The Medical Research Council

PRESS RELEASE IMU Biosciences joins ground-breaking UK research consortium investigating patient response to cancer immunotherapies Consortium includes leading research institutions, NHS Trusts and industry members and aims to make pioneering immunotherapies safer and more effective London, UK, 7 October 2024 – IMU Biosciences (or “the Company”), a biotechnology company pioneering systems-level immune profiling with AI to drive breakthroughs in precision medicine, is pleased to announce its participation in MANIFEST (Multiomic ANalysis of Immunotherapy Features Evidencing Success and Toxicity), a new UK-wide platform to understand immunotherapy response and side effects in patients with cancer. The MANIFEST consortium, led by the Francis Crick Institute and the Royal Marsden NHS Foundation Trust, has been awarded £9 million in funding from the UK government's Medical Research Council and Office for Life Sciences, with an additional £12.9 million in matched funds from industry partners. This four-year project aims to evaluate the many barriers to the success of immunotherapy and develop predictive biomarkers related to patient response, resistance, and immune-related adverse events following immuno-oncology treatments. IMU Biosciences will play a crucial role in this nationwide effort by analysing thousands of blood samples from patients undergoing immunotherapy. The Company's cutting-edge technology platform, which incorporates high-resolution spectral cytometry integrated with AI-powered analytics, can identify and analyse over 2,000 immune cell subsets, to develop novel systems-level immune signatures and insights. IMU’s technology will be instrumental in the study to help identify and understand how an individual’s immune system influences the responsiveness to immuno-therapy treatments. Using its AI and machine learning analytics, IMU is developing predictive models to improve treatment selection and patient outcomes. The research will initially focus on melanoma, renal cell carcinoma, bladder cancer, and triple-negative breast cancer, involving 6,000 patients across the UK. The consortium's findings aim to help understand which patients are most likely to benefit from immunotherapy and provide insights for potential new treatments, such as vaccines and cell therapies. Adam Laing, President and CSO of IMU Biosciences commented: “The IMU team is thrilled to contribute our cutting-edge, AI-driven immune profiling platform to this groundbreaking UK consortium, helping to deepen the understanding of the immune system’s role in cancer therapy and response, with the ultimate goal of improving clinical outcomes for patients. This collaboration with world-class institutions and industry partners underscores IMU Biosciences' commitment to driving innovation in precision medicine and showcases our potential to make a real impact in healthcare." The MANIFEST consortium brings together 15 academic institutions, including The Francis Crick Institute and the Cancer Research UK National Biomarker Centre, alongside six NHS Trusts, 11 industry collaborators including IMU Biosciences, as well as patient advocacy groups and other networks. -ENDS- Contacts: Adam Laing, CSO and Co-founder, IMU Biosciencesmedia@imubiosciences.com ICR Consilium Tel: +44 (0) 20 3709 5700Sukaina Virji/Lucy Featherstone/Jonathan EdwardsIMUBiosciences@consilium-comms.com About IMU Biosciences IMU Biosciences has developed proprietary platform technologies that generate and translate vast system-level immune data into actionable insights and tools to drive the development of precision medicines across a variety of diseases. Built on over a decade of research at King’s College London and the Francis Crick Institute, IMU leverages advanced immune profiling with proprietary AI and machine learning analytics to uncover novel clinical immune signatures. IMU continues to establish partnerships with leading Pharma and Biotech companies to advance disease diagnosis, optimise product selection, and improve patient stratification and monitoring—while also building its own pipeline of innovative products. To learn more please visit https://www.imubiosciences.com/. Follow us on LinkedIn.

