About

Liling Wan, PhD, is an Assistant Professor of Cancer Biology and an Assistant Investigator at the Abramson Family Cancer Research Institute at the University of Pennsylvania's Perelman School of Medicine. Her research interests lie at the intersection of cancer biology and epigenetics, focusing on understanding chromatin function and its dysregulation in human cancer. Her work explores how mechanisms such as histone modifications, genome organization, and transcriptional condensates regulate cellular fate transitions and plasticity that promote tumorigenic potential. Wan's research aims to decode the molecular basis of cancer-associated mutations in chromatin regulators, examine the regulation and function of chromatin-associated transcriptional condensates, and characterize epigenomic reprogramming's influence on cancer behaviors like metastasis. Her laboratory employs diverse techniques including mouse models, genome-wide sequencing, advanced imaging, functional genomics, and biochemistry to advance basic mechanistic understanding and therapeutic development in cancer epigenetics.

Research topics

• Genetics
• Cancer research
• Biology

Selected publications

• Supplementary Table S5 from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia

  2025-12-11

  articleOpen access

  <p>Supplementary Table S5 shows all the oligos used in this study</p>

  PublisherDOI

• Supplementary Table S3 from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia

  2025-12-11

  articleOpen access

  <p>Supplementary Table S3 shows the differential expressed genes in NPM1c-koncked in HOXB8 cell lines vs parental cells</p>

  PublisherDOI

• Editor’s Note: Small-Molecule Inhibition of the Acyl-Lysine Reader ENL as a Strategy against Acute Myeloid Leukemia

  Cancer Discovery · 2025-06-03

  erratumOpen accessSenior author
  PublisherOA PDFDOI

• Supplementary Figure S1-S8 from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia

  2025-12-11

  articleOpen access

  <p>Supplementary Figure S1 is associated with Figure1 and it shows the NPM1-WT binds to the rDNA arrays and NPM1c binds to non-repetitive genomic regions. Supplementary Figure S2 is associated with Figure1 and it shows NPM1c’s chromatin binding and association with gene expression. Supplementary Figure S3 is associated with Figure2 and shows NPM1c regulates the transcription of its target genes with BRU-seq. Supplementary Figure S4 is associated with Figure2 and it shows the characterization of NPM1c condensate with biochemical assay and imaging assay. Supplementary Figure S5 is associated with figure 3. The figure shows NPM1c and chromatin landacpe dymanics during dTag-13 treatment and wash-off. Supplementary Figure S6 is associated with figure 4. It shows the supplemental data of HOXB8-NPM1c-knock-in model. Supplementary figure S7 is associated with figure 5. It shows the supplemental data of XPO1's binding to chromatin in various leukemia cell lines and normal HSPCs. Supplementary Figure S8 is associated with figure 6. It shows the supplemental information of synergy between Menin and XPO1 inhibitor in the NPM1c AML cell line model.</p>

  PublisherDOI

• Supplementary Table S2 from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia

  2025-12-11

  articleOpen access

  <p>Supplementary Table S2 shows the differential expressed genes in dTAG-13 vs DMSO treatment at 24hr in OCI-AML3-NPM1c-degron2 cells.</p>

  PublisherDOI

• Supplementary Table S4 from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia

  2025-12-11

  articleOpen access

  <p>Supplemenary Table S4 shows the differential expressed genes in 25nM Selinexorvs DMSO treatment at 24hr in OCI-AML3-NPM1c-degron2 cells.</p>

  PublisherDOI

• Efficacy and safety of Tanreqing injection in ventilator-associated pneumonia: A systematic review and meta-analysis

  European Journal of Integrative Medicine · 2025-05-01

  reviewSenior authorCorresponding
  PublisherDOI

• Supplementary Table S1 from Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia

  2025-12-11

  articleOpen access

  <p>Supplementary Table S1 shows the high-confident NPM1c binding peaks in OCI-AML3 cells.</p>

  PublisherDOI

• RNA Reinforces Condensate Nucleation on Chromatin To Amplify Oncogenic Transcription

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Supplementary tables S1-S38 from Condensate-Promoting ENL Mutation Drives Tumorigenesis <i>In Vivo</i> Through Dynamic Regulation of Histone Modifications and Gene Expression

