From the ddn Blog: A potential double-play on triple negative breast cancer

A research team at Weill Cornell Medical College has discovered a molecular ‘switch’ that allows triple negative breast cancer cells—which doesn’t express the genes for the estrogen receptor, progesterone receptor or HER2/neu—to develop the protrusions necessary to detach from the primary tumor and metastasize throughout the rest of the body.

Kelsey Kaustinen
This column appeared on the ddn Blog on Jan. 21, 2013. Visit the ddn Blog at www.drugdiscoverynews.com/blog.
 
No matter what kind of cancer you're talking about,metastasis is one of the primary problems, often leading to relapse asthe tumors reappear in different parts of the body. And of all the types of cancer out there, breast cancer is one of the worst offenders whenit comes to metastasis due to its proximity to the lymph nodes andproclivity to spreading. So far, the best bet for preventing metastasisis the timely removal of tumors and the application of chemotherapy, but now there might be a new method: stopping the metastasis itself.
 
A research team at Weill Cornell Medical College has discovered a molecular 'switch' that allows triple negative breastcancer cells—which doesn't express the genes for the estrogen receptor,progesterone receptor or HER2/neu—to develop the protrusions necessaryto detach from the primary tumor and metastasize throughout the rest ofthe body. Triple negative breast cancer is one of the deadliest types of breast cancer, with high recurrence rates and metastatic spread, andaccounts for 15 to 25 percent of all breast tumors.
 
The researchers focused on finding agents that could restore function to a microRNA that plays a significant role in the spread of cancer,and found that the miRNA miR-708 is inhibited in triple negative breastcancer. When functioning regularly, miR-708 acts as a metastatic tumorinhibitor, and tumors don't spread or form macrometastases. Bydelivering a synthetic form of the miRNA in bubbles of fat, theresearchers were able to block the cancer cells' metastatic growth inthe lungs of mice.
 
In addition, the team also discovered that polycombrepressor complex proteins are responsible for the inhibition ofmiR-708, which offers additional promise since several pharmacologicalagents currently undergoing testing as lymphoma cancer drugs aredesigned to inhibit histone-lysine N-methyltransferase EZH2, the memberof the polycomb group that directly silences miR-708.
 
Obviously, no matter what type of cancer is being treated, the hopeis always to stop it before it spreads. But in cancers such as triplenegative breast cancer and others prone to metastasis, having a way tocurtail the spread of cancer is the best kind of backup there is.

Kelsey Kaustinen

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