Researchers from the Institute of Cancer Research (ICR) have revealed in a study published in the Journal of Clinical Investigation that an existing targeting drug could successfully treat more individuals living with advanced prostate cancer. In the UK, prostate cancer is responsible for around 12,000 deaths every year. In advanced prostate cancer, abnormal cells begin to spread and grow in surrounding tissues or organs, as well as other areas of the body. According to previous research, up to 30% of men living with the advanced disease have tumours that contain defects in repairing DNA, some of which respond well to PARP inhibitor drugs, including AstraZeneca and Merck & Co’s – known as MSD outside the US and Canada – Lynparza (olaparib). Funded by AstraZeneca, Prostate Cancer UK, Cancer Research UK, the Medical Research Council, Movember and the Prostate Cancer Foundation, researchers analysed biopsies from 124 patients living with advanced prostate cancer and found that RNASEH2B loss was common in 44% of patients, in at least 50% of their cancer cells, while 20% of patients experienced RNASEH2B loss in 75% of cancer cells. The RNASEH2B gene plays a role in repairing certain forms of DNA damage and when it is deleted or ‘lost’ during cell division or replication, it no longer functions as it should. In addition, researchers evaluated both pre- and post-treatment biopsy samples from patients living without BRCA1 and BRCA2 mutations (tumour suppressor genes) who participated in the TOPARP-A and TOPARP-B clinical trials conducted by the ICR’s Clinical Trials and Statistics Unit and found that the number of cells with RNASE2B loss decreased in 13 out of 18 patients following PARP inhibitor treatment, while six of 18 patients experienced a decline in circulating tumour cells – three of which benefitted from relapse-free survival between eight and 22 months. These new findings could lead to further trials of Lynparza in prostate cancer to determine whether it could be targeted at a larger population of advanced prostate cancer patients with RNASEH2B aberrations. Johann de Bono, regius professor of cancer research, ICR, commented: “This is a substantial advance… [and] further research is urgently needed to validate these findings… [to] provide a new treatment option for patients with advanced prostate cancer.”

Genes can indirectly influence the age at which girls have their first period by accelerating weight gain in childhood, a known risk factor for early puberty. Other genes can directly affect age of puberty, some with profound effects. Genes can indirectly influence the age at which girls have their first period by accelerating weight gain in childhood, a known risk factor for early puberty, a Cambridge-led study has found. Other genes can directly affect age of puberty, some with profound effects. In the largest study of its kind to date, an international team led by researchers at the Medical Research Council (MRC) Epidemiology Unit, University of Cambridge, studied the DNA of around 800,000 women from Europe, North America, China, Japan, and Korea. Published today in Nature Genetics, the researchers found more than 1,000 variants -- small changes in DNA -- that influence the age of first menstrual period. Around 600 of these variants were observed for the first time. The age at which girls hit puberty and start having periods normally occurs between ages 10 to 15, though this has been getting earlier and earlier in recent decades. The reasons for this are not fully understood. Early puberty is linked with increased risk of a number of diseases in later life, including type 2 diabetes, cardiovascular disease, and certain cancers. Later puberty on the other hand, has been linked to improved health in adulthood and a longer lifespan. Just under half (45%) of the discovered genetic variants affected puberty indirectly, by increasing weight gain in early childhood. Corresponding author Professor John Perry said: "Many of the genes we've found influence early puberty by first accelerating weight gain in infants and young children. This can then lead to potentially serious health problems in later life, as having earlier puberty leads to higher rates of overweight and obesity in adulthood." Previous work by the team -- together with researchers at Cambridge's MRC Metabolic Diseases Unit -- showed that a receptor in the brain, known as MC3R, detects the nutritional state of the body and regulates the timing of puberty and rate of growth in children, providing a mechanism by which this occurs. Other identified genes appeared to be acting in the brain to control the release of reproductive hormones. The scientists also analysed rare genetic variants that are carried by very few people, but which can have large effects on puberty. For example, they found that one in 3,800 women carry variants in the gene ZNF483, which caused these women to experience puberty on average, 1.3 years later. Dr Katherine Kentistou, lead study investigator, added: "This is the first time we've ever been able to analyse rare genetic variants at this scale. We have identified six genes which all profoundly affect the timing of puberty. While these genes were discovered in girls, they often have the same impact on the timing of puberty in boys. The new mechanisms we describe could form the basis of interventions for individuals at risk of early puberty and obesity." The researchers also generated a genetic score that predicted whether a girl was likely to hit puberty very early or very late. Girls with the highest 1% of this genetic score were 11 times more likely to have extremely delayed puberty -- that is, after age 15 years. On the other hand, girls with the lowest 1% genetic score were 14 times more likely to have extremely early puberty -- before age 10. Senior author and paediatrician Professor Ken Ong said: "In the future, we may be able to use these genetic scores in the clinic to identify those girls whose puberty will come very early or very late. The NHS is already trialling whole genome sequencing at birth, and this would give us the genetic information we need to make this possible. "Children who present in the NHS with very early puberty -- at age seven or eight -- are offered puberty blockers to delay it. But age of puberty is a continuum, and if they miss this threshold, there's currently nothing we have to offer. We need other interventions, whether that's oral medication or a behavioural approach, to help. This could be important for their health when they grow up." The research was supported by the Medical Research Council and included data from the UK Biobank.