Presented in collaboration with Be The Match BioTherapies®
A hallmark of the ageing hematopoietic system is a skewing of lineage output from balanced to myeloid-biased, which is hypothesized to result in compromised adaptive immunity and predisposition toward myeloid malignancies in aging individuals. More recently, changes in the composition of a heterogeneous HSC population with age (the population shift model) is being increasingly recognized to account for lineage output changes and the observed hematopoietic ageing phenotype may result from an expansion of myeloid-biased HSCs with exhaustion of lymphoid-biased and balanced HSCs. Importantly, research efforts continue investigate the molecular mechanisms associated with aging HSCs. This session will highlight theories recent discoveries of the ageing HSC compartment and molecular mechanisms underlying these processes which potentially can be targeted to rejuvenate aged HSC functions.
Define the current models of hematopoietic stem cell (HSC) heterogeneity and changes that occur with the ageing process.
Discuss the molecular mechanisms that contribute to HSC output skewing and senescence that occur with age and approaches to revert the aging-associated hallmarks of aged HSCs.
Describe HSC clonal dominance and expansion of HSCs that occurs with age and contribution to malignant transformations.