Antibiotics may help treat melanoma by ‘quickly killing’ the cancer cells

Skin cancer: Dr Chris outlines the signs of a melanoma

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In a lab-based experiment, RNA biologist Eleonora Leucci found that “antibiotics quickly killed many cancer cells” and, in some cases, “cured” the disease. For her research project, cancerous tumours were implanted into laboratory mice. Then some of the mice were treated with antibiotics, or a combination of existing anti-cancer treatments.

Then some of the mice were treated with antibiotics, or a combination of existing anti-cancer treatments.

The focus was on melanomas – a type of skin cancer – that has the ability to evolve to escape current cancer treatment.

Leucci explained: “As the cancer evolves, some melanoma cells may escape the treatment and stop proliferating [i.e. multiplying] to ‘hide’ from the immune system.

“These are the cells that have the potential to form a new tumour mass at a later stage.”

The cancer researcher pointed out that in order for the inactive cancer cells to survive cancer treatment, their “power plant” needs to be switched on “at all times”.

This power plant is known as the mitochondria, which can be “very vulnerable to a specific class of antibiotics”.

“This is what gave us the idea to use these antibiotics as anti-melanoma agents,” said Leucci.

As the antibiotics were shown to kill cancer cells, Leucci theorised that it could be “used to buy precious time needed for immunotherapy to kick in”.

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“In tumours that were no longer responding to targeted therapies, the antibiotics extended the lifespan of – and in some cases even cured – the mice,” she added.

Leucci stated that cancer cells “show high sensitivity” to antibiotics, so research can now be funded to repurpose them to treat cancer instead of bacterial infections.

However, Leucci cautioned that her findings are based on research in mice, not humans.

“We need more research and clinical studies to examine the use of antibiotics to treat cancer patients,” she noted.

This is a breaking news story with more to follow…

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