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Liling Wan, PhD
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Assistant Professor of Cancer Biology
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Department: Cancer Biology
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Graduate Group Affiliations
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Contact information
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751 BRB II/III
3b 421 Curie Boulevard
Philadelphia, PA 19104-6160
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3b 421 Curie Boulevard
Philadelphia, PA 19104-6160
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Office: (215)-898-3116
34 Fax: (215)-573-6725
34 Lab: (215)-898-3698
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34 Fax: (215)-573-6725
34 Lab: (215)-898-3698
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Education:
21 9 B.S. 32 (Biological Sciences and Biotechnology) c
3c Tsinghua University, Beijing, China, 2008.
21 8 PhD 1e (Molecular Biology) c
3c Princeton University, Princeton, NJ, 2014.
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21 9 B.S. 32 (Biological Sciences and Biotechnology) c
3c Tsinghua University, Beijing, China, 2008.
21 8 PhD 1e (Molecular Biology) c
3c Princeton University, Princeton, NJ, 2014.
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Links
58 Wan Lab Website
6f Penn Epigenetics Institute
68 Institute for Regenerative Medicine
37 Department of Cancer Biology
2b Abramson Family Cancer Research Institute
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Permanent link58 Wan Lab Website
6f Penn Epigenetics Institute
68 Institute for Regenerative Medicine
37 Department of Cancer Biology
2b Abramson Family Cancer Research Institute
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69 The research interests in the Wan Lab lie in the intersection of cancer biology and epigenetics.
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11 Keywords:
a5 cancer, epigenetics, genome organization, histone modifications, transcriptional condensates, cell fate plasticity, Leukemia, Kidney development, metastasis.
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19 Research Details:
335 Chromatin - the complex of DNA and histone proteins - is the physiological template of the eukaryotic genome through which transcription factors, signaling pathways, and other internal and external cues alter gene activity and cellular phenotypes. Cancer genome studies have shown that at least 40% of human cancers harbor mutations in genes encoding chromatin-associated factors, highlighting the widespread impact of chromatin misregulation in cancer. Our research focuses on understanding chromatin function and its dysregulation in human cancer, particularly in exploring how these mechanisms regulate cellular fate transitions and plasticity that promote tumorigenic potential. In addition to our basic mechanistic discoveries, we are also committed to leveraging this knowledge for therapeutic development.
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1fe Our lab currently pursues several key areas of research: (1) Investigating the molecular basis and functional consequences of cancer-associated mutations in chromatin regulators; (2) Decoding the regulation and function of chromatin-associated transcriptional condensates; (3) Examining how epigenomic reprogramming influences transcriptional and cellular plasticity to affect cancer behaviors such as metastasis; and (4) Characterizing drugs targeting newly identified epigenetic mechanisms in cancer.
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1c Research techniques:
a2 We use a host of different approaches including mouse models of disease, genome-wide sequencing, advanced imaging, functional genomics, and biochemistry.
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1a Rotation Projects:
6f Rotation projects are available in each area of interest in the lab. Please contact Dr. Wan for details.
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Description of Research Expertise
24 Research Interests:69 The research interests in the Wan Lab lie in the intersection of cancer biology and epigenetics.
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11 Keywords:
a5 cancer, epigenetics, genome organization, histone modifications, transcriptional condensates, cell fate plasticity, Leukemia, Kidney development, metastasis.
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19 Research Details:
335 Chromatin - the complex of DNA and histone proteins - is the physiological template of the eukaryotic genome through which transcription factors, signaling pathways, and other internal and external cues alter gene activity and cellular phenotypes. Cancer genome studies have shown that at least 40% of human cancers harbor mutations in genes encoding chromatin-associated factors, highlighting the widespread impact of chromatin misregulation in cancer. Our research focuses on understanding chromatin function and its dysregulation in human cancer, particularly in exploring how these mechanisms regulate cellular fate transitions and plasticity that promote tumorigenic potential. In addition to our basic mechanistic discoveries, we are also committed to leveraging this knowledge for therapeutic development.
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1fe Our lab currently pursues several key areas of research: (1) Investigating the molecular basis and functional consequences of cancer-associated mutations in chromatin regulators; (2) Decoding the regulation and function of chromatin-associated transcriptional condensates; (3) Examining how epigenomic reprogramming influences transcriptional and cellular plasticity to affect cancer behaviors such as metastasis; and (4) Characterizing drugs targeting newly identified epigenetic mechanisms in cancer.
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1c Research techniques:
a2 We use a host of different approaches including mouse models of disease, genome-wide sequencing, advanced imaging, functional genomics, and biochemistry.
