Richard Pietzak
EurekAlert
Cornell Center on the Microenvironment and Metastasis and Neuberger Berman Lung Cancer Research Center findings suggest targeting a single protein may help stop cancer spread.
NEW YORK (Feb. 22, 2012) — Oncologists have known that in order for cancer cells to spread, they must transform themselves so they can detach from a tumor and spread to a distant organ. Now, scientists at Weill Cornell Medical College have revealed critical steps in what happens next — how these cells reverse the process, morphing back into classical cancer that can now grow into a new tumor.
Their findings, now published online and in a upcoming issue of Cancer Research and funded through a National Cancer Institute grant to the Cornell Center on the Microenvironment and Metastasis and the Neuberger Berman Foundation, show that a single protein, versican, is key to this process in breast cancer, the tumor they studied. When researchers stopped versican from functioning in mice, breast cancer could not “seed” themselves into the lungs and form secondary tumors.
“Our findings both help us understand how breast cancer metastasizes to the lungs and ways to possibly prevent that deadly spread,” says the study’s senior investigator, Dr. Vivek Mittal, an associate professor of cell and developmental biology in cardiothoracic surgery and director of the Neuberger Berman Lung Cancer Laboratory at Weill Cornell Medical College.
Read More: Researchers reveal how cancer cells change once they spread to distant organs