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Ovarian Cancer


Study data from University of Sherbrooke provide new insights into cancer



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This article was published in Clinical Oncology Week, which you can subscribe to online.

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2009 AUG 3 - (NewsRx.com) -- "Alternative splicing of pre-mRNA increases the diversity of protein functions. Here we show that about half of all active alternative splicing events in ovarian and breast tissues are changed in tumors, and many seem to be regulated by a single factor; sequence analysis revealed binding sites for the RNA binding protein FOX2 downstream of one-third of the exons skipped in cancer," scientists in Sherbrooke, Canada report.

"High-resolution analysis of FOX2 binding sites defined the precise positions relative to alternative exons at which the protein may function as either a silencer or an enhancer. Most of the identified targets were shifted in the same direction by FOX2 depletion in cell lines as they were in breast and ovarian cancer tissues. Notably, we found expression of FOX2 itself is downregulated in ovarian cancer and its splicing is altered in breast cancer samples," wrote J.P. Venables and colleagues, University of Sherbrooke.

The researchers concluded: "These results suggest that the decreased expression of FOX2 in cancer tissues modulates splicing and controls proliferation.."

Venables and colleagues published their study in Nature Structural & Molecular Biology (Cancer-associated regulation of alternative splicing. Nature Structural & Molecular Biology, 2009;16(6):670-U98).

For additional information, contact J.P. Venables, University of Sherbrooke, Laboratory Genom Fonct, Sherbrooke, PQ J1K 2R1, Canada.

The publisher's contact information for the journal Nature Structural & Molecular Biology is: Nature Publishing Group, 75 Varick St., 9TH Flr, New York, NY 10013-1917, USA.

Keywords: Canada, Sherbrooke, Cancer, Oncology, University of Sherbrooke.

This article was prepared by Clinical Oncology Week editors from staff and other reports. Copyright 2009, Clinical Oncology Week via NewsRx.com.

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