ArticleOncoimmunology2016
Anti-α-enolase antibody limits the invasion of myeloid-derived suppressor cells and attenuates their restraining effector T cell response.
Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 22 citations in OpenAlex.
- Inhibiting CXCR2 Remodels the Tumor Microenvironment and Blunts Tumor Progression and Dissemination of High-Grade Serous Carcinoma.Cancer research communications · 2026Article
- Enolase-1 and Inflammation.Biomolecules · 2026Review
- ENO1 as an Immunoregulatory Hub in Cancer: Mechanisms and Translational Implications.Biomolecules · 2026Review
- Application of serum anti-ENO1 and anti-SSNA1 antibody biomarkers in predicting the prognosis of gastric cancer.Oncology letters · 2025Article
- ENO1 promotes PDAC progression by inhibiting CD8Translational oncology · 2025Article
- Therapeutic cancer vaccines in pancreatic cancer.Frontiers in immunology · 2025Review
- Heterogeneity and Differentiation Trajectories of Infiltrating CD8+ T Cells in Lung Adenocarcinoma.Cancers · 2022Article
- Halting the vicious cycle within the multiple myeloma ecosystem: blocking JAM-A on bone marrow endothelial cells restores angiogenic homeostasis and suppresses tumor progression.Haematologica · 2021Article
- The role of myeloid-derived suppressor cells in gastrointestinal cancer.Cancer communications (London, England) · 2021Review
- The Glycolytic Pathway as a Target for Novel Onco-Immunology Therapies in Pancreatic Cancer.Molecules (Basel, Switzerland) · 2021Review
- Review
- Characterizing heterogeneity of non-small cell lung tumour microenvironment to identify signature prognostic genes.Journal of cellular and molecular medicine · 2020Article
- In pancreatic cancer, chemotherapy increases antitumor responses to tumor-associated antigens and potentiates DNA vaccination.Journal for immunotherapy of cancer · 2020Article
- Preclinical validation of Alpha-Enolase (ENO1) as a novel immunometabolic target in multiple myeloma.Oncogene · 2020Article
- Myeloid-Derived Suppressor Cells and Pancreatic Cancer: Implications in Novel Therapeutic Approaches.Cancers · 2019Review
- MDSCs: Key Criminals of Tumor Pre-metastatic Niche Formation.Frontiers in immunology · 2019Review
- Next Generation Immunotherapy for Pancreatic Cancer: DNA Vaccination is Seeking New Combo Partners.Cancers · 2018Review
- Cancer vaccines and immunotherapeutic approaches in hepatobiliary and pancreatic cancers.Human vaccines & immunotherapeutics · 2017Review
- Article
- Next generation of cancer immunotherapy calls for combination.Oncoscience · 2017Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic Ductal Adenocarcinoma (PDA) is a very aggressive tumor for which effective therapeutical strategies are still lacking. Globally, the 5 y survival rate is 5-7% and surgery is the only potentially curative treatment. Immunotherapy represents a novel possibility for treating PDA, and myeloid-derived suppressor cells (MDSC), which are increased in cancer patients and correlate with metastatic burden and cancer stage, offer a new target in cancer therapy. We have previously shown that antibodies against the PDA-associated antigen α-enolase (ENO1) are detected in more than 60% of PDA patients and correlate with a better prognosis. Furthermore, ENO1-DNA vaccination in mice induced anti-ENO1 antibodies that mediated antitumor activity. In this study, the effects of anti-ENO1 binding on MDSC functions and on the T cell response were evaluated. Here, we show that MDSC express ENO1 on their surface, which increased after LPS stimulation. Moreover, anti-ENO1 mAb inhibited adhesion to endothelial cells, as well as in vitro and in vivo migration. Similarly, after ENO1 mAb treatment of MDSC, arginase activity decreased, while the secretion of pro-inflammatory cytokines (particularly IL-6) increased, and co-stimulatory molecule expression and suppression functions were only partially affected. Finally, we found that activated T cells in the presence of anti-ENO1 mAb-treated MDSC increased IFNγ and IL-17 secretion and decreased IL-10 and TGFβ secretion compared to control MDSC. In conclusion, anti-ENO1 antibodies may inhibit in vivo the infiltration into the tumor microenvironment of MDSC, and attenuate their restraining of effector T cell response, opening a new perspective to render PDA immunotherapy more effective.
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.