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Genetic 'sensor' spots and kill cells with key cancer gene

20 November 2017
Appeared in BioNews 927

A team of scientists in Germany has developed a 'sensor' that detects mutations in the key tumour suppressor gene p53 and then kills potentially cancerous cells. The research was published this month in Nature Communications.

The p53 gene is part of a family of genes that prevents cells from proliferating in an uncontrolled manner, which results in cancer. Mutations that stop p53 from working are implicated in 50 percent of human cancers, and many biotechnology companies have developed drugs to target the gene.

In this study, the multicentre team from Dresden created a molecular sensor that detects when early changes occur in the p53 gene. This sensor takes the form of a genetic element that makes a cell reliant on normal p53 – any mutations which disable the gene activate the sensor and trigger cell death mechanisms, so preventing tumour formation.

This would be a novel way to deal with cancer, according to project leader Professor Frank Buchholz at University Hospital Carl Gustav Carus. 'We treat cancer cells long after they have gone through the transformation process,' he noted. With the team's new approach, prevention would be the key.

'The p53 sensor enables an active precocious intervention for the first time,' said Professor Buchholz. 'Our results show that cells with p53 mutations can be selectively detected and eliminated at an early stage. Hence, the transformation process is prevented.'

The team has, so far, tested this sensor in vitro and in vivo in a mouse model. These new findings, though, open doors to develop new techniques for cancer diagnosis. It might even be possible to adapt this sensor for other genes.

Development of a genetic sensor that eliminates p53 deficient cells
Nature Communications |  13 November 2017
German cancer sensor raises the alarm and then puts the fire out
Labiotech.eu |  16 November 2017
Sensor for the most important human cancer gene
Science Daily |  14 November 2017
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