  2024-08-02

  supplementary-materialsOpen accessSenior author

  <p>Supplementary Table S1. Genes differentially expressed between Enl-T1 and Enl-WT LSK cells. Supplementary Table S2. Genes differentially expressed between Enl-T1 and Enl-WT GMP cells. Supplementary Table S3. Genes differentially expressed between Enl-T1 and Enl-WT L-GMP cells. Supplementary Table S4. Genes differentially expressed between Enl-T1 and Enl-WT cKit + Mac1+ cells. Supplementary Table S5. Genes differentially expressed between Enl-T1 and Enl-WT cKit-Mac1+ cells. Supplementary Table S6. Shared Enl-T1 up-regulated DEGs in LSK, GMP, and L-GMP cells. Supplementary Table S7. Expression of Hoxa genes in Enl-WT and Enl-T1 hematopoietic populations. Supplementary Table S8. GSEA gene sets used in Supplementary Figure S12. Supplementary Table S9. GSVA score of patients from TARGET-AML database. Supplementary Table S10. H3K27ac peaks in all hematopoietic populations. Supplementary Table S11. H3K27ac differential regions of ENL-T1 versus ENL-WT in LSK cells. Supplementary Table S12. H3K27ac differential regions of ENL-T1 versus ENL-WT in GMP cells. Supplementary Table S13. H3K27ac differential regions of ENL-T1 versus ENL-WT in L-GMP cells. Supplementary Table S14. H3K27ac differential regions of ENL-T1 versus ENL-WT in cKit + Mac1+ cells. Supplementary Table S15. H3K27ac differential regions of ENL-T1 versus ENL-WT in cKit-Mac1+ cells. Supplementary Table S16. T1-UP DEGs associated with H3K27ac T1 gained DRs in all hematopoietic populations. Supplementary Table S17. H3K27ac T1 gained differential regions associated with T1-UP DEGs in all hematopoietic populations. Supplementary Table S18. p300 ChIP-seq normalized signal at T1 gained H3K27ac differential regions in Enl-WT and Enl-T1 GMP, L-GMP cells. Supplementary Table S19. T1 gained H3K27ac differential regions with both p300 UP and associated gene expression UP in Enl-T1 cells for GMP and L-GMP. Supplementary Table S20. T1 gained H3K27ac differential regions with p300 UP and associated gene expression UP in Enl-T1 cells for L-GMP under A-485 treatment. Supplementary Table S21. H3K27me3 peaks in wildtype hematopoietic populations. Supplementary Table S22. Hematopoietic differentiation associated-H3K27me3 peaks. Supplementary Table S23. H3K27me3 peaks in all hematopoietic populations. Supplementary Table S24. H3K27me3 differential regions of ENL-T1 versus ENL-WT in LSK cells. Supplementary Table S25. H3K27me3 differential regions of ENL-T1 versus ENL-WT in GMP cells. Supplementary Table S26. H3K27me3 differential regions of ENL-T1 versus ENL-WT in L-GMP cells. Supplementary Table S27. H3K27me3 differential regions of ENL-T1 versus ENL-WT in cKit + Mac1+ cells. Supplementary Table S28. H3K27me3 differential regions of ENL-T1 versus ENL-WT in cKit-Mac1+ cells. Supplementary Table S29. T1-UP DEGs associated with H3K27me3 lost differential regions in all hematopoietic populations. Supplementary Table S30. Group1 and group2 gene list in cKit + Mac1+ and cKit-Mac1+ cells. Supplementary Table S31. FLAG-ENL peaks in LSK cells expressing the indicated FLAG-ENL transgenes. Supplementary Table S32. FLAG-ENL gained regions of T1 versus WT in LSK cells expressing the indicated FLAG-ENL transgenes. Supplementary Table S33. H3K27ac T1 gained differential regions associated with T1 gained FLAG-ENL DRs in LSK cells expressing the indicated FLAG-ENL transgenes. Supplementary Table S34. Genes differentially expressed between Enl-T1-DMSO and Enl-WT-DMSO LSK cells. Supplementary Table S35. Genes differentially expressed between Enl-T1-DMSO and Enl-WT-DMSO in GMP cells. Supplementary Table S36. Expression of Hoxa genes under Enl-WT-DMSO, Enl-T1-DMSO and Enl-T1-TDI conditions in LSK and GMP cells. Supplementary Table S37. Oligos used in this study. Supplementary Table S38. Antibodies used in this study.</p>

  PublisherDOI

Recent grants

• Illuminating transcriptional condensates using an integrated approach

  NIH · $2.4M · 2021–2026

• Transcriptional control by the epigenetic reader ENL in human cancer

  NIH · $747k · 2020–2023

• Transcriptional control by the epigenetic reader ENL in human cancer

  NIH · $294k · 2018–2020

Frequent coauthors

• Yiman Liu

  Xiamen University

  128 shared

• Lele Song

  Peking University

  74 shared

• Qinglan Li

  Guangdong Pharmaceutical University

  68 shared

• Haitao Li

  Jiangnan University

  58 shared

• Sylvia Tang

  55 shared

• Hangpeng Li

  Cancer Research Institute

  46 shared

• Fatemeh Alikarami‬

  Children's Hospital of Philadelphia

  44 shared

• Peter T. Meinke

  Tri-Institutional Therapeutics Discovery Institute

  43 shared