Shriram K. Sundararaman

TL;DR: It is reported that LKB1 loss results in marked silencing of stimulator of interferon genes (STING) expression and insensitivity to cytoplasmic double-strand DNA (dsDNA) sensing, which is mediated at least in part by hyperactivation of DNMT1 and EZH2 activity related to elevated S-adenylmethionine levels and reinforced byDNMT1 upregulation.

TL;DR: A novel microfluidic model is developed to study KL tumor-vascular interactions and shows that tumor cell cGAS-STING signaling not only produces T cell chemoattractants, but also primes tumor vasculature for immune cell escape.

TL;DR: This work immortalizes HUVECs and FBs by exogenously expressing human telomerase reverse transcriptase (hTERT) to obtain stable endothelial cell and FB sources for μVN formation in vitro and characterize the functions of Thy1 positive and negative FBs in vasculogenesis in vitro.

TL;DR: It is revealed that tumor cells produce 2'3'-cGAMP, which activates the STING pathway in non-tumor cells and leads to type I IFN production and the priming of natural killer cells for tumor rejection.

TL;DR: In this paper , transient MPS1 inhibition (MPS1i) was shown to re-engage this pathway in KL cells via micronuclei generation, and a single course of decitabine treatment followed by pulse MPS 1i therapy restores T cell infiltration in vivo, enhances anti-PD 1 efficacy, and results in a durable response without evidence of significant toxicity.