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Telomere failure, telomerase activation drive prostate cancer progression
Date:2/21/2012

humans

Chin, Ding and colleagues analyzed gene copy number aberrations - genes deleted or amplified - in 18 advanced tumors from the mice and 194 human prostate tumors.

They found 22 of the 94 copy number alterations involving deletion or amplification of 741 genes identified in mice were similar to those found in humans. A series of analyses of changes found in bone metastases pointed to deletions of the Smad4 tumor-suppressor gene, which regulates the transforming growth factor beta (TGF-) pathway.

The team took this finding back to the mouse model with tumor suppressors p53 and pten knocked out. These mice don't develop bone metastasis, but when the researchers also knocked out Smad4, more aggressive tumors developed, including bone metastasis in three of 24 mice.

Genes prognostic for human prostate cancer

Next, they looked at 14 genes in nine molecular pathways found to be enriched in bone metastasis to see if they were prognostic for recurrence (as measured by PSA levels after surgery) among 140 prostate cancer patients.

The 14-gene set was significantly prognostic of biochemical recurrence, providing evidence of their biological relevance to human prostate cancer, but the researchers noted that their individual contributions and mechanisms of action will require further research.

"Overall, our findings validate the integrative approach of employing genotype-phenotype correlations found in the mouse model with the power of genomic and bioinformatic analyses to discover and explain molecular mechanisms that drive prostate cancer," said co-first author Chang-Jiun Wu, Ph.D., a postdoctoral fellow in MD Anderson's Department of Genomic Medicine.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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