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Kidney Cancer UK News

Genes

Kidney cancers caught stealing genes from other cell types in order to spread

The study, led by scientists from the MRC Cancer Unit at the University of Cambridge, suggests that this may also help to explain how other types of cancers spread – or metastasise – and provide new targets for cancer therapies.

To metastasise, cancer cells need to develop the ability to break away from the original tumour, survive moving around the body in the blood stream, invade another organ and form a secondary tumour.

Despite extensive studies searching for genetic mutations that lead to kidney cancer, much of what causes kidney cancers to spread in the body is still unexplained.

In this study, published in the journal Cancer Discovery, the researchers searched for explanations beyond mutations by studying how genes are switched on and off. They used human kidney and breast cancer cell lines taken from samples of human cancer in a mouse model to study how cancers spread.

Every cell in the body contains the same genes, but different types of cells exist because DNA has control systems that switch genes on and off in different cell types. These control systems, called enhancers, tell the cell when and where each gene should to be ‘expressed’ – they tell a gene to be switched on, so the genetic instructions can be copied and made into a protein.

In cancer cells that were able to spread and colonise other tissues, the scientists found that genes that are normally turned off in kidney cells were being expressed – the cancer cells hijacked genes that are normally turned on in white blood cells (cells that are part of the immune system and fight diseases). Hijacking these white blood cell genes helped the cancer to metastasise.

The researchers compared their findings to kidney cancer samples from hundreds of people with the most common type of kidney cancer – clear cell renal cell carcinoma – and found similar profiles of gene activation, suggesting that what they saw in the mouse models may be happening in human cancers. Results from experimental models of breast cancer suggested that similar mechanisms might also be at play in breast cancer patients.

Full story on the cambridgenetwork.co.uk here

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