Led by scientists from the Universities of Bristol and Cambridge, the Wellcome Sanger Institute, the Health Research Institute of Asturias in Spain and AstraZeneca, the study shows that specific genetic changes affect the ability to develop develop ‘clonal hematopoiesis’, a common condition characterized by the development of enlarged clones of blood cells in the body, driven by mutations in their DNA.
Although asymptomatic, the disorder becomes common with age and is a risk factor for developing blood cancers and other age-related diseases. Its onset is the result of genetic changes in our hematopoietic cells.
All human cells experience genetic changes in their DNA throughout life, known as somatic mutations, with a specific subset of somatic mutations that promote cell multiplication. This is especially common in professional hematopoietic cells, called hematopoietic stem cells, and leads to the development of populations of cells with identical mutations known as ‘clones’.
Using data from the UK Biobank, a large-scale biomedical database and research resource containing genetic and health information from half a million UK participants, the team were able to show that these genetic changes are associated not only with blood cancers but also with tumor growth. elsewhere in the body such as lung, prostate, and ovarian cancers.
The findings also clearly confirm that smoking is one of the strongest modifiable risk factors for developing this disorder, highlighting the importance of reducing tobacco use to prevent the onset of the disorder. disease and its harmful consequences.
Dr Siddhartha Kar, UK Future Leadership Specialist at the University of Bristol and one of the lead authors of the study from Bristol’s MRC Integrated Epidemiology Unit (IEU), said: Our findings relate to the genes and mechanisms involved in the expansion of unstable blood cell lines and may help guide therapeutic advances to prevent or delay the health consequences of diabetes. clonal hematopoiesis, such as progression to cancer and the development of other aging diseases.”
Professor George Vassiliou, Professor of Hematological Medicine at the University of Cambridge and one of the study’s lead authors, added: “Our study shows that cellular mechanisms drive the process of angiogenesis. clonal blood can vary depending on the mutated gene responsible.This is a challenge we face, much to the point of monitoring, but also an opportunity because we can develop methods. specific treatment for each of the major subtypes of this common phenomenon.”