News about the next big breakthrough in cancer treatments are a dime a dozen. But this particular achievement seems worthy of hype and attention. Here is hoping its results can be further verified and replicated.
According to the Telegraph:
For the first time aggressive breast, lung and bladder cancer cells have been turned back into harmless benign cells by restoring the function which prevents them from multiplying excessively and forming dangerous growths.
Scientists at the Mayo Clinic in Florida, US, said it was like applying the brakes to a speeding car.
So far it has only been tested on human cells in the lab, but the researchers are hopeful that the technique could one day be used to target tumours so that cancer could be ‘switched off’ without the need for harsh chemotherapy or surgery.
“We should be able to re-establish the brakes and restore normal cell function,” said Professor Panos Anastasiadis, of the Department for Cancer Biology.
The scientists discovered that the glue which holds cells together is regulated by biological microprocessors called microRNAs. When everything is working normally the microRNAs instruct the cells to stop dividing when they have replicated sufficiently. They do this by triggering production of a protein called PLEKHA7 which breaks the cell bonds. But in cancer that process does not work.
Scientists discovered they could switch on cancer in cells by removing the microRNAs from cells and preventing them from producing the protein.
And, crucially they found that they could reverse the process switching the brakes back on and stopping cancer. MicroRNAs are small molecules which can be delivered directly to cells or tumours so an injection to increase levels could switch off disease.
As always, medical experts are rightly cautious about the results, noting that there is still quite a gap between cells grown in a laboratory and those of a human with cancer. Nevertheless, this is a big step forward, and presents yet another promising approach to consider in combating this scourge.