Jianmin Wang

This study quantifies cancer stemness in prostate cancer across progression stages, showing its association with therapy resistance, poor survival, and lineage plasticity.

This study identifies sex-associated epigenetic and transcriptional programs in muscle-invasive bladder cancer, showing distinct DNA methylation and gene expression patterns between males and females, with conservation in a mouse model.

This paper investigates why oncogenic mutations often fail to induce cancer by showing that normal cells undergo a transient, plastic state but are constrained by lineage-specific barriers preventing stable transformation.

The paper investigates how two alleles of the CHRFAM7A gene, through divergent cytoskeletal evolution, lead to distinct brain organization and potential susceptibility to neuropsychiatric diseases.

This study shows RB1 loss in EGFR mutant lung cancer leads to reversible lineage plasticity, accelerating resistance to EGFR TKI therapy through non-genetic mechanisms.

This study shows that EZH2 influences the evolution of aggressive prostate cancer subtypes but is not essential for neuroendocrine prostate cancer development.

This study identifies a Th1/Th17 imbalance driven by IFN{gamma} that causes cytokine release syndrome and neutropenia in CAR-T therapy, suggesting IFN{gamma} blockade as a potential treatment.

The paper compares the cellular response to DNA damage and chromatin damage using bleomycin and curaxin, finding distinct p53-dependent and -independent effects.

This study shows that FACT is essential for maintaining chromatin integrity during transcription in mammalian adult stem cells, and its loss leads to lethality due to stem cell failure.

This study shows that mitochondrial hypoxia induces APOBEC3G-mediated RNA editing in lymphocytes, leading to metabolic changes and reduced proliferation.

The paper shows that chromatin destabilizing drugs like curaxin induce an interferon response (TRAIN) through repeat transcription, independent of p53 status, and may prevent cancer by eliminating epigenetically unstable cells.