Publication highlights

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Explore a selection of research case studies from the past five years.

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Researchers at the Crick are tackling the big questions about human health and disease, and new findings are published every week.

Our faculty have picked some of the most significant papers published by Crick scientists, all of which are freely available thanks to our open science policy.

Lung cancer cell.

Why many lung cancer patients who have never smoked have worse outcomes

Researchers at the Francis Crick Institute, UCL and AstraZeneca have discovered the reason why targeted treatment for non-small cell lung cancer fails to work for some patients, particularly those who have never smoked. The study shows that lung cancer cells with two particular genetic mutations are more likely to double their genome, which helps them to withstand treatment and develop resistance to it. The researchers re-analysed data from the trials of a new EGFR inhibitor, which blocks a common genetic mutation in this type of lung cancer. They compared the impact of treatment for patients with either EGFR-only or with EGFR and p53 mutations, finding that tumours got smaller in response to treatment for patients with just EGFR mutations. But for patients with both mutations, some tumours had grown, providing evidence of rapid drug resistance. This was confirmed in mice with both mutations - resistant cells had doubled their genomes.

Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling

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Published in Nature Communications

Published

APOBEC in lung cancer

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance

Increasing understanding of how drivers of mutations affect lung tumour evolution is critical to prevent tumour reoccurrence and resistance. Using the TRACERx lung cancer study, a research team at the Francis Crick Institute uncovered increased expression of a mutation-driving gene called APOBEC3B (A3B) in lung tumours treated with targeted therapy.

Using multiple pre-clinical lung cancer models, they found that the role of A3B in lung tumor evolution is context dependent. When tumours first start growing, A3B restrains their growth, causes instability in their DNA, and drives tumour cell death. In contrast, with targeted lung cancer therapy, A3B actually helped cancer cells resist treatment.

These findings reinforce the concept that targeted therapies can induce adaptive changes that promote resistance.

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance

Published in Nature Genetics

Published

COVID testing

Pandemic peak SARS-CoV-2 infection and seroconversion rates in London frontline health-care workers

This important paper showed very high levels of infection amongst healthcare workers in a local hospital. It has influenced government policy – asymptomatic healthcare workers are to be screened as per our recommendation (announced October 12th).

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Published in The Lancet

Published

A role for p53 in the adaptation to glutamine starvation through the expression of SLC1A3

In this paper we show that the ability of cells to survive glutamine depletion depends on aspartate metabolism, which is supported by the aspartate/glutamate transporter SLC1A3. The tumor suppressor p53 is shown to induce the expression of SLC1A3, explaining in part how p53 can help cancer cells survive under glutamine starvation.

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Published in Cell Metabolism

Published

Cell clustering promotes a metabolic switch that supports metastatic colonization

We show that the clustering of cancer cells following detachment from ECM results in hypoxia, which activates mitophagy to remove damaged mitochondria and reductive metabolism to support glycolysis. These responses limit mitochondrial ROS production, allowing cell survival and metastasis.

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Published in Cell Metabolism

Published

Serine synthesis pathway inhibition cooperates with dietary serine and glycine limitation for cancer therapy

Targeting the nutritional requirements of cancers through selective dietary intervention is an emerging therapeutic approach. Dietary limitation of the non-essential amino acids serine and glycine can limit the growth of some, but not all, cancers. This study extends this approach by showing combined treatment with an inhibitor of the intrinsic serine synthesis pathway with a serine/glycine free diet improves the therapeutic response and inhibits the growth of cancers that are not responsive to the diet alone. Extension of this work to human studies may offer an important new avenue for the treatment of a broad range of cancers.

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Published in Nature Communications

Published

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Find out how we share our research, or go in-depth with some reports on particular research areas.

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Accessing our research

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Research case studies 

Explore a selection of recent case studies that spotlight particular areas of research at the Crick.