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Kong, Nikki

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Kong

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Kong, Nikki

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2015 - 201912020 - 20211

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Author's Publications: search.filters.isAuthorOfPublication.1b931b50-ba41-4e37-894b-ab85743f19c5

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    The next new target in leukemia: The embryonic stem cell gene SALL4
    (2015) Wang, Fei; Zhao, Wenxiu; Kong, Nikki; Cui, Wei; Chai, Li
    The embryonic stem (ES) cell gene SALL4 has recently been identified as a new target for cancer therapy, including leukemia. SALL4 is expressed in ES cells and during embryonic development, but is absent in most adult tissues. It is, however, aberrantly expressed in various solid tumors and hematologic malignancies such as myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Aberrant expression of SALL4 is frequently associated with a more aggressive cancer phenotype, which includes high-risk MDS and its progression to AML. SALL4 contributes to leukemogenesis through multiple pathways including the repression of PTEN and the activation of HOXA9 expression. Targeting the SALL4/PTEN pathway by blocking the protein–protein interaction of SALL4 and its associated epigenetic complex, nucleosome remodeling and deacetylase complex (NuRD), might be a novel approach to treating AML and holds great potential for the treatment of other SALL4-mediated oncogenic processes such as high-risk MDS and solid tumors.
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    Dual DNA and Protein Tagging of Open Chromatin Unveils Dynamics of Epigenomic Landscapes in Leukemia
    (Springer Science and Business Media LLC, 2021-03-01) Lee, Jonathan D.; Paulo, Joao; Posey, Ryan R.; Mugoni, Vera; Kong, Nikki; Cheloni, Giulia; Lee, Yu-Ru; Slack, Frank; Tenen, Daniel; Clohessy, John; Gygi, Steven; Pandolfi, Pier Paolo
    The architecture of chromatin specifies eukaryotic cell identity by controlling transcription factor access to sites of gene regulation. Here we describe a dual transposase/peroxidase approach, integrative DNA And Protein Tagging (iDAPT), which detects both DNA (iDAPT-seq) and protein (iDAPT-MS) associated with accessible regions of chromatin. In addition to direct identification of bound transcription factors, iDