ArticleMolecular cancer2024
Acyl-coenzyme a binding protein (ACBP) - a risk factor for cancer diagnosis and an inhibitor of immunosurveillance.
Article in Molecular cancer, 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 21 papers.
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Who cites it
21 citing papers in PubMed.
- Cell death-induced release of the pro-aging protein acyl CoA binding protein (ACBP) into the circulation.Cell death and differentiation · 2026Article
- Neutralization of acyl-CoA-binding protein attenuates glucocorticoid-mediated suppression of cancer immunosurveillance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- ACBP/DBI Neutralization Stimulates Anticancer Immune Responses by Upregulating Lamin A in T Cells.ImmunoTargets and therapy · 2026Article
- Stress management by benzodiazepines in septic shock and critical illness: mechanistic and clinical evidence supporting alternative sedative strategies.Cell stress · 2026Article
- Article
- Benzodiazepines interfere with the efficacy of pembrolizumab-based cancer immunotherapy. Results of a nationwide cohort study including over 50,000 participants with advanced lung cancer.Oncoimmunology · 2025Article
- ACBP/DBI neutralization for the prevention and treatment of malignant and non-malignant liver diseases.Cell death & disease · 2025Review
- Increased plasma concentrations of acyl-coenzyme A binding protein (ACBP) predict future lung cancer development in smokers at risk of cardiovascular disease.Molecular cancer · 2025Article
- Metabolites as agents and targets for cancer immunotherapy.Nature reviews. Drug discovery · 2025Review
- Neutralization of acyl CoA binding protein (ACBP) for the experimental treatment of osteoarthritis.Cell death and differentiation · 2025Article
- Acyl-CoA-binding protein as a driver of pathological aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Neutralization of acyl coenzyme A binding protein for the experimental prevention and treatment of hepatocellular carcinoma.Cell reports. Medicine · 2025Article
- Review
- Integrative analysis of genetic variability and functional traits in lung adenocarcinoma epithelial cells via single-cell RNA sequencing, GWAS, bayesian deconvolution, and machine learning.Genes & genomics · 2025Article
- Atlas of expression of acyl CoA binding protein/diazepam binding inhibitor (ACBP/DBI) in human and mouse.Cell death & disease · 2025Article
- Article
- The danger theory of immunity revisited.Nature reviews. Immunology · 2024Review
- Correction: Acyl-coenzyme a binding protein (ACBP) - a risk factor for cancer diagnosis and an inhibitor of immunosurveillance.Molecular cancer · 2024Article
- Benzodiazepines compromise the outcome of cancer immunotherapy.Oncoimmunology · 2024Article
- Acyl CoA binding protein (ACBP): an autophagy checkpoint that can be targeted for improving cancer immunosurveillance.Oncoimmunology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
34 authors.
Funding
Abstract
backgroundThe plasma concentrations of acyl coenzyme A binding protein (ACBP, also known as diazepam-binding inhibitor, DBI, or 'endozepine') increase with age and obesity, two parameters that are also amongst the most important risk factors for cancer.
methodsWe measured ACBP/DBI in the plasma from cancer-free individuals, high-risk patients like the carriers of TP53 or BRCA1/2 mutations, and non-syndromic healthy subjects who later developed cancer. In mice, the neutralization of ACBP/DBI was used in models of non-small cell lung cancer (NSCLC) and breast cancer development and as a combination treatment with chemoimmunotherapy (chemotherapy + PD-1 blockade) in the context of NSCLC and sarcomas. The anticancer T cell response upon ACBP/DBI neutralization was characterized by flow cytometry and single-cell RNA sequencing.
resultsCirculating levels of ACBP/DBI were higher in patients with genetic cancer predisposition (BRCA1/2 or TP53 germline mutations) than in matched controls. In non-syndromic cases, high ACBP/DBI levels were predictive of future cancer development, and especially elevated in patients who later developed lung cancer. In preclinical models, ACBP/DBI neutralization slowed down breast cancer and NSCLC development and enhanced the efficacy of chemoimmunotherapy in NSCLC and sarcoma models. When combined with chemoimmunotherapy, the neutralizing monoclonal antibody against ACBP/DBI reduced the frequency of regulatory T cells in the tumor bed, modulated the immune checkpoint profile, and increased activation markers.
conclusionThese findings suggest that ACBP/DBI acts as an endogenous immune suppressor. We conclude that elevation of ACBP/DBI constitutes a risk factor for the development of cancer and that ACBP/DBI is an actionable target for improving cancer immunosurveillance.
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