Bioscientist plays major role in groundbreaking lung cancer research

Cancer researcher Dr Tim Humpton played a major role in a new groundbreaking international study that has revealed potential targets for preventing lung cancer tumour reoccurrence and resistance.

Dr Humpton, Reader in the School of Health and Life Sciences (SHLS) Biological and Biomedical Sciences Department and Research Centre for Health (ReaCH) was involved in the new study which focused on understanding mechanisms of drug resistance in patients with lung cancer.

Dr Humpton said: “This study reveals new potential vulnerabilities in otherwise treatment-resistant lung cancer. It is an important breakthrough accomplished by a motivated international team, of which I’m delighted to have contributed my expertise.”

These findings, derived from the TRACERx lung cancer study conducted at the Francis Crick Institute, shed light on the critical importance of understanding the molecular consequences of interactions between cancer-causing mutations to better prevent tumour reoccurrence and drug resistance.

The study, entitledThe role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance has been published in the Nature Genetics journal.

Dr Humpton, is a key researcher in the ReaCH Molecular Mechanisms of Long-Term Conditions Research Group, focuses on the biology of p53, a potent tumour suppressor and ‘guardian of the genome’. P53 normally acts to prevent cancer, and its mutation or disruption is a key feature of the majority of cancer types.

The research on the project was led by Dr Deborah Caswell, from the Cancer Evolution and Genome Instability Laboratory at The Francis Crick Institute in London, and by Dr Trever Bivona, from the University of California, San Francisco and the Chan-Zuckerberg Biohub in San Francisco, USA.

The project included contributions from over 45 research groups across the UK, USA, and Europe.  In the paper, the team used pre-clinical models, cell lines and patient-derived samples to show that a particular gene called Apolipoprotein B mRNA-editing catalytic subunit-like enzyme (APOBEC3B) acts to restrict lung tumour development in certain contexts when the p53 gene is functional.

However, in patients who receive certain targeted therapies and lack or have mutated p53, APOBEC3B changes roles to promote therapy resistance and tumour progression.

Dr Humpton said the study highlights the complex role of APOBEC3B in lung cancer and also suggests a new potential target for more durable responses to targeted cancer therapy.