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Potential new eye tumor treatment discovered
Date:8/4/2011

es in all human retinoblastomas examined and in some mouse retinoblastomas. The authors engineered mice to express high levels of miR-17~92 in their retinas. When coupled with inactivation of Rb family members, expression of miR-17~92 led to extremely rapid and aggressive retinoblastoma. Then they showed that this abundance of miR-17~92 acts to suppress an inhibitor of proliferation, called p21Cip1, which is supposed to compensate for the loss of Rb.

"These findings which show that miR-17~92 overcomes the cell's attempts to compensate for the loss of Rbcould be similar in other types of cancers," MacPherson said. "This microRNA cluster could represent a new therapeutic target for treating tumors caused by Rb deficiency."


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Contact: David MacPherson
macpherson@ciwemb.edu
410-246-3084
Carnegie Institution
Source:Eurekalert

Page: 1 2

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