London: British researchers have identified a key protein that can control how breast cancer cells spread in the body.
The study sheds light on how cancer cells leave the blood vessels to travel to a new part of the body, said the researchers from the University of Manchester in Britain.
When tumor cells spread, they first enter the blood stream and grip onto the inner walls of blood vessels, the researchers elicited.
The cancer cells control a receptor protein called EPHA2 in order to push their way out of the vessels, they added.
When these cancer cells interact with the walls of the blood vessels, EPHA2 is activated and the tumor cells remain inside the blood vessels. When the EPHA2 is inactive, the tumor cells can push out and spread, revealed the study published in the journal Science Signaling.
The researchers used a technique that allowed them to map how cancer cells interact and exchange information with cells that make up the blood vessels.
“The next step is to figure out how to keep this receptor switched on, so that the tumor cells can’t leave the blood vessels – stopping breast cancer spreading and making the disease easier to treat successfully,” concluded the lead researcher Claus Jorgensen from the University of Manchester. (IANS)
Breast cancer drugs may force some cancer cells into ‘sleeper mode’, allowing them to potentially come back to life years after initial treatment.
The research could open avenues for finding ways of keeping the cancer cells dormant for longer, or even potentially finding a way of awakening the cells so they can then be killed by the treatment.
The team studied human breast cancer cells in the laboratory and examined the effects of a group of breast cancer drugs called hormone treatments.
“For a long time scientists have debated whether hormone therapies – which are a very effective treatment and save millions of lives – work by killing breast cancer cells or whether the drugs flip them into a dormant ‘sleeper’ state,” said Luca Magnani, lead author of the study from Imperial College London.
“This is an important question as hormone treatments are used on the majority of breast cancers. Our findings suggest the drugs may actually kill some cells and switch others into this sleeper state,” Magnani added.
“If we can unlock the secrets of these dormant cells, we may be able to find a way of preventing cancer coming back, either by holding the cells in permanent sleep mode, or be waking them up and killing them,” Magnani said.
In the study, published in the journal Nature Communications, the team studied around 50,000 human breast cancer single cells in the lab, and found that treating them with hormone treatment exposed a small proportion of them as being in a dormant state.
The ‘sleeper cells’ may also provide clues as to why some breast cancer cells become resistant to treatment, causing a patient’s drugs to stop working, and their cancer to return, the researchers said.
Hormone therapies are used to treat a type of breast cancer called oestrogen-receptor positive. These make up over 70 per cent of all breast cancers, and are fuelled by the hormone oestrogen.
These cancers are usually treated with surgery to remove the tumour, followed by a course of targeted hormone therapy – usually either aromatase inhibitors or tamoxifen, which target oestrogen receptors.
However, around 30 per cent of breast cancer patients taking hormone therapies see their cancer eventually return – sometimes as long as 20 years after treatment.
This returning cancer is usually metastatic, meaning it has spread around the body, and the tumours are often now resistant to medication. (IANS)