ReviewOncotarget2016
Targeting tumor-associated macrophages to combat pancreatic cancer.
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed.
- Review
- A Patient-Derived Organ-on-Chip Platform for Modeling the Tumor Microenvironment and Drug Responses in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Emerging Chimeric Antigen Receptor-Immune Cell Therapy for Pancreatic Cancer: Mechanisms, Clinical Advances, and Future Perspectives.Oncology research · 2026Review
- An Investigation to Study Morphology, Nanomechanical Attributes, Transcriptomics, and Proteomics of Tumor Associated Macrophages Derived Extracellular Vesicles in the Tumor Microenvironment.Journal of analytical oncology · 2026Article
- TREM-1 as a novel immunotherapeutic target to treat pancreatic ductal adenocarcinoma.Molecular therapy. Oncology · 2025Article
- PLS-α-GalCer: a novel targeted glycolipid therapy for solid tumors.Journal for immunotherapy of cancer · 2025Article
- RAW264.7 Macrophages as a Polarization Model in the Context of Pancreatic Cancer and Chemokine Release.Biology · 2025Article
- Intercellular TIMP-1-CD63 signaling directs the evolution of immune escape and metastasis in KRAS-mutated pancreatic cancer cells.Molecular cancer · 2025Article
- Single-cell transcriptomics reveal the prognostic roles of epithelial and T cells and DNA methylation-based prognostic models in pancreatic cancer.Clinical epigenetics · 2024Article
- The complex role of macrophages in pancreatic cancer tumor microenvironment: a review on cancer progression and potential therapeutic targets.Discover oncology · 2024Review
- An update to experimental and clinical aspects of tumor-associated macrophages in cancer development: hopes and pitfalls.Clinical and experimental medicine · 2024Review
- From monocyte-derived macrophages to resident macrophages-how metabolism leads their way in cancer.Molecular oncology · 2024Review
- Glycosylation in the tumor immune response: the bitter side of sweetness.Acta biochimica et biophysica Sinica · 2024Review
- Immune cells and checkpoints in pancreatic adenocarcinoma: Association with clinical and pathological characteristics.PloS one · 2024Article
- Antibody drug conjugates: hitting the mark in pancreatic cancer?Journal of experimental & clinical cancer research : CR · 2023Review
- Galectin-1 in Pancreatic Ductal Adenocarcinoma: Bridging Tumor Biology, Immune Evasion, and Therapeutic Opportunities.International journal of molecular sciences · 2023Review
- Review
- CCR4 Blockade Diminishes Intratumoral Macrophage Recruitment and Augments Survival of Syngeneic Pancreatic Cancer-Bearing Mice.Biomedicines · 2023Article
- Regulation of epithelial-mesenchymal transition by tumor microenvironmental signals and its implication in cancer therapeutics.Seminars in cancer biology · 2023Review
- Review
5 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
6 authors.
Funding
Abstract
The tumor microenvironment is replete with cells that evolve with and provide support to tumor cells during the transition to malignancy. The hijacking of the immune system in the pancreatic tumor microenvironment is suggested to contribute to the failure to date to produce significant improvements in pancreatic cancer survival by various chemotherapeutics. Regulatory T cells, myeloid derived suppressor cells, and fibroblasts, all of which constitute a complex ecology microenvironment, can suppress CD8+ T cells and NK cells, thus inhibiting effector immune responses. Tumor-associated macrophages (TAM) are versatile immune cells that can express different functional programs in response to stimuli in tumor microenvironment at different stages of pancreatic cancer development. TAM have been implicated in suppression of anti-tumorigenic immune responses, promotion of cancer cell proliferation, stimulation of tumor angiogenesis and extracellular matrix breakdown, and subsequent enhancement of tumor invasion and metastasis. Many emerging agents that have demonstrated efficacy in combating other types of tumors via modulation of macrophages in tumor microenvironments are, however, only marginally studied for pancreatic cancer prevention and treatment. A better understanding of the paradoxical roles of TAM in pancreatic cancer may pave the way to novel preventive and therapeutic approaches. Here we give an overview of the recruitment and differentiation of macrophages, TAM and pancreatic cancer progression and prognosis, as well as the potential preventive and therapeutic targets that interact with TAM for pancreatic cancer prevention and treatment.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.