Jonathan D. Licht

The paper identifies a SUN1-ApoD feedback loop that promotes cellular aging through microtubule-nuclear mechanotransduction by inducing aging-related phenotypes in fibroblasts and muscle.

The paper develops selective glucocorticoid receptor modulators (SGRMs) that modulate immune checkpoint function by altering GR activity states through structural design and machine learning.

This study shows that H2B variants, particularly H2B1O, alter chromatin accessibility and induce EMT in breast cancer, suggesting their role as onco-histones and potential therapeutic targets.

This study identifies NF90 as a coactivator of EZH2's polycomb-independent transactivation function in prostate cancer, promoting cell growth and poor clinical outcomes.

This paper develops a genetically engineered mouse model of uveal melanoma that recapitulates human disease progression and immune microenvironment features, revealing phenotypic plasticity and cooperative genetic drivers.

Structure-optimized CD27-based CAR-T cells targeting CD70 show >80-fold improved expansion in vivo and offer a potential therapy for high-risk multiple myeloma patients.

This study identifies GDF15 as a driver of uveal melanoma liver metastasis by reprogramming hepatic stellate cells to promote angiogenesis and matrix deposition.

This study shows that H2B variants alter chromatin structure and oncogenic gene expression, suggesting they may be early cancer biomarkers and therapeutic targets.

This study shows KDM6A regulates immune response genes in multiple myeloma by activating NLRC5 and CIITA, and its loss reduces MHC expression, which can be reversed by HDAC3 inhibitors.

This study shows that HIRA-mediated H3.3 incorporation at enhancers regulates androgen receptor (AR) and BRD4 complex assembly, affecting transcription in prostate cancer.