What type of study is this?

This is a Cohort Study study (also classified as: Experimental Study).

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September 20, 2025

Abstract PR014: ARID4B induces immune escape in high-grade serous ovarian cancer by upregulating B3GNT5-mediated glycosphingolipid synthesis

Key Points

ARID4B expression is linked to shorter survival in high-grade serous ovarian cancer and drives immune evasion.
Loss of ARID4B reduces tumor formation in immunocompetent mice, indicating an immune-dependent mechanism at play.
ARID4B directly binds to B3GNT5, leading to increased glycosphingolipid synthesis that impairs CD8+ T cell functions.
Inhibition of glycosphingolipid synthesis shows synergistic effects with immune checkpoint blockade, enhancing immunotherapy.

Abstract

Abstract Introduction: Modulating the tumor immune microenvironment in a molecularly defined manner remains a major challenge in cancer immunotherapy. For example, how epigenetic regulators remodel tumor microenvironment to evade immune surveillance remains poorly understood. ARID4B is often overexpressed in high-grade serous ovarian cancer (HGSOC). The current study aims to investigate the mechanism by which ARID4B drives immunosuppressive landscape HGSOC and develop novel therapeutic strategies to overcome the immunosuppressive microenvironment in an ARID4B-dependent manner. Methods: To investigate the effect of ARID4B in HGSOC, we generate ARID4B wild-type/knockout isogeneic cell lines and analyzed transcriptional changes by RNA sequencing and profile ARID4B genome-wide distribution by Cut 2025 Sep 19-21; Denver, CO. Philadelphia (PA): AACR; Cancer Res 2025;85 (18Suppl): Abstract nr PR014.

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