Poster Session 1.D - Pathological and Oncological Sciences
Varga, Viktória
SE Department of Pathology and Experimental Cancer Research
Viktória Varga1, Dorottya Moldvai1, Zsófia Gábriel1, Fatime Szalai1, Ildikó Krencz1, Ágnes Márk1, Gábor Barna2, Daniella Kuzmanovszki3, Beáta Kun3, Péter Holló3, Anna Sebestyén2
1: SE Department of Pathology and Experimental Cancer Research
2: Semmelweis University, Department of Pathology and Experimental Cancaer Research
3: Semmelweis University, Department of Dermatology, Venereology and Dermatooncology
CD36 is a multifunctional lipid receptor that promotes tumor progression by enhancing fatty acid uptake, driving metabolic reprogramming, and supporting cancer cell stemness and metastasis. CD36 expression on CD8⁺ T cells within the tumor microenvironment has been shown to promote lipid peroxidation and induce ferroptotic cell death, thereby impairing effector antitumor immunity.
Our aim was to investigate alterations in peripheral CD36⁺ T cells before and during immune checkpoint inhibitor (ICI) therapy in patients with advanced melanoma and to evaluate their associations with oncological and clinical parameters. In a prospective clinical cohort, serial peripheral blood samples were collected before and during the ICI therapy and analyzed by multiparametric flow cytometry, including the following markers: CD3, CD4, CD8, CD36, KLRG1, PD-1, CD56, CD16, CD57, and CD28. The results were compared with data from a healthy control group.
Based on our small cohort (n=24 melanoma patients, n=15 healthy controls), median CD36 expression on T and NK cells showed considerable inter-individual variability. In melanoma patients, the proportion of CD36⁺ T cells (median 19%, IQR 9–56) was higher than in healthy controls (median 14%, IQR 5–29). According to changes in median CD36 expression during immune checkpoint inhibitor therapy, patients could be stratified into two main patterns: 54% demonstrated a marked increase in T-cell CD36 expression (from median 16%, IQR 5–26, to 21%, IQR 14–56), while 34% exhibited elevated baseline levels that declined substantially under treatment (from median 39%, IQR 27–45, to 15%, IQR 8–33); in the remaining 12% of patients, CD36⁺ T-cell frequencies remained essentially unchanged. The processing and correlation of the clinical data are currently underway.
These observations suggest that ICI therapy elicits dynamic, coordinated changes in CD36 expression on T cells, with patient-specific response patterns. The concordant modulation of CD36 across these lymphocyte subsets suggests that CD36 may represent a promising biomarker of immunotherapy-induced immune cell remodeling and supports further investigation into its relevance to treatment response and resistance.
Supported by NKFIH-142799, Semmelweis250+, TKP2021-EGA-24, SE250+