The key to locking up cancer

Sara Braniecki

Structure of TGF-B

In the current issue of Nature Cell Biology, a team of researchers led by Philip Howe from the Department of Cancer Biology at the Lerner Research Institute explain how they worked backwards to discover the protein that triggers cancer cells to be released from the original tumor, thus giving rise to new tumors.  Knowing this can lead to the development of drugs that contain cancer to one location, making it more efficiently treatable.

The researchers already knew that a process called epithelial-mesenchymal transdifferentiation (EMT) was important for cells on the surface of a tumor to transform into cells that are able to grow a new tumor elsewhere in the body.  The researchers worked backwards through the EMT process to find out what initiates it.  The researchers discovered that a protein called disabled-2 (Dab2) activated the EMT process and Dab2’s formation was triggered by transforming growth factor-b (TGF-b).

The EMT process is often what leads to death in patients with breast, ovarian, pancreatic, and colon-rectal cancers.  With the information these researchers have discovered about cancer cells, researchers can now begin to create drugs to stop EMT and stop cancer from spreadings.  This information could also lead to understanding how other diseases progress and can be contained.

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