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1a Rotation Projects:
6f Rotation projects are available in each area of interest in the lab. Please contact Dr. Wan for details.
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13f Song L, Li Q, Xia L, Sahay A, Qiu Q, Li Y, Li H, Sasaki K, Susztak K, Wu H, Wan L: Single-Cell multiomics reveals ENL mutation perturbs kidney developmental trajectory by rewiring gene regulatory landscape. Nature Communications 15(1), July 2024.
8c Mathias KM, Liu Y, Wan L: Dysregulation of transcriptional condensates in human disease: 8e mechanisms, biological functions, and open questions. Current Opinion in Genetics & Development 86(102203), June 2024.
197 Wang X*, Fan D*, Liu Y*, Han Q*, Miao H, Wang X, Li Q, Chen D, Gore H, Himadewi P, Pfeifer G, Cierpicki T, Grembecka J, Su J#, Chong S#, Wan L#, Zhang X# (*co-first; #co-corresponding): Mutant NPM1 hijacks transcriptional hub to maintain pathogenic gene programs in acute myeloid leukemia. Cancer Discovery 13(2): 724-745, March 2023.
177 Song L*, Yao X*, Li H, Peng B, Boka AP, Liu Y, Chen G, Liu Z, Mathias KM, Xia L, Li Q, Mir M, Li Y#, Li H#, Wan L# (*co-first; #co-corresponding): Hotspot mutations in the structured ENL YEATS domain link aberrant transcriptional condensates and cancer. Molecular Cell 82(21): 4080-4098, November 2022.
21c Liu Y, Li H, Alikarami F, Barrett DR, Khan TA, Michino M, Hill C, Mahdavi L, Song L, Tang S, Yang L, Li Y, Pokharel SP, Li Q, Stamford AW, Liverton N, Renzetti LM, Taylor S, Watt GF, Ladduwahetty T, Kargman S, Meinke PT, Foley MA, Shi J, Li H, Chen CW, Gardini A, Huggins DJ, Bernt KM#, Wan L# (#co-corresponding): Small-molecule inhibition of the acyl-lysine reader ENL as a strategy against acute myeloid leukemia. Cancer Discovery 12(11): 2684-2709, November 2022.
197 Wan L#, Chong S, Fan X, Liang A, Cui X, Gates L, Carroll TS, Li Y, Feng L, Chen G, Wang S, Ortiz MV, Daley S, Wang X, Xuan H, Kentsis A, Muir TW, Roeder RG, Li H, Li W, Tjian R, Wen H#, Allis CD# (#co-corresponding): Impaired Cell Fate through Gain-of-function Mutations in a Chromatin Reader. Nature 577(7788): 121-126, January 2020.
17c Wan L*, Wen H*, Li Y*, Lyu J, Xi Y, Hoshii T, Joseph JK, Wang X, Loh YE, Erb MA, Souza AL, Bradner JE, Shen L, Li W, Li H#, Allis CD#, Armstrong SA#, Shi X# (*co-first; #co-senior): ENL Links Histone Acetylation to Oncogenic Gene Expression in Acute Myeloid Leukemias. Nature 543(7644): 265-269, March 2017.
199 Wan L, Lu X, Yuan S, Wei Y, Guo F, Shen M, Yuan M, Chakrabarti R, Hua Y, Smith HA, Blanco MA, Chekmareva M, Wu H, Bronson RT, Haffty BG, Xing Y, Kang Y: MTDH-SND1 Interaction is Crucial for Expansion and Activity of Tumor-Initiating Cells in Diverse Oncogene- and Carcinogen-Induced Mammary Tumors. Cancer Cell 26(1): 92-105, July 2014.
139 Guo F*, Wan L*, Zheng A, Stanevich V, Wei Y, Satyshur KA, Shen M, Lee W, Kang Y#, Xing Y# (*co-first; #co-senior): Structural Insights into the Tumor-Promoting Function of the MTDH-SND1 Complex. Cell Reports 8(6): 1704-1713, September 2014.
12c Wan L, Hu G, Wei Y, Yuan M, Bronson RT, Yang Q, Siddiqui J, Pienta KJ, Kang Y: Genetic Ablation of Metadherin Inhibits Autochthonous Prostate Cancer Progression and Metastasis. Cancer Research 74(18): 5336-5347, September 2014.
d5 Wan L, Pantel K, Kang Y: Tumor Metastasis: Moving New Biological Insights into the Clinic. Nature Medicine 19(11): 1450-1464, November 2013.
