ArticleOncoimmunology
JAK-STAT-mediated chronic inflammation impairs cytotoxic T lymphocyte activation to decrease anti-PD-1 immunotherapy efficacy in pancreatic cancer.
Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 3 of them syntheses that pooled it.
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Who cites it
109 citing papers in PubMed, 3 syntheses or guidelines pooled it, 169 citations in OpenAlex.
- Signaling pathway mechanisms in pancreatic ductal adenocarcinoma tumor microenvironment and emerging targeting strategies for improved prognosis.Oncology reviews · 2026Pooled it
- Integration of healthy volunteers in early phase clinical trials with immuno-oncological compounds.Frontiers in oncology · 2022Pooled it
- Therapeutic targeting of STAT3 pathways in pancreatic adenocarcinoma: A systematic review of clinical and preclinical literature.PloS one · 2021Pooled it
- Review
- Effects of Nicotine administration on α7nAChR, miR-124, STAT3, and inflammatory markers in Rat Lung Tissue.Molecular biology reports · 2026Article
- Beyond suppression: the paradox of JAK inhibitors as amplifiers of cancer immunotherapy.Nature reviews. Immunology · 2026Review
- Myeloid-Derived Suppressor Cells in Sepsis: Pathophysiology, Duality, and Therapeutic Frontiers.Shock (Augusta, Ga.) · 2026Review
- Research progress on the correlation between OPN and immune escape of gastric cancer.Clinical and experimental medicine · 2026Review
- Revitalizing T cells: breakthroughs and challenges in overcoming T cell exhaustion.Signal transduction and targeted therapy · 2026Review
- JAK inhibition in PD-1 immunotherapy and tumor microenvironment.Frontiers in immunology · 2026Review
- Therapeutic expansion of JAK inhibitors in Chinese dermatological practice: beyond atopic dermatitis to novel autoimmune frontiers.Frontiers in medicine · 2026Review
- VAMP5 promotes glioma progression through bioinformatics analysis clinical correlation and functional validation.Discover oncology · 2025Article
- Fumarate activates the IL-6/JAK/STAT3 pathway by inhibiting KDM4C-mediated H3K36me3 demethylation in FH-knockdown renal cancer cells.British journal of cancer · 2025Article
- A novel anti-PD-L1/IL-8 bispecific antibody BP2402 enhances antitumor immunity and modulates inflammatory signaling in triple-negative breast cancer mice model.Journal of translational medicine · 2025Article
- Inflammation-Driven Genomic Instability: A Pathway to Cancer Development and Therapy Resistance.Pharmaceuticals (Basel, Switzerland) · 2025Review
- RAD18 promotes cell malignant behaviors of esophageal squamous cell carcinoma by modulating ATM/STAT3/PD-L1.Chromosoma · 2025Article
- Parkinson's disease: exploring the systemic immune mechanisms through molecular investigations.Inflammopharmacology · 2025Review
- Formosanin C inhibits triple-negative breast cancer progression by suppressing the phosphorylation of STAT3 and the polarization of M2 macrophages.Breast cancer research and treatment · 2025Article
- Sequential JAK inhibition enhances antitumor immunity after combined anti-PD-1 and anti-CTLA4.JCI insight · 2025Article
- Mechanisms of Resistance to Anti-PD-1 Immunotherapy in Melanoma and Strategies to Overcome It.Biomolecules · 2025Review
49 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Human pancreatic cancer does not respond to immune check point blockade immunotherapy. One key feature of pancreatic cancer is the association between its progression and chronic inflammation. Emerging evidence supports a key role for the JAK-STAT pathway in pancreatic cancer inflammation. We aimed at testing the hypothesis that sustained JAK-STAT signaling suppresses cytotoxic T lymphocyte (CTL) activation to counteract anti-PD-1 immunotherapy-induced CTL activity in pancreatic cancer. We show that human pancreatic carcinomas express high level of PD-L1 and exhibit low level of CTL infiltration. JAK-STAT inhibitor Ruxolitinib selectively inhibits STAT1 and STAT3 activation and increases CTL infiltration to induce a Tc1/Th1 immune response in the tumor microenvironment in an orthotopic pancreatic cancer mouse model. Ruxilitinib-mediated tumor suppressive efficacy diminishes in T-cell-deficient mice. Pancreatic tumor grows significantly faster in IFNγ-deficient mice. However, neutralizing IFNγ does not alter tumor growth but diminishes Ruxolitinib-induced tumor suppression
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.