Ovarian cancer often goes undetected until it reaches a level wherein it has spread within the pelvis and stomach. Every year, roughly 550 women develop ovarian cancer in Finland. Ovarian cancer is difficult to treat and it is commonly fatal, with 320 women dying of ovarian cancer annually in Finland. Now, researchers at the University of Helsinki have uncovered how tumour cells interact with the immune system in ovarian cancer.

Their study has been published in ‘Nature Communications’.

Cancer can only develop and progress when the tumour cells are able to hide from the body’s immune system. Cancer immunotherapies, which boost the body’s immune defence against cancer, have emerged as promising therapies in multiple tumour types. However, the effectiveness of immunotherapies against ovarian cancer has remained modest. This was mainly since the mechanisms how ovarian cancer cells hide from the immune system have been unknown.

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Utilising a novel imaging technology, the researchers characterized more than 110,000 individual cells from clinical ovarian cancer samples. The researchers investigated how the genetic characteristics of ovarian cancer the shape human immune system, and how tumour and immune cells communicated with each other.

“With the help of this revolutionary imaging technology and advanced data analysis, we were able to study individual tumour cells, their functional properties and interactions with unprecedented precision,” said Associate professor Anniina Farkkila, the corresponding author of the study.

“By studying individual cells directly in the tissue, we demonstrated how cancer cells hide in different ways, depending on the specific gene mutation. We found that the body’s immune system is more effective against tumours with a mutation in BRCA1/2 genes. By contrast, tumours without such mutations have a connective tissue barrier prohibiting the interaction between the cancer and immune cells,” said doctoral researcher Inga-Maria Launonen, BM.

BRCA1/2 mutations occured in approximately 20 per cent of poorly differentiated serous carcinomas, the most common form of ovarian cancer. The killer T-cells closely guarded the aggressive tumour cells particularly in tumours with BRCA1/2 mutations, which is why these patients had a markedly better prognosis.

“By increasing our understanding of how tumour genes trick the immune system, we will be able to develop more effective ways to activate the body’s own immune defences to kill the cancer cells,” Inga-Maria said.

The results of the study confirmed the significance of the interaction between tumour and immune cells in identifying new and more effective therapies as well as in choosing the right therapy for each patient.

“Our findings will enable us to tailor precision immuno- and combination therapies that have the potential to even cure ovarian cancer in the future,” Farkkila said. 

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