Seyed Javad M. Moghaddam, MD

Note that back in 2020 due to the COVID-19 pandemic, my laboratory was completely shut down for 3 months, and partially shut down working with a shift schedule and limited staff for 6 more months during which we had to stop expanding our mouse colonies. This led to an extended delay of several projects due to the time we had to spend reviving our mouse colonies which lasted until mid-2021. We also had issues hiring personnel to perform these studies due to COVID-influenced restrictions and hesitancy. However, we still managed to expand the colony of the genetic mouse model required for a portion of this project and performed most of the related studies planned for Aim 1, and a small part of Aim 3. We collected and analyzed samples, and produced very promising data (see below). I have presented these data on 2-3 occasions, and a manuscript describing the results was prepared and submitted to a peer-reviewed journal (JCI Insight) for publication which was very recently accepted for publication and went online ahead of print this month. We are currently working to produce more mice to perform the studies proposed in Aim 2, and the remainder of Aim 1, and 3.

Update: In summary, we demonstrated that IL-1ß blockade effectively suppresses K-ras mutant lung tumorigenesis by shifting the immunosuppressive tumor microenvironment to an anti-tumor phenotype, possibly via modulating the NF-?B and STAT3 pathways and subsequently leading to reduced tumor cell proliferation, and angiogenesis while increasing tumor cell death. These findings support the importance of IL-1ß as a potential target with preventive and therapeutic benefits for patients with K-ras mutant lung adenocarcinoma with highly translational potential in the clinical setting.