Back to search

Article

Combined MEK and STAT3 inhibition reprograms stromal inflammation to overcome immunotherapy resistance in pancreatic cancer

2021-03-08

Abstract excerpt

<h4>ABSTRACT</h4> Pancreatic ductal adenocarcinoma (PDAC) is characterized by immune exclusion, pro-inflammatory polarization of cancer-associated fibroblasts (CAF), and resistance to immune checkpoint inhibition (ICI). We have previously demonstrated that reciprocally activated RAS/MEK/ERK and JAK/STAT3 pathways mediate therapeutic resistance, while combined MEK and STAT3 inhibition (MEKi+STAT3i) overcomes such...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
e3800dfd-888b-539d-bc8a-13bf44460223
DOI
10.1101/2021.03.07.434236
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
Combined MEK and STAT3 inhibition reprograms stromal inflammation to overcome immunotherapy resistance in pancreatic cancerDOI 10.1101/2021.03.07.434236
Distinct small molecule inhibitors of Kras specifically prime CTLA4 blockade therapy to transcriptionally reprogram Tregs and overcome resistance to suppress pancreas cancerSemantic proximity
Inverse Correlation of STAT3 and MEK Signaling Mediates Resistance to RAS Pathway Inhibition in Pancreatic Cancer.Semantic proximity
The Extracellular Niche and Tumor Microenvironment Enhance KRAS Inhibitor Efficacy in Pancreatic Cancer.Semantic proximity
Combined KRAS Inhibition and Immune Therapy Generates Durable Complete Responses in an Autochthonous PDAC ModelSemantic proximity
Current advances in immunotherapy for KRAS-Mutant pancreatic cancer.Semantic proximity
TAK1 Promotes an Immunosuppressive Tumor Microenvironment through Cancer-Associated Fibroblast Phenotypic Conversion in Pancreatic Ductal Adenocarcinoma.Semantic proximity
An allele-agnostic mutant-KRAS inhibitor suppresses tumor maintenance signals and reprograms tumor immunity in pancreatic cancer.Semantic proximity
Oncogenic dependency plays a dominant role in the immune response to cancer.Semantic proximity
MYC Instructs and Maintains Pancreatic Adenocarcinoma Phenotype.Semantic proximity
Epigenetic and Transcriptional Control of the Epidermal Growth Factor Receptor Regulates the Tumor Immune Microenvironment in Pancreatic Cancer.Semantic proximity
Targeting tumor-intrinsic TAK1 triggers anti-tumor immunity and sensitizes pancreatic cancer to checkpoint blockadeSemantic proximity
Targeting CREB remodels the immune microenvironment to enhance immunotherapy responses in pancreatic cancerSemantic proximity
Select a neighboring publication to make it the new centre.