Triple-negative breast cancer cells show a significant expression of the proteins CCL5 and IL6, according to research published in the September 2, 2014 online edition of Nature Communications.
Specifically, TNBC cells secrete IL6 (a cytokine protein interleukin-6) that triggers cells located within lymph nodes and the lungs to secrete CCL5 (a chemokine protein) and VEGF (vascular endothelial growth factor). CCL5 then helps recruit cancer cells that express CCL5 receptor CCR5, and VEGF promotes vascular growth (angiogenesis) in lymph nodes and increases vessel permeability in the lungs.
In plainer language, the interplay between these proteins and receptors leads to metastatic growth, which is more likely in TNBC.
That also means we have another potential for the holy grail: drugs targeted specifically at TNBC.
What’s more, FDA-approved drugs already exist to target these proteins and are now used in other illnesses such as HIV and rheumatoid arthritis. For example, IL6 receptor inhibitor tocilizumab is an FDA-approved anti-inflammatory drug and the HIV drug maraviroc inhibits CCR5. So showing that these drugs can treat TNBC can jump-start the approval process for a targeted cancer drug.
Currently, it takes 10-12 years and billions of dollars to develop a new drug from discovery to market; however, using repurposed or repositioned drugs promises significant savings in time and resources.
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