Triple-negative breast cancer refers to any breast cancer that does not express the genes of three common hormone receptors: estrogen receptor (ER), progesterone receptor (PR) and HER2/neu. Constituting about 20% of all breast cancer cases, it is most likely to affect young people and African Americans. Basically, targeted breast cancer treatments demand blocking the hormones. Hence, it is one of the most hostile cancers whose treatment options are restricted.
Debra Auguste, a professor of chemical engineering at the Northeastern University, commented “It’s treated with surgery, chemotherapy, and in some cases radiation. But there is no targeted therapy that acts on the cellular biology”.
In a research, a method was demonstrated in which it can deliver a cancer-killing drug and at the same time interfere with the cancer’s ability to grow and spread. The cancer treating drugs are often dispersed throughout a patient’s body. Hence, it is necessary to direct them specifically and therefore, the drugs should be packaged in a way that it causes them to bind to, or interact with, the cancerous cells. This can be done by targeting receptors on the surface of cancer cells where the researchers identify a specifically prevalent receptor and attach a matching molecule to the drug they want to deliver. However, this can fail. Auguste and her colleagues chose two common receptors instead of one, and determined the ratio of one to the other on the surface of two separate lines of triple-negative breast cancer cells. Then, they designed therapeutics for each cell line that were coated in matching molecules, distributed at that same ratio.
“Most targeting is looking for a single over-expression of one receptor. Here, we’re really trying to understand what is on the cell, and how we can make a personalised therapeutic that would have the greatest effect” – Auguste.
When the researchers tested their therapeutic on mice, it was a success. It prevented the cancer from spreading, to which Auguste said- “The act of binding makes a difference. Now we have something that affects proliferation, affects cell migration, and also delivers the chemotherapeutic that can act to kill the cell.” She further added “We’re trying to understand how these patterns evolve on cell surfaces. Then we can connect them to the actual biology and cell functions and behaviours that are going to lead to progress and paradigm shifts in our field.”
Shahjadi Jemim Rahman