Publications by authors named "Noah Cheng"
Article Synopsis
- Tumor cell-derived prostaglandin E2 (PGE2) promotes immunosuppression in the tumor microenvironment by influencing immune cells, but its specific role in tumor cells remains unexplored.
- Deleting the PGE2 synthesis enzyme or blocking its receptor (EP4) in pancreatic cancer cells activates T cells, changes the immune environment, and inhibits tumor growth.
- Combining EP4 receptor blockade with immunotherapy leads to complete tumor regressions and enhances immune memory, highlighting the importance of targeting the PGE2 signaling pathway for potential cancer treatments.
The 40-year desire to target the mutant Kirsten rat sarcoma (KRAS) gene (mKRAS) therapeutically is being realized with more and more broadly applicable and tumor-specific small-molecule inhibitors. Immunologically, mKRAS has equal desirability as a target. Tumor KRAS signaling plays a large role in shaping the immunosuppressive nature of the tumor microenvironment, especially in pancreatic cancer, leaving mKRAS inhibitors with potentially powerful immune modulatory capabilities that could be exploited in immunological-oncological combinations.
View Article and Find Full Text PDFUnlabelled: Mutations in the KRAS oncogene are found in more than 90% of patients with pancreatic ductal adenocarcinoma (PDAC), with Gly-to-Asp mutations (KRASG12D) being the most common. Here, we tested the efficacy of a small-molecule KRASG12D inhibitor, MRTX1133, in implantable and autochthonous PDAC models with an intact immune system. In vitro studies validated the specificity and potency of MRTX1133.
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