Triple-negative breast cancer (TNBC) refers to any breast cancer that does not express the genes for estrogen receptor (ER), progesterone receptor (PR) or Her2/neu. TNBC is difficult to treat since most hormone therapies target one of these receptors. Researchers at UCI have developed a therapeutic that bypasses these receptors, and instead targets fatty acid oxidation, a process linked to TNBC.
Triple-negative breast cancer (TNBC) refers to any breast cancer that does not express the genes for estrogen receptor (ER), progesterone receptor (PR) or Her2/neu. There are currently no targeted therapies to treat TNBC and approximately 34% of TNBC patients experience recurrence or metastasis within five years of radiation and chemotherapy treatment.
Researchers at UCI have identified a protein found on cell surfaces called CUB-domain containing protein 1 (CDCP1). CDCP1 controls fat metabolism by lowering fat levels inside cells, thus causing more fatty acid oxidation (FAO), which has been linked to metastasis of TNBC. As a method to target cancer cells that lack hormone receptors, blocking fragment that inhibit CDCP1 activity have been developed. Specifically, the fragment blocks CDCP1 dimerization, reducing FAO. Reduction of FAO is accompanied with inhibition of tumor growth and reduced metastasis.
Treatment for triple-negative breast cancer and other breast cancers
Efficacy of CDCP1 function-blocking has been shown in vitro and in vivo in two animal models of TNBC.