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New data underlines Modrenal's genetic mechanism of action in breast cancer.

Women's Health Weekly

| January 01, 2004 | COPYRIGHT 2004 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2004 JAN 1 - (NewsRx.com & NewsRx.net) -- Bioenvision, Inc., (BIV) has presented new data underlining the ability of its lead breast cancer treatment, Modrenal (trilostane), to suppress the activity of estrogen at two groups of genes involved in breast cancer growth.

The research from Queen Mary, University Of London, and presented for the first time at the 26th San Antonio (Texas) Breast Cancer Symposium, helps to explain reported clinical benefit rates of over 50% and differentiates Modrenal's mechanism of action from existing therapies, such as tamoxifen and the aromatase inhibitors.

In hormone sensitive breast cancer, estrogen affects tumor growth through two main pathways. The preferred path is via estrogen receptors that activate genes that drive tumor cell proliferation. When this pathway is blocked, for example by drugs such as tamoxifen, estrogen eventually finds an alternative route (via a site in the nucleus known as the AP1 receptor). This activates a different set of genes that are also able to initiate cell growth. This is now referred to as the "cell survival pathway" and is believed to be the mechanism whereby cancer cells develop resistance to existing endocrine treatments ("acquired endocrine resistance").

The new data shows that tamoxifen blocks the preferred pathway but, in certain circumstances, will also promote cell growth via AP1 dependent genes. This could explain why patients develop a ...

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