ArticleBiochemistry and biophysics reports2025
Soluble CTLA-4 and high-risk genetic variants: A new frontier in pancreatic ductal adenocarcinoma (PDAC) biomarkers.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- IL-6 as a central driver of immune evasion in PDAC: from IDO-mediated tolerance to multi-pathway immunosuppression.Frontiers in immunology · 2026Review
- Soluble CTLA-4 as a context-dependent immune checkpoint: biology, biomarker potential, and therapeutic implications.Frontiers in immunology · 2026Review
- Integrating CTLA-4 Genetics and Soluble Isoforms for the Stratification of HCV-Related Hepatocellular Carcinoma Risk and Aggressiveness.International journal of molecular sciences · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: CTLA-4 is regarded as the "leader" of immune checkpoint inhibitors, as it suppresses autoreactive T cells at the initial phase of naïve T-cell activation. Its genetic variability may impair its effectiveness in the anti-tumor response. Additionally, the presence of soluble CTLA-4 (sCTLA-4) in the tumor microenvironment suppresses effector T-cell activation, allowing for tumor evasion. Therefore, this study aimed to explore the relationship between CTLA-4 polymorphisms and sCTLA-4 and the risk of pancreatic ductal adenocarcinoma (PDAC) in an Egyptian population. Method: Three single-nucleotide polymorphisms of the CTLA-4 gene (rs231726, rs11571317, and rs13384548) were analyzed, and sCTLA-4 levels were assessed in 125 PDAC patients and 125 healthy controls. Results: The rs231726 TT genotype was associated with a six-fold greater risk of PDAC, advanced disease grades, and elevated carbohydrate antigen 19-9 (CA19-9) and carcinoembryonic antigen (CEA). Also, the T-allele increased the likelihood of developing PDAC by four times. Conversely, the CC genotype and C-allele conferred protection against PDAC development. The rs11571317 CC genotype and C-allele elevated the PDAC risk by 4.91 and 3.49-fold, respectively, with no relationship to disease severity. The rs13384548 polymorphism showed no significant association with PDAC susceptibility. sCTLA-4 correlated positively with CA19-9 and CEA levels, with the highest levels found in individuals possessing the rs231726 TT genotype and high malignancy grades. Conclusions: These findings highlight the potential of CTLA-4 SNPs and sCTLA-4 as biomarkers for PDAC diagnosis and prognosis. Integrating these biomarkers into screening programs can offer improved strategies for early detection and disease management in high-risk populations.
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.