EMERYVILLE, Calif., Dec. 29 /PRNewswire-FirstCall/ -- Bionovo, Inc. (Nasdaq: BNVI) announced today the publication of results from its study on the anti-tumor mechanism of BN107. The results of the study, published in the International Journal of Cancer, describe the potential molecular mechanisms mediating the selective pro-apoptotic (cell death) effect induced by BN107 on estrogen receptor negative (ER-) breast cancer cells.
Despite favorable advances that treatment options have had on survival, oncologists continue to face challenges in providing safe and effective treatment options for ER- breast cancer patients. In this patient population, the PI3K/Akt/mTOR pathway is often abnormally activated which allows cancer cells to grow uncontrollably and evade death. There are two mTOR protein complexes, mTORC1 and mTORC2, both of which are essential for the control of aberrant survival signals. Agents that can inhibit mTORC1 and mTORC2 at the same time might lead to effective suppression of the Akt/mTOR pathway and result in tumor cell death. The study showed that BN107 decreases the levels of proteins present in the mTORC1 and mTORC2 complexes, resulting in their demise specifically in ER- breast cancer cells. The mTOR pathway as a target for cancer therapies has been actively pursued by many pharmaceutical companies. To the Company's knowledge, this is the first report demonstrating effective inhibition of both mTOR complexes concomitantly through a novel mechanism.
As explained by Dr. Sylvia Fong, Research Scientist at Bionovo, "The ability of BN107 to induce cancer cell death is selective. We demonstrate that breast cancer cells lacking estrogen receptors are highly sensitive to BN107. Our studies show that disruption of mTOR signaling mediated by both mTORC1 and mTORC2 complexes is most likely responsible f
|SOURCE Bionovo, Inc.|
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