Edward Speed’s connection to the Crick began long before his cancer diagnosis. As part of the original effort to build the institute, he was a member of the board that successfully raised £100 million, playing a quiet but pivotal role in connecting philanthropists to a bold scientific vision.
“I am in awe of people like Edward who have taken part in the PEACE study”
Mariam Jamal-Hanjani
When Edward was told he had lymphoma in 2018, the world of science he had supported became the world he relied on. Following years of intensive treatment – periods of remission punctuated by relapse – he died in November 2025 at the age of 68, surrounded by his family.
“He’d benefited so much from advances in science and felt strongly that he had a duty to give back,” says his wife, Debbie Speed. This sense of responsibility guided not only his philanthropy, but also one of the most profound decisions he would make. When treatment options were exhausted, Edward chose to donate his body to the PEACE study – a Cancer Research UK-funded programme that collects tissue samples from terminally ill people, both before and after their death. This provides researchers with a rare opportunity to study not only patients’ tumours but also the wider biological imprint of cancer across the body.
“The only way we can fully understand the impact of cancer across a lifetime, particularly in the later stages when treatments often stop working, is by analysing tumour samples after people have died,” says Mariam Jamal-Hanjani, chief investigator on the study and an Associate Researcher at the Crick.
A recent analysis of data from 22 participants in PEACE has now revealed unexpected ‘mutational fingerprints’ in healthy organs of people with advanced cancer, a discovery that is advancing our understanding of how cancer and its treatments affect the body.
By reading the DNA sequences in these healthy tissue samples, Crick postdoctoral research scientist Oriol Pich identified previously unseen patterns of mutations across multiple organs. He and the team then matched these genetic readouts to clinical data from individual patients, including details of their treatments and lifestyle factors such as whether they smoked.
“We expected to see many mutations from risk factors like drinking alcohol and smoking in samples from the liver and lungs,” describes Oriol. “But our analysis also showed that some types of cancer treatment produce bursts of mutations in other healthy tissues and organs.”
Surprisingly, they found genetic changes associated with immunotherapy – a treatment not thought to directly damage DNA. The researchers believe this may be explained by the way immunotherapy places selective pressure on cells, allowing certain mutated populations to grow.
The team also found higher-than-expected levels of mutations in organs such as the spleen, raising new questions about how different parts of the body respond to cancer and its treatment.
While not all these mutations would have led to future cancers, the findings highlight the broader impact of cancer treatment on the body, and underline the need for therapies that are more targeted and less harmful to healthy cells.
The advanced DNA sequencing method used in this study was sensitive enough to detect very rare genetic changes, but it could not identify which specific cell types those mutations came from. The team is now exploring whether some types of cells accumulate mutations faster than others in different tissues and what that means for the tissue and patient.