Summary
Investigate the effects of Myelodysplastic Syndrome (MDS)-associated U2AF1 mutations on natural killer (NK) cell dysfunction to understand the underlying cellular and molecular mechanisms, aiming to advance immune-based therapies for MDS.
MDS-associated U2AF1 mutations induce natural killer cell dysfunction
US · IL
NIH
grant
awarded
#nih-1R21CA301519-01A1
What they want
The project investigates the effects of MDS-associated spliceosome mutations on NK cell dysfunction in mice and humans. Preliminary studies found that these mutations drive substantial NK cell dysfunction. The hypothesis is that MDS-associated spliceosome mutations impair NK cell function by altering expression or functionality of critical NK cell-intrinsic gene products. The work proposes to determine the cellular (Aim 1) and molecular (Aim 2) mechanisms underlying these effects to provide critical mechanistic insights for developing more targeted and effective immune-based therapies to treat MDS and related malignancies.
Deliverables
- Determine the cellular mechanisms underlying NK cell dysfunction induced by MDS-associated spliceosome mutations (Aim 1)
- Determine the molecular mechanisms underlying NK cell dysfunction induced by MDS-associated spliceosome mutations (Aim 2)
