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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.

Bowel cancer tumour

Protein level predicts immunotherapy response in bowel cancer

Researchers at the Crick and Barts Cancer Institute, Queen Mary University of London, have shown that the amount of a protein called CD74 can indicate which people with bowel cancer may respond best to immunotherapy. Bowel cancer falls into two categories: a deficient subtype and proficient subtype, and immunotherapy isn't yet used to treat both subtypes. The team found that three types of immune cells needed to be present for the tumour to respond to treatment: T cells, NK cells and macrophages. When all three were present and near to cancer cells, the T cells produced interferons, triggering a signal in macrophages and tumour cells. The researchers then found that a measurable component of this signal was a protein called CD74. This finding was mirrored in clinical trial data, showing that people who responded to immunotherapy had significantly higher levels of CD74. Therefore measuring CD74 levels could predict whether someone will respond to immunotherapy regardless of subtype.

A constitutive interferon-high immunophenotype defines response to immunotherapy in colorectal cancer

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Published in Cancer Cell

Published

God with two faces

Surprising ‘two-faced’ cancer gene role supports paradigm shift in predicting disease

Loss of the tumour suppressor gene CDKN2A is a common early event in development of the pre-cancerous condition Barrett's oesophagus. Around 1% of Barrett's patients go on to develop oesophageal adenocarcinoma, but rather than enhancing this progression, as would be expected, early CDKN2A loss is actually protective. Having made this striking observation, the team at the Crick and collaborators showed that the reason lies with a second tumour suppressor gene, TP53. Loss of TP53 is a key driver of transformation into oesophageal cancer, but if CDKN2A is also missing, the Barrett's cells are too weakened to progress. CDKN2A changes sides to become a villain later in the process: if it's lost after the cancer has developed, it promotes a more aggressive tumour.

Context-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer

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Published in Nature Cancer

Published

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Uncovering cancer-immune system interactions could inform how patients respond to immunotherapy

Researchers at the Francis Crick Institute and King’s College London have revealed the complex interactions between cancer and the immune cells that surround a tumour, with the potential to inform how patients will respond to immunotherapy. The researchers analysed thousands of samples across 32 types of cancer to examine the way that cancer dynamically interacts with the tumour immune microenvironment (TIME), allowing the disease to flourish.

Focusing on a class of genes called cancer drivers, they identified 477 of these cancer drivers that interact with multiple features of the TIME, suggesting that they drive the formation of cancer by disrupting biological processes within the cell as well as interfering with the immune system.

Mechanistic insights into the interactions between cancer drivers and the tumour immune microenvironment

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Published in Genome Medicine

Published

Stochastic neighbour embedding plot.

Patient-specific cancer genes contribute to recurrently perturbed pathways and establish therapeutic vulnerabilities in esophageal adenocarcinoma

Oesophageal adenocarcinoma shows high genetic heterogeneity making the identification of cancer drivers challenging. We developed a machine learning algorithm to identify cancer drivers in 261 oesophageal adenocarcinomas. Although most predicted drivers were rare or patient-specific, they all perturbed well-known cancer pathways. Using the recurrence of the same pathway perturbations rather than individual genes, we stratified patients into six groups different for their clinical features. We validated experimentally the contribution of these genes to disease progression and revealed acquired dependencies exploitable in therapy. This study described a new way to identify cancer drivers that we have recently further developed for application in precision oncology.

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Published in Nature Communications

Published

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Research case studies 

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