Yu-Jui Ho

Senescence-directed nanotherapy ameliorates fibrosis and overcomes immune exclusion in cancer

P-selectin-targeted fucoidan nanoparticles carrying Navitoclax or dBET6 deplete a senescent-like, lipid-associated macrophage subset, reverse mouse liver and lung fibrosis with less toxicity, and restore checkpoint therapy response in fibrotic tumors.

Epigenetic Reactivation of Lineage Differentiation to Target Leukemia

This study identifies TRIM28 as a critical regulator in acute leukemia, showing its depletion promotes neutrophil differentiation and reduces leukemic potential, with a small-molecule inhibitor developed to target it.

Oncogenic and tumor-suppressive forces converge on a progenitor niche at the benign-to-malignant transition

In mouse pancreatic cancer models, p53, CDKN2A and SMAD4 programs converge on a rare Kras-mutant progenitor-like state whose niche KRAS inhibition collapses and p53 loss expands.

An immunocompetent murine model of virus-elicited liver fibrosis and hepatocellular carcinoma

This study develops an immunocompetent mouse model of virus-induced liver fibrosis and hepatocellular carcinoma using Norway rat hepacivirus.

Harnessing the Embryo Antitumor Factor NEPN for Broad-Spectrum Cancer Immunotherapy via Dual Modulation of Tumor Progression and Immune Suppression

This study identifies NEPN as a tumor-suppressive embryonic factor that enhances cancer immunotherapy by modulating TGFβ1 signaling and immune responses in both non-solid and solid tumors.

MYC and p53 alterations cooperate through VEGF signaling to repress cytotoxic T cell and immunotherapy responses in prostate cancer

This study shows that MYC and p53 alterations in prostate cancer cooperate via VEGF signaling to suppress T cell activity and immunotherapy responses, and that targeting VEGFR2 can enhance immunotherapy efficacy.

Stromal KITL/SCF promotes pancreas tissue homeostasis and restrains tumor progression

The paper identifies loss of stromal KITL as a mechanism promoting tumor progression in the pancreas by disrupting tissue homeostasis.

Mutant IDH uncouples p53 from target gene regulation to disable tumor suppression

This paper shows that mutant IDH disrupts p53 target gene regulation by altering chromatin states, disabling tumor suppression, and that this effect can be reversed with IDH inhibition.

SAKE (Single-cell RNA-Seq Analysis and Klustering Evaluation) Identifies Markers of Resistance to Targeted BRAF Inhibitors in Melanoma Cell Populations

SAKE identifies markers of resistance to BRAF inhibitors in melanoma cells by analyzing scRNA-Seq data from multiple platforms.