Unraveling the Potential of a Dual-Action Mechanism Against Triple-Negative Breast Cancer

Unraveling the Potential of a Dual-Action Mechanism Against Triple-Negative Breast Cancer

Understanding Triple-Negative Breast Cancer (TNBC)

Triple-negative breast cancer (TNBC) is a particularly aggressive cancer type that lacks estrogen, progesterone receptors, and doesn’t produce the HER2 protein in excess. It constitutes 10-15% of all breast cancers and is more commonly found in women under the age of 40 who possess the BRCA1 mutation. Due to its aggressive nature and resistance to conventional treatment, TNBC often leads to a poor prognosis and limited treatment options. However, a promising breakthrough in research could offer new hope for patients battling this relentless disease.

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Dr. Schug’s Groundbreaking Findings

Dr. Zachary Schug, a professor at The Wistar Institute, has made a significant breakthrough in the potential treatment of TNBC. His research, published in Nature Cancer, exhibits a dual-action mechanism that could effectively combat this hard-to-treat form of breast cancer. The study suggests that by “silencing” a specific gene named ACSS2, we could improve the effectiveness of available treatments for patients.

The Challenge of TNBC

The absence of estrogen, progesterone, and HER2 receptors, which are present in other forms of breast cancer and targeted during treatment, makes treating TNBC a formidable challenge. TNBC grows quicker and is more resistant to treatment than other types of breast cancer, leading to a worse prognosis for patients. However, Dr. Schug’s research could change this narrative.

Unveiling the Dual-Action Concept

Dr. Schug and his team have demonstrated the effectiveness of a dual-action concept. Silencing the ACSS2 gene disrupts the metabolism of TNBC while simultaneously bolstering the immune system’s ability to fight it. ACSS2 is responsible for regulating acetate, a nutrient that cancer cells, particularly TNBC cells, utilize for growth and spread. The team employed two methods to deactivate ACSS2 – CRISPR-Cas9 gene editing and a compound known as VI-3-135, a potent ACSS2 inhibitor identified in 2021.

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Targeting ACSS2 and Immunosensitization

The researchers found that targeting ACSS2 not only disrupted the aggressive cancer’s ability to metabolize acetate and grow, but it also triggered the immune system to recognize and attack the cancer. With inhibited ACSS2, cancer cells could not process acetate effectively, leading the tumor region to “bathe” in acetate. This signals the immune system that something is wrong, initiating a process known as “immunosensitization”.

Implications of the Findings

This process of steering the immune system towards cancer has puzzled other TNBC researchers. However, Dr. Schug showed that slowing down ACSS2 was so effective against TNBC that tumor growth was drastically reduced, even to the point of completely eradicating the cancer in some experiments. The research suggests that a treatment involving ACSS2 inhibition could improve outcomes for patients diagnosed with TNBC. By testing the ACSS2 inhibitor with standard breast cancer chemotherapy, Dr. Schug and his colleagues found that ACSS2 inhibition increased treatment effectiveness. While further research is needed, combining this approach with other cancer therapies could lead to significant improvements in TNBC treatment.

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