ReviewJournal of experimental & clinical cancer research : CR2024
Tumor immune microenvironment-based therapies in pancreatic ductal adenocarcinoma: time to update the concept.
Review in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 49 citations in OpenAlex.
- Impact of Liver Metastases on Outcomes With Chemotherapy or Immune Checkpoint Inhibitors in Pancreatic Cancer.Immunity, inflammation and disease · 2026Observational
- Biomarker-Driven Strategies for Stromal Reprogramming in Pancreatic Ductal Adenocarcinoma.Cells · 2026Review
- Article
- Single-Cell Glycomics of the Pancreatic Tumor Microenvironment: Technologies, Glyco-Immune Checkpoints, and Tumor-Immune Communication.Advanced biology · 2026Review
- Reprogramming the Tumor Oncobiosphere: Bioactive Nanohybrid Materials for Reversing Therapeutic Pseudo-Resistance.ACS omega · 2026Review
- Review
- GSK3βGut · 2026Article
- Pan-cancer 8q24 amplification predicts primary immunotherapy resistance and therapeutic vulnerabilities.iScience · 2026Article
- Reprogramming tumor microenvironment of pancreatic cancer by CAF-targeted sonodynamic therapy combined with chemotherapy.Materials today. Bio · 2026Article
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- C-X-C chemokine receptor type 4 (CXCR4) antagonism in precision oncology: Clinical applications and future directions.Cancer pathogenesis and therapy · 2026Review
- Individualized treatment and key prognostic biomarkers based on folate metabolism in patients with pancreatic cancer.Translational cancer research · 2026Article
- Cytokine mRNA-based therapy alleviates dendritic cell and T cell paucity to eliminate aggressive pancreatic cancer in preclinical mouse models.EBioMedicine · 2026Article
- Epigenetic modulation to overcome immune suppression in pancreatic cancer.Clinical epigenetics · 2026Review
- Cancer antigen 125 levels change rule after laparoscopic biopsy and its prognostic value for patients with unresectable pancreatic ductal adenocarcinoma: a retrospective preliminary exploratory study.BMC gastroenterology · 2026Article
- Bioengineered Pancreatic Cancer Immunosuppressive Microenvironment Models for Screening Immunotherapies.Advanced healthcare materials · 2026Article
- Decoding the ERS-CAF immunoregulatory axis via multimodal AI and its pan-cancer prognostic and therapeutic predictive value.NPJ digital medicine · 2026Article
- Identification and characterization of MARCO-expressing tumor-associated macrophages in pancreatic ductal adenocarcinoma with pan-cancer relevance.NPJ precision oncology · 2026Article
- Antimetastatic effects of MRTX1133 KRAS G12D specific inhibitor in a liver metastatic model of pancreatic ductal adenocarcinoma.Scientific reports · 2026Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid tumors. The tumor immune microenvironment (TIME) formed by interactions among cancer cells, immune cells, cancer-associated fibroblasts (CAF), and extracellular matrix (ECM) components drives PDAC in a more immunosuppressive direction: this is a major cause of therapy resistance and poor prognosis. In recent years, research has advanced our understanding of the signaling mechanism by which TIME components interact with the tumor and the evolution of immunophenotyping. Through revolutionary technologies such as single-cell sequencing, we have gone from simply classifying PDACs as "cold" and "hot" to a more comprehensive approach of immunophenotyping that considers all the cells and matrix components. This is key to improving the clinical efficacy of PDAC treatments. In this review, we elaborate on various TIME components in PDAC, the signaling mechanisms underlying their interactions, and the latest research into PDAC immunophenotyping. A deep understanding of these network interactions will contribute to the effective combination of TIME-based therapeutic approaches, such as immune checkpoint inhibitors (ICI), adoptive cell therapy, therapies targeting myeloid cells, CAF reprogramming, and stromal normalization. By selecting the appropriate integrated therapies based on precise immunophenotyping, significant advances in the future treatment of PDAC are possible.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.