Gene can 'switch off' cancer in mice
Your support helps us to tell the story
From reproductive rights to climate change to Big Tech, The Independent is on the ground when the story is developing. Whether it's investigating the financials of Elon Musk's pro-Trump PAC or producing our latest documentary, 'The A Word', which shines a light on the American women fighting for reproductive rights, we know how important it is to parse out the facts from the messaging.
At such a critical moment in US history, we need reporters on the ground. Your donation allows us to keep sending journalists to speak to both sides of the story.
The Independent is trusted by Americans across the entire political spectrum. And unlike many other quality news outlets, we choose not to lock Americans out of our reporting and analysis with paywalls. We believe quality journalism should be available to everyone, paid for by those who can afford it.
Your support makes all the difference.Scientists have engineered an on-off cancer "switch" in mice that may help to develop human treatment. The switch is a gene forming a vital link in the step-by-step process leading to leukaemia in humans.
Scientists have engineered an on-off cancer "switch" in mice that may help to develop human treatment. The switch is a gene forming a vital link in the step-by-step process leading to leukaemia in humans.
In the genetically engineered mice, the BCR-ABL1 gene can be turned on or off at will. Exposure to tetracycline, an antibiotic, keeps the gene in the off position.
Dr Daniel Tenen and colleagues at the Harvard Institute of Medicine in Boston, Massachusetts, found that gene-switch mice given the antibiotic in drinking water stayed healthy. When tetracycline was withdrawn - switching on the gene - the animals quickly developed leukaemia and died. But returning the antibiotic to the water stopped the disease in its tracks.
The experiments, reported in the journal Nature Genetics , show that the protein produced by BCR-ABL1 is necessary to induce and maintain the cancer.
Full reversibility may depend on how long cells must be exposed to the gene's protein to develop the cancer. Longer exposure might raise the chance of other cancer-causing genetic abnormalities occurring that were independent of BCR-ABL1. The scientists said: "Our findings suggest that complete and lasting remissions may be achieved if the genetic abnormality is abolished or silenced before secondary mutations are acquired."
Join our commenting forum
Join thought-provoking conversations, follow other Independent readers and see their replies
Comments