Rui Li

This study identifies mitosis as a critical window for ecDNA hub organization in cancer cells and shows WEE1 regulates hub integrity and oncogene expression.

The paper shows ecDNA localizes to the nuclear periphery in cancer, resisting silencing and enhancing transcriptional output through interactions with the nuclear lamina.

This study uses somatic mutations to track marrow-derived cell infiltration into the human brain, finding widespread microglia replenishment and a protective link between clonal hematopoiesis and Alzheimer's disease.

This study shows ecDNA copy number plasticity drives tumour evolution by generating functional heterogeneity and promoting drug resistance.

The paper identifies enhancer-like elements on ecDNA in colorectal cancer that are derived from transposable elements and are functionally active in cancer cell fitness.

The paper shows that ecDNA-borne PVT1 fusions stabilize oncogenic mRNAs by interacting with SRSF1, enhancing RNA stability and supporting MYC dependency in cancer.

This paper identifies transcription-replication conflict as a vulnerability in ecDNA-containing cancers and demonstrates that CHK1 inhibition selectively kills these tumors.

This study identifies a STAG2-PAXIP1/PAGR1 tumor-suppressive axis in lung cancer by showing their combined role in suppressing oncogenic KRAS-driven tumorigenesis.

The paper investigates the evolution of chromosome 4p loss in basal breast cancer, identifying C4orf19 as a novel gene that suppresses proliferation and is part of a kinase module.

This study shows that Xist ribonucleoprotein complexes drive sex-biased autoimmunity in males, leading to autoimmune pathology and reprogramming of immune cells to resemble female patterns.

The paper uses a single-cell multiome atlas of the human retina and deep learning to identify causal noncoding variants in eye diseases.

This study shows XIST is required in adult human B cells to silence X-linked immune genes and identifies TRIM28 as a B cell-specific XIST cofactor involved in X-inactivation and atypical B cell formation.

The paper demonstrates that the XIST RNA-protein complex has a modular architecture that determines RBP binding and m6A modification, beyond sequence motifs.

This study shows Spen binds to endogenous retroviral RNAs and recruits chromatin silencing machinery, linking RNA-mediated retrovirus silencing to X chromosome inactivation.

The paper identifies TFAP2C and p63 as key regulators of epidermal lineage commitment and shows TFAP2C initiates differentiation while p63 drives maturation through chromatin dynamics.

This paper uses HiChIP to map enhancer-promoter interactions in primary human cells, linking disease-associated DNA variants to their target genes.