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Selected Publications
17f Liu Y, Li Q, Song L, Gong C, Tang S, Budinich KA, Vanderbeck A, Mathias KM, Wertheim GB, Nguyen SC, Outen R, Joyce EF, Maillard I, Wan L.: Condensate-promoting ENL mutation drives tumorigenesis in vivo through dynamic regulation of histone modifications and gene expression. Cancer Discovery 14(8), April 2024.13f Song L, Li Q, Xia L, Sahay A, Qiu Q, Li Y, Li H, Sasaki K, Susztak K, Wu H, Wan L: Single-Cell multiomics reveals ENL mutation perturbs kidney developmental trajectory by rewiring gene regulatory landscape. Nature Communications 15(1), July 2024.
8c Mathias KM, Liu Y, Wan L: Dysregulation of transcriptional condensates in human disease: 8e mechanisms, biological functions, and open questions. Current Opinion in Genetics & Development 86(102203), June 2024.
197 Wang X*, Fan D*, Liu Y*, Han Q*, Miao H, Wang X, Li Q, Chen D, Gore H, Himadewi P, Pfeifer G, Cierpicki T, Grembecka J, Su J#, Chong S#, Wan L#, Zhang X# (*co-first; #co-corresponding): Mutant NPM1 hijacks transcriptional hub to maintain pathogenic gene programs in acute myeloid leukemia. Cancer Discovery 13(2): 724-745, March 2023.
177 Song L*, Yao X*, Li H, Peng B, Boka AP, Liu Y, Chen G, Liu Z, Mathias KM, Xia L, Li Q, Mir M, Li Y#, Li H#, Wan L# (*co-first; #co-corresponding): Hotspot mutations in the structured ENL YEATS domain link aberrant transcriptional condensates and cancer. Molecular Cell 82(21): 4080-4098, November 2022.
21c Liu Y, Li H, Alikarami F, Barrett DR, Khan TA, Michino M, Hill C, Mahdavi L, Song L, Tang S, Yang L, Li Y, Pokharel SP, Li Q, Stamford AW, Liverton N, Renzetti LM, Taylor S, Watt GF, Ladduwahetty T, Kargman S, Meinke PT, Foley MA, Shi J, Li H, Chen CW, Gardini A, Huggins DJ, Bernt KM#, Wan L# (#co-corresponding): Small-molecule inhibition of the acyl-lysine reader ENL as a strategy against acute myeloid leukemia. Cancer Discovery 12(11): 2684-2709, November 2022.
197 Wan L#, Chong S, Fan X, Liang A, Cui X, Gates L, Carroll TS, Li Y, Feng L, Chen G, Wang S, Ortiz MV, Daley S, Wang X, Xuan H, Kentsis A, Muir TW, Roeder RG, Li H, Li W, Tjian R, Wen H#, Allis CD# (#co-corresponding): Impaired Cell Fate through Gain-of-function Mutations in a Chromatin Reader. Nature 577(7788): 121-126, January 2020.
17c Wan L*, Wen H*, Li Y*, Lyu J, Xi Y, Hoshii T, Joseph JK, Wang X, Loh YE, Erb MA, Souza AL, Bradner JE, Shen L, Li W, Li H#, Allis CD#, Armstrong SA#, Shi X# (*co-first; #co-senior): ENL Links Histone Acetylation to Oncogenic Gene Expression in Acute Myeloid Leukemias. Nature 543(7644): 265-269, March 2017.
199 Wan L, Lu X, Yuan S, Wei Y, Guo F, Shen M, Yuan M, Chakrabarti R, Hua Y, Smith HA, Blanco MA, Chekmareva M, Wu H, Bronson RT, Haffty BG, Xing Y, Kang Y: MTDH-SND1 Interaction is Crucial for Expansion and Activity of Tumor-Initiating Cells in Diverse Oncogene- and Carcinogen-Induced Mammary Tumors. Cancer Cell 26(1): 92-105, July 2014.
139 Guo F*, Wan L*, Zheng A, Stanevich V, Wei Y, Satyshur KA, Shen M, Lee W, Kang Y#, Xing Y# (*co-first; #co-senior): Structural Insights into the Tumor-Promoting Function of the MTDH-SND1 Complex. Cell Reports 8(6): 1704-1713, September 2014.
12c Wan L, Hu G, Wei Y, Yuan M, Bronson RT, Yang Q, Siddiqui J, Pienta KJ, Kang Y: Genetic Ablation of Metadherin Inhibits Autochthonous Prostate Cancer Progression and Metastasis. Cancer Research 74(18): 5336-5347, September 2014.
d5 Wan L, Pantel K, Kang Y: Tumor Metastasis: Moving New Biological Insights into the Clinic. Nature Medicine 19(11): 1450-1464, November 2013.
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