Publications by authors named "B Z Stanger"
Unlabelled: In pancreatic ductal adenocarcinoma (PDAC), KRAS mutations drive both cancer cell growth and formation of a dense stroma. Small molecule KRAS inhibitors (KRASi) represent a breakthrough for PDAC treatment hence clinical tools that can assess early response, detect resistance and/or predict prolonged survival are desirable for management of patients undergoing KRASi therapy. We hypothesized that diffusion-weighted MRI (DWI) can detect cell death while dynamic contrast enhanced MRI (DCE) and magnetization transfer ratio (MTR) imaging are sensitive to tumor microenvironment changes, and these metrics shed insights into tumor size (standard care assessment) change induced by KRASi treatment.
View Article and Find Full Text PDFPurpose: Pancreatic ductal adenocarcinoma (PDAC) patients with tumors enriched for the basal-like molecular subtype exhibit enhanced resistance to standard of care treatments and have significantly worse overall survival (OS) compared to patients with classical subtype enriched tumors. It is important to develop genomic resources, enabling identification of novel putative targets in a statistically rigorous manner.
Experimental Design: We compiled a single cell RNA sequencing (scRNAseq) atlas of the human pancreas with 229 patient samples, aggregated from publicly available raw data.
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with abundant cancer-associated fibroblasts (CAFs) creating hallmark desmoplasia that limits oxygen and nutrient delivery. This study explores the importance of lipid homeostasis under stress. Exogenous unsaturated lipids, rather than de novo synthesis, sustain PDAC cell viability by relieving endoplasmic reticulum (ER) stress under nutrient scarcity.
View Article and Find Full Text PDFArticle 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.