Scientists discover a "switch" that promotes the spread of breast cancer in the body

Preliminary research, conducted by scientists at Imperial College London and the London Cancer Research Institute, has identified a genetic "switch" in bad cancer cells that stimulates the production of bad cancer. a type of internal scaffolding.

This scaffold is a type of protein, called Keratin-80, badociated with the protein that helps keep hair strong. The increase in the amount of this scaffold strengthens the stiffness of the cancer cells, which, according to the researchers, could help the cells to agglutinate and move into the blood stream to other parts from the body.

The researchers, who published their work in the journal Nature Communications, have studied human bad cancer cells treated with a common type of anticancer drugs called aromatase inhibitors.

The team discovered that bad cancer cells become resistant to the drug (which means the drugs are no longer effective if the cancer recurs).

Targeting this switch with another drug could help reverse this resistance and make the cancer less likely to spread, said Dr. Luca Magnani, lead author of the Department of Surgery and Cancer research at the University of Ottawa. Imperial: "Breast cancer is the most common cancer In the UK, aromatase inhibitors are effective at killing cancer cells, but about 30 percent of patients relapse after surgery and will see their cancer recur, usually because the cancer cells have adapted to worse, when the cancer recurs, it has usually spread throughout the body – which is difficult to treat. "

Dr. Magnani said: "Until now, we did not know the reasons for this situation, but our early-stage study suggests that a type of genetic switch – called a transcription factor – can activate genes. that make cancer cells not only resistant, treatment should now continue with larger studies, but if confirmed, targeting this genetic switch could prevent cancer cells from becoming drug-resistant and spreading to other regions of the body. "

Aromatase inhibitors are used to treat a type of bad cancer called a positive estrogen receptor. These account for more than 70% of all bad cancers and are fed by the hormone estrogen.

These cancers are usually treated surgically to remove the tumor, followed by targeted hormone therapy, usually either aromatase inhibitors or tamoxifen, which blocks the estrogen receptors.

Inhibitors of aromatase are usually administered to postmenopausal women and prevent the production of estrogen in other tissues. Although women 's ovaries have stopped producing estrogen, a portion of the hormone is still produced in several other tissues by an enzyme called aromatase. The drug prevents this enzyme from making estrogen.

However, about 30% of bad cancer patients who take aromatase inhibitors are seeing their cancer reappear. This recurrent cancer is usually metastatic, which means that it has spread throughout the body and that tumors are often now resistant to aromatase inhibitors.

In previous research, the same group had discovered that cancer cells became resistant to aromatase inhibitors by constituting an alternative source of "fuel". The team found that when aromatase inhibitors rob cancer cells of estrogen, some adapt by increasing cholesterol production, which they then use to survive. This means that if the cancer recurs, it can not be killed by the same type of medication.

In recent research, which used bad cancer cell cultures in humans in the laboratory, the research team discovered that the switch that activates the genes that increase cholesterol production also activates the genes that make the more rigid cells and more likely to invade neighboring tissues.

The team also found that in women whose cancers had spread throughout the body, the cells contained higher amounts of 80-keratin.

The team said that larger-scale patient studies were now needed to confirm the results, but that this research could provide new opportunities to help treat bad cancer that recurs and spreads around the body.

Dr. Magnani explained, "Although the spread of cancer around the body affects many patients, scientists still do not know what molecular processes are behind the movement of cells." This research highlights this process and also suggests that it is controlled by the same drug resistance switch These results need to be replicated in larger trials, but could potentially be a way to end both drug resistance and drug resistance. and the spread of cancer. "

Dr. Fernando Calvo, who led the research as Team Leader on the Tumor Microenvironment at the Institute of Cancer (ICR), said:

"The evolution of tumors is one of the biggest challenges facing cancer researchers. By determining how tumors develop drug resistance, we can find new ways to treat cancer effectively, or even to prevent the development of resistance.

"Our study shows how drug resistance and invasiveness of cancer cells are interconnected in bad cancer through changes in cell shape.If we understand how to block resistance, we could also prevent cancer from occurring. spread throughout the body – this would be an important step in the more effective treatment of bad cancer. "

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