Investigating clonal dynamics and effects of environmental factors in clonal haematopoiesis Dr Kasper Rasmussen presents his work on dissecting the mechanisms by which the proteins regulating the DNA methylation landscape affects chromatin structure and gene expression patterns in hematopoietic cells. Hosted by Professor Dave Kent.

Seminar
This event has now finished.
  • Date and time: Friday 26 April 2024, 1pm to 4pm
  • Location: Dianna Bowles Lecture Theatre, B/K/018, Biology Building, Campus West, University of York (Map)
  • Audience: Open to alumni, staff, students (postgraduate researchers, taught postgraduates, undergraduates)
  • Admission: Free admission, booking not required

Event details

Abtsract

Blood production is driven by a small subset of long-lived haematopoietic stem cells that can self-renew and give rise to all terminal differentiated cells found in the blood. A significant proportion of the human population (~6%) carries mutations in HSCs that promote age-related clonal expansion, blood cancer, and all-cause mortality in a phenomenon termed clonal haematopoiesis (CH). Large-scale efforts have identified a subset of ~60 genes – including the DNA methylation effectors TET2 and DNMT3A - that when mutated drive CH. However, the mechanism of how competitive advantage is achieved as well as the interplay between specific mutations and environmental factors, such as inflammation and genotoxic stress, are still unclear. In this seminar, I will present our efforts to understand the molecular and epigenomic changes leading to clonal outgrowth and delineate the effects of proinflammatory cytokines, common chemotherapeutic agents, and targeted therapies to identify risk factors as well as preventative measures that may limit cancer formation and promote healthy aging.

About the speaker

Dr Kasper Rasmussen

Kasper is a Principal Investigator in Molecular Cell and Developmental Biology in the School of Life Sciences at the University of Dundee. The aim of his work is to dissect the mechanisms by which the proteins regulating the DNA methylation landscape affect chromatin structure and gene expression patterns in hematopoietic cells. To do this, he utilizes CRISPR genome editing in embryonic stem cells, mouse and human hematopoietic cell lines and complex mouse models of leukaemia and combine these with the application of new biochemical, genomics and proteomics techniques. The biological insights obtained may provide the basis for developing targeted therapies for blood cancers with mutations in the DNA methylation machinery.