Cells that are irrepairably damaged or pre-cancerous can become senescent -- meaning that they stop dividing for overall health of the organism.

Researchers then fed the mice either a normal diet or a high-fat diet.

But before senescent cells die, they can spew out chemicals that may cause inflammation and promote cancer development.

Then they primed the mice by exposing them to a carcinogenic chemical, a process that Hara says may be similar to humans' exposure to environmental toxins, such as air pollution.

To examine whether senescent cells are involved in obesity-induced cancers, researchers worked with genetically engineered mice.

The gut bacteria of obese mice unleash high levels of an acid that promotes liver cancer, reveals one of the first studies to uncover a mechanism for the link between obesity and cancer.

After 30 weeks, only 5% of the lean mice developed cancer -- in their lungs -- whereas all the obese mice developed liver cancer.

Eijione Hara, one of the study authors, and his colleagues initially set out to study how dying cells influence obesity-linked cancers.

Although the results showed that cell senescence was involved in obesity-linked cancer in the mice, researchers did not initially understand why the liver became a hotbed for tumours.

But when they compared the blood serum of the two groups of mice, they found that the obese mice had much higher levels of deoxycholic acid (DCA), a chemical that causes DNA damage and can induce cell senescence.

The researchers also found that obese mice had a greater number of DCA-producing Clostridium bacteria, and that obese mice given antibiotics to clear intestinal bacteria developed fewer liver tumours. Thank you.