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Sep 2026

Abstract A107: Multi-Omic Single-cell Sequencing Reveals KMT2D Loss Activates AP-1-Driven Enhancer Reprogramming to Promote Epithelial-to-Mesenchymal Plasticity in Pancreatic Cancer

KMT2D, a histone H3K4 methyltransferase and critical epigenetic regulator, is mutated in approximately 11% of pancreatic ductal adenocarcinoma (PDAC) cases. Prior work from our group demonstrated that KMT2D loss drives epithelial-to-mesenchymal plasticity (EMP) and tumor progression in PDAC; however, the downstre...

Raghunath Ranga Sudharshan, H. Kim, Heizel Acosta et al. · 0 citations
Sep 2026

Abstract B076: Tumor cell-intrinsic KMT2D loss regulates T cell function through FN1 signaling in pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest malignancies and is characterized by a profoundly immunosuppressive tumor microenvironment (TME) that limits the efficacy of current therapies. KMT2D (Mll4 in mice) is a histone H3K4 methyltransferase and critical epigenetic regulator that is altere...

Heizel Acosta, R. Sudharshan, Hongsun C. Kim et al. · 0 citations
Open access Jul 2026

Epigenetic Tumor Suppressor KMT2D Shapes the Immune Landscape in Pancreatic Cancer 2335260

KMT2D plays a pivotal role in orchestrating both tumor-intrinsic and microenvironmental processes that drive pancreatic cancer progression, and understanding how KMT2D loss reprograms the immune landscape may uncover novel immunomodulatory therapeutic targets for pancreatic cancer.

H. Acosta-Vilanova, H. Kim, Shungang Zhang et al. · 0 citations

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