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����Ӱҵ College Fellow Dr Sanne van Neerven’s research focuses on the earliest interactions between normal and mutant cells in the intestine in a bid to investigate causes of colorectal cancer and ultimately find ways to prevent it.

Sanne focuses on the first moments that a cell acquires a mutation, and “how the normal and mutant cells subsequently compete with each other”.

“People generally assume the cancer cells always win this battle. It's not the case,” she says. 

“Actually, our normal cells can be extremely fit and are able to outcompete the mutant cells as well. Studying how cells compete with each other, and what makes a cell a winner or a loser, provides interesting clues on how to prevent cancer.”

Sanne is a Senior Research Associate at the Gurdon Institute at the University of Cambridge, in the laboratory of Professor Ben Simons. She completed her bachelor’s degree in Biomedical Sciences (University of Amsterdam) and obtained her Masters’ in Oncology (Vrije Universiteit Amsterdam) before pursuing a PhD in the Amsterdam University Medical Centers with Professor Louis Vermeulen.

Her work discovered a new mechanism of tumour initiation in the mammalian intestine, supercompetition, by which mutant cells actively disadvantage normal neighbours to facilitate colorectal cancer development. 

For her work on cell competition, Sanne was awarded the International Birnstiel award (2021), the L’Oréal-UNESCO Women in Science - Rising Talent Award (2022) and the Cancer Center Amsterdam Best Preclinical Thesis award (2023). 

She also received the Andreas Bonn medal, pictured, from the for the best thesis in the category ‘life sciences’ between 2019-2023.

“We figured out that in the gut, some mutants are not just expanding quicker than the normal cells, but they're in fact ‘supercompetitors’ that actively disadvantage the normal cells,” Sanne adds. “It’s basically an unfair game”.

“We discovered that these mutant cells produced several proteins to which the normal cells were very sensitive and these factors forced the normal cells out of the way. We found that if we made the normal cells resistant to these factors, we could prevent cancer from starting in mice. So instead of targeting the mutant cells, we proposed to make the normal cells fitter. Based on these fundamental discoveries, we are currently performing a clinical trial in Amsterdam, testing this new strategy in 12 patients with hereditary colorectal cancer.”

The 18-month clinical trial has begun in the Netherlands, while Sanne is now expanding her research on cell competition to develop rational chemoprevention strategies for hereditary cancer syndromes. She has recently received a three-year Cancer Research UK ‘Biology to Prevention Award’ which will allow her to further her work and seek answers to key questions.

She adds: “During my PhD I studied the competition between normal and mutant cells within the intestinal crypt, but it seems you need more than one mutant crypt to form a cancer. Therefore, I am currently investigating how mutant cells expand beyond the crypt. It seems that several mutant crypts might cooperate to form a cancerous lesion. Understanding how they cooperate and attempting to interfere with this cooperation will hopefully inspire the development of novel detection and prevention strategies for cancer.”