- Friday, October 20, 2023
- 2:45 PM–3:35 PM
- Science Building 110
SETD2 Deficiency and Hypo-methylating Agents Induce Mis-splicing in Kidney Cancer: Implications for Cancer Vaccine Development with Audrey Nguyen Investigating the Role of the NLRP3 Inflammasome in Endothelial to Mesenchymal Activation and Aortic Aneurysm Formation with Daniel John
SETD2 Deficiency and Hypo-methylating Agents Induce Mis-splicing in Kidney Cancer: Implications for Cancer Vaccine Development
The SETD2 protein plays a significant role in the cell's genetic regulation through its histone methyltransferase activity and is recurrently mutated in aggressive clear cell Renal Cell Carcinoma (ccRCC), or kidney cancer. Treating SETD2 deficient cells with hypo-methylating agents like 5-aza-20-deoxycytidine (DAC) increases the likelihood of mis-splicing events, leading to the inclusion of introns in the mature mRNA, which translates to cancer specific protein and drives viral mimicry. The implications of these findings are significant, as mis-splicing products may serve as potential biomarkers or targeted antigens to develop a cancer vaccine against this malignancy.
Investigating the Role of the NLRP3 Inflammasome in Endothelial to Mesenchymal Activation and Aortic Aneurysm Formation
Aortic aneurysms (AAs) are becoming increasingly prevalent, with an estimated 35.12 million cases worldwide in people from the ages of 30 to 79 in 2019. Endovascular and open repair are possible for larger aneurysms, but for smaller aneurysms, surgical repair is typically not recommended due to the risks entailed by surgery. There are currently no effective pharmacological therapies available. Recent studies from our lab have also demonstrated that endothelial cell specific elimination of IL-R1 inhibited AAA formation and the endothelial to mesenchymal transition (EndMT). The nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3)-caspase-1 inflammasome cascade activates IL-1 signaling by cleaving pro-IL-1B to its active form. We sought to demonstrate the role of NLRP3 in AAAs and to determine the effects of NLRP3 elimination on EndMT.
