A presentation on how cancer cells move to other tissues has won UCD's AccesScience prize, writes Claire O'Connell
In cancer, one of the greatest threats is a tumour cell that can up sticks and move to another part of the body, where it seeds another cancerous growth. A researcher at University College Dublin (UCD) wants to figure out how breast cancer cells do this by becoming less "sticky" to break away from the main tumour. Her work on how cells become unhinged from each other could lead to more effective treatment regimes and drug development, ultimately improving the outcome for the patient.
"Breast cancer is the biggest female cancer in Ireland. It accounts for 28 per cent of female cancers, which is about 1,700 new cases a year, and almost 20 per cent of female cancer deaths," says Elaine McSherry, who is doing a PhD at UCD's Conway Institute.
Last week her talk, The Missing Links? How Breast Cancer Spreads, won the annual AccesScience competition that encourages students to describe their research to the public in a jargon-free way.
The majority of breast cancers arise in the ducts, or hollow tubes in the gland, explains McSherry. If cells lining the insides of the ducts become cancerous they can grow and block the tube.
"That's called ductal carcinoma in situ," she says. "It's a contained cancer because it's still inside the duct wall. You more than likely won't feel the lump, it's really tiny, so that's why the mammograms are so good at detecting that early cancer."
If the tumour stays put it is unlikely to kill the patient, and once the cancer has been detected it can be effectively treated with surgery, according to McSherry.
But things become more serious if cells from the duct-blocking tumour start to tunnel out through the duct wall and into surrounding areas. "Then it's much more likely that it can get into the blood or lymph system and move to other organs. This is where the big problem occurs," she says.
For her PhD thesis, McSherry has been looking at what genes are turned on or off as tumour cells switch from staying put to getting going. Looking at the literature she identified around 90 candidate genes that could be playing roles in unlinking the tumour cells from each other, changing the structure of those cells and allowing them to move.
Then in the lab she screened for the activity of those genes both in cancer-derived cell lines and in donated tumour tissue samples from consenting patients.
The most interesting results appeared in the genes that help cells stick together. McSherry found that key "adhesion" genes from the P-cadherin and integrin families were turned down in the more invasive cells. She will spend the rest of her PhD looking at the effects of turning down such sticky genes in non-cancerous cells in the lab.
Understanding the basics of what happens as the cells break free from each other could help scientists identify "biomarkers" for invasiveness, she explains. In the future, tests to screen for these markers could help identify early on which breast cancer patients need more aggressive therapy or more intense follow-ups.
And ultimately, key genes in the invasion process could also be targets for new anti-cancer drugs. "You probably won't be able to replace cell adhesion but maybe you could target how the cells move and how the invasive cells are spreading," says McSherry. Her work is funded by an Ircset scholarship and by Cancer Research Ireland.