Studying a deadly type of breast cancer called triple negative, Johns Hopkins Medicine scientists say they have identified key molecular differences between cancer cells that cling to an initial tumor and those that venture off to form distant tumors.
The research, using mouse models and human tissues, could pave the way for developing new treatments that target such molecular variations.
A report on the findings is published Aug. 3 in Science Translational Medicine.
“We have long needed new treatment targets and options for triple negative breast cancers,” says Andrew Ewald, Ph.D., the Virginia DeAcetis Professor in Basic Science Research and Director, Department of Cell Biology at the Johns Hopkins University School of Medicine and co-leader of the Cancer Invasion and Metastasis Program at the Johns Hopkins Kimmel Cancer Center. “These cancers often return within three years of diagnosis, and treatments used for other breast cancers don’t typically work for triple negative.”
An estimated 10%-20% of the 280,000 breast cancers diagnosed in the U.S. each year are triple negative, and the rate is higher among African American women, who are twice as likely as others to experience this form of the disease.
The lethal nature of this type of cancer is marked by the fact that its cells lack molecular flags on its surface that connect with the hormones estrogen and progesterone and a cancer growth-promoting protein called Her2-neu. Many current breast cancer therapies work by targeting those flags, rendering them of little use to those with triple negative tumors.
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