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Tragara Pharmaceuticals' Apricoxib Reverses EMT, a Key Process for Cancer Progression and Metastasis
Date:5/26/2011

versal also reduced proliferation and survival of tumor cells in the primary lesion, perhaps due to a reduction in levels of cancer stem cells which are thought to arise via EMT."

The Capoxigem posters, originally presented earlier in 2011 and available on the Tragara company website, are:

2011 AACR 102nd Annual Meeting (April 4, 2011)

"Inhibition of COX-2 with Apricoxib Enhances the Efficacy of Standard Therapy in Preclinical Models of Human Pancreatic Cancer", Amanda R. Kirane, Ph.D., University of Texas Southwestern Medical Center, Dallas.

2011 ASCO Gastrointestinal Cancers Symposium (January 22, 2011)

"Preclinical Antitumor Activity and Mechanisms of Action of Apricoxib, a Clinical Cox-2 Inhibitor", Francis Burrows, Ph.D., Tragara Pharmaceuticals, Inc., San Diego.

About Epithelial-Mesenchymal Transition (EMT) and COX-2

The epithelial-mesenchymal transition (EMT) is a developmental program resulting in a cellular shift from an epithelial phenotype to a motile, mesenchymal form that is essential for embryogenesis, tissue remodeling and tumor progression. Under the influence of oncogenic factors such as inflammatory cytokines, polarized epithelial cancer cells detach from their underlying basement membrane and progressively lose lineage-specific markers such as E-cadherin and acquire mesenchymal markers (e.g. vimentin) and the ability to invade and metastasize to new sites. Both EMT and hyperactivity of the COX-2 pathway are associated with poor prognosis in a range of solid tumor types. Many of the properties of solid tumor cells that have undergone EMT, including apoptosis resistance and heightened angiogenic and metastatic capacity, are also associated with chronic inflammation and overexpression of COX-2 and its
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SOURCE Tragara Pharmaceuticals, Inc.
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