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Subset Signatures

A large-scale study of triple-negative breast cancer shows that small molecules called microRNAs can be used to define four subtypes of this aggressive malignancy.

Subset Signatures

Triple-Negative Breast Cancer Subtypes Identified Using microRNA

A large-scale study of triple-negative breast cancer shows that small molecules called microRNA can be used to define four subtypes of this aggressive malignancy.

The findings, by researchers at the OSUCCC – James who are working with collaborators in Italy, could lead to new screening methods, prognostic markers and perhaps targeted treatments for this aggressive and often-fatal form of breast cancer.

“Treating women with triple-negative breast cancer is challenging because this malignancy can be very different genetically from one patient to another,” says co-senior investigator Charles Shapiro, MD, director of Breast Medical Oncology at the OSUCCC – James and professor of Internal Medicine at Ohio State. “We believe these microRNA signatures define novel subsets of triple-negative breast cancer and offer new insights into the biology of the disease and better ways to treat these patients.”

The microRNAs that compose the signatures are involved in regulating cell growth, proliferation and survival, and also in cell movement and migration.

“These findings strongly suggest that microRNAs play an important role in triple-negative breast cancer and might be used to better identify the most effective treatment for a patient’s tumor,” says co-senior investigator and researcher Kay Huebner, PhD, professor of Molecular Virology, Immunology and Medical Genetics at Ohio State.

“Several of the deregulated microRNAs we found in the cancer samples are involved in chemoresistance or radioresistance. MicroRNA profiles can help us improve and personalize therapies for individual patients,” she says.

Triple-negative breast cancer accounts for about 15 percent of all breast cancers. It is characterized by cancer cells that lack estrogen and progesterone receptors, and by overexpression of the HER2 receptor. For this reason, these tumors do not respond to hormone therapies or HER2-targeted treatments.

Published in the journal PLOS ONE.

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