;470:214-220.
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A paired analysis of seven prostate cancer tumors and matched normal DNA from those seven patients yielded insight into the genesis of tumor development, according to study results.
Researchers from several sites in the US performed paired-end, massively parallel sequencing on tumors that were at least stage T2c and Gleason grade 7.
The researchers observed a positive correlation between the location of rearrangement breakpoints in TMPRSS2–ERG-positive tumor cells and open chromatin in VCaP cells, and breakpoints present in ETS fusion-negative cells and VCaP regions of closed chromatin.
It was noted that these data may suggest that regions of open chromatin in some TMPRSS2–ERG-positive tumor cells may be the site of preferential breakpoints. The findings may also suggest that there are alternative possibilities for where breakpoints in ETS fusion-negative cells are generated.
Three tumors had disruptions in CADM2 and four had unbalanced events that disrupted PTEN or MAGI2. Interrogating the MAGI2 and PTEN locations may improve prognostic capabilities and stratification for trials involving phosphatidylinositol 3-kinase pathway inhibitors, according to the researchers.
“Genomic rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms,” the researchers wrote. They suggested that complete genomic sequencing of relapsing primary and metastatic prostate cancers may aid in developing a genetic map for clinicians to follow. The map may be useful in classifying tumors, defining mechanisms of carcinogenesis and identifying novel targets for therapeutic intervention.
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