Combining two separate drugs made by GlaxoSmithKline ($GSK) and Abbott ($ABT) appeared to defeat a particularly tough version of breast cancer cells in lab and mouse studies.
The GSK drug--lapatinib (Tykerb), a kinase inhibitor--is approved to treat human epithelial growth factor receptor 2 (HER2) positive breast cancers and used in at least one other treatment combination. Abbott's veliparib is a PARP inhibitor in clinical trials for a number of cancers including breast cancer. What's novel here is scientists at the University of Alabama at Birmingham (UAB) are exploring the combined drugs as a treatment for triple-negative breast cancer. Most breast cancer treatments target estrogen, progesterone or human epidermal growth factor as expressed by the disease. But as the researchers explain, the triple-negative variety is particularly aggressive and tough to treat, in part because it expresses none of those receptors.
UAB researchers say the GSK/Abbott combination killed triple-negative breast cancer cells in the lab and also in mouse models. They believe the mix worked because lapatinib breaks down a cancer cell's ability to repair its DNA, and veliparib, the PARP inhibitor, accelerates further cancer cell damage by blocking its ability to rebuild. (PARPs, the researchers explain, are enzymes that repair some DNA damage, making them a viable cancer target.)
"This potent combination causes an interaction that is lethal to triple-negative breast cancer cells," lead UAB researcher Shih-Hsin Yang said in a statement.
The results are significant because both drugs on their own have previously tested as safe and well tolerated in breast cancer patients. But it will be a while before the combination can advance into human clinical trials. More animal studies must be completed first, and the potent combo may not work the same way in humans. Still, the research team is advancing ahead, and they plan to present their data and ideas at the Translational Breast Cancer Research Consortium in November. For details of their study, read the journal PLoS ONE.
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