New drug could break cancer’s resistance

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A promising experimental drug could help make treatment-resistant cancer cells vulnerable to existing therapies again.

For many people undergoing cancer treatment, one of the biggest concerns is whether the medicine will continue working. A therapy can initially keep the disease under control, only for cancer cells to adapt and become harder to treat.

Researchers at Baylor College of Medicine are investigating a potential new way around that problem. According to Baylor and research published in Science Advances, an experimental compound called CS18 is designed to interfere with several mechanisms cancer cells use to survive treatment, reports Science Daily.

A new target

Rather than focusing on just one biological pathway, CS18 targets a specific region of a protein called TopBP1. The protein is involved in processes cancer cells can exploit to support growth, survival and the repair of damaged DNA.

Researchers developed CS18 after screening thousands of chemical compounds using computer modelling and laboratory experiments. The aim was to find a molecule capable of disrupting a key part of TopBP1 known as BRCT7/8.

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Resistance reversed

CS18 was tested in cells representing several cancers, including breast, ovarian and lung cancers, as well as acute myeloid leukemia.

One notable finding involved lung cancer cells that had developed resistance to osimertinib, an existing cancer drug. When CS18 was added, the resistant cells became sensitive to osimertinib again, increasing cancer cell death.

Researchers also tested the compound in animal models. Tumor growth was significantly reduced, while no major weight loss or other obvious signs of toxicity were observed.

Early days

The findings do not mean CS18 is ready for use in patients. The compound remains experimental, and considerably more research will be needed to determine whether it is safe and effective in humans.

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However, the results suggest a possible future strategy for tackling treatment resistance by weakening several of the defenses cancer cells rely on rather than attacking a single pathway.

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This article is made and published by Mie Hermansen, who may have used AI in the preparation.

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