Gregory P. Chang

TL;DR: In this paper, the authors investigated Treg cell function in a genetically engineered mouse model of lung adenocarcinoma and found that Treg cells suppressed anti-tumor responses in tumor-associated tertiary lymphoid structures (TA-TLSs).

TL;DR: It is shown that PIDD expression promotes growth arrest and chemotherapy resistance by a mechanism that depends on Caspase-2 and wild-type p53 and insight is provided into a mechanism of Mdm2 inhibition that impacts p53 dynamics upon genotoxic stress.

TL;DR: The data demonstrate the applicability of GMAP toward the validation of synthetic promoters, identification of potent RNAi constructs, establishment of inducible lentiviral systems, tumor initiation in genetically engineered mouse models, and gene-targeting for the generation of knock-in mice.

TL;DR: It is proposed that Treg cells in TA-TLSs can inhibit endogenous immune responses against tumors, and targeting these cells might provide therapeutic benefit for cancer patients.

TL;DR: In this article, the authors show that PIDD expression promotes growth arrest and chemotherapy resistance by a mechanism that depends on Caspase-2 and wild-type p53, and they establish Mdm2 as a cleavage target of Caspases-2, and provide insight into a mechanism of MDM2 inhibition that impacts p53 dynamics upon genotoxic stress.