Triple-Negative Breast Cancer Shows Response to a Breakthrough Dual-Target Therapy


A recent experimental dual-target therapy has revealed new hopes in fighting in the aggressive form of triple-negative breast cancer.  A recent study revealed that the given treatment was responsible for decreasing the overall growth and spreading of the triple-negative breast cancer in mice.

The given breakthrough approach makes use of a specific protein for blocking two major growth mechanisms that aid the breast cancer cells to migrate and multiply.  The protein “TINAGL1 –tubulointerstitial nephritis antigen-like 1” is known to occur naturally in the human body.  The given study reveals that a recombinant or synthetic version of the protein TINAGL1 can help in reducing the growth as well as the spreading of the triple-negative breast cancer.


The study report in the journal Cancer Cell was recently released.  Yibin Kang –Senior Study Author & the professor of molecular biology at Princeton University, New Jersey, stated, “People all around have constantly been trying.  With several efforts towards blocking the spread of triple-negative breast cancer, the attempts so far have only been in vain.  This is because by trying out one approach, the cancer cells were known to compensate by always finding some way to escape.  However, with this all-new, revolutionary approach, the given treatment is successful in blocking both the pathways at the same time.”

What is Triple-negative Breast Cancer?

Breast cancer is a serious health condition that tends to develop when the cells in the breast tissues start growing at an exponential rate and multiplying at the same time.  About 2/3rd of the breast cancer cases will test positive for either progesterone or estrogen receptors, or even both in some cases.  Around 20 percent of the cases are known to test positive for the excessive presence of HER2 –Human Epidermal Growth Factor Receptor 2.  However, in some typical cases, in around 12-17 percent of the individuals who receive the diagnosis for breast cancer, the test might turn out negative for both the hormone receptors along with high HER2.  This is the condition of triple-negative breast cancer.

With the treatment options for triple-negative breast cancer being limited, the all-new dual-target therapy might be new hope in the given scenario.  TINAGL1 is known to work in two ways –one, by reducing the overall activity of EGFR protein, and the other by causing interference in the path of FAK (Focal Adhesion Kinase) protein along with a group of molecules known as integrins.

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