Molecular pathology and clinical characteristics play a crucial role in guiding treatment selection and predicting the prognosis of diffuse large B-cell lymphoma (DLBCL). The programmed cell death protein 1 (PD-1) and its ligand (PD-L1), have emerged as pivotal regulators of immune checkpoints in cancer. The objectives of this study are to investigate the correlation between the expression levels of PD-1 and soluble PD-L1 (sPD-L1) in the peripheral blood of DLBCL patients, analyze their clinicopathological characteristics, and identify the optimal beneficiary group for PD-1/PD-L1 blockade. Peripheral blood samples were collected from 36 DLBCL patients before their initial treatment at Shandong Cancer Hospital between December 2018 and July 2019. The expression levels of PD-1 and sPD-L1 were measured using flow cytometry and enzyme-linked immunosorbent assay (ELISA), respectively. The clinicopathological characteristics, including age, sex, Ann Arbor stage, International Prognostic Index (IPI) score, response to treatment, etc., were recorded for each patient. The surface expression of PD-1 on peripheral blood T cells was significantly higher in DLBCL patients compared to healthy controls. There was a significant association between elevated PD-1 expression levels and the advanced Ann Arbor stage (P=0.0153) as well as the B group (P=0.0184). Higher sPD-L1 levels were associated with the GCB subtype according to Hanss classification (P=0.0435). The expression levels of PD-1 and sPD-L1 in the peripheral blood of DLBCL patients are significantly correlated with advanced disease stage, B group, and GCB subtype according to Hanss classification. This suggests that the PD-1/PD-L1 axis play a critical role in specific subgroups of DLBCL. Targeting this axis could serve as a potential therapeutic strategy to enhance the clinical outcomes of DLBCL patients. Further studies are necessary to explore the prognostic implications of PD-1 and sPD-L1 expression levels in DLBCL patients.

The solute carrier family 2 member 1 (SLC2A1), which encodes glucose transporter 1 (GLUT1), has long been recognized as a key driver of aerobic glycolysis in cancer. However, accumulating evidence has substantially expanded this view, revealing that GLUT1 functions not only as a critical mediator of metabolic reprogramming but also as an important regulator linking tumor metabolism to immune evasion. Notably, GLUT1 expression, regulation, and functional dependence are highly context-dependent across tumor types, disease states, and cellular compartments. Recent studies further link GLUT1-dependent glycolytic flux to immune regulation through glucose competition, lactate accumulation, and metabolite-dependent epigenetic programs within the tumor microenvironment. Reflecting this evolving understanding, therapeutic strategies targeting GLUT1 have progressed from simple metabolic inhibition to approaches that exploit tumor-specific metabolic dependencies and extend to regulated cell death, combination therapy, precision delivery, and selective modulation of malignant and non-malignant cellular compartments. These advances support a shift from expression-centered targeting toward strategies guided by functional GLUT1 dependence and cellular context, while recognizing the metabolic and physiological constraints that shape the therapeutic window. In this review, we systematically summarize recent advances in GLUT1 expression heterogeneity, multilayered regulatory networks, metabolic–immune crosstalk, diagnostic and prognostic relevance, and therapeutic targeting, and discuss how these insights may refine biomarker development, patient selection, and the clinical translation of GLUT1-directed precision metabolic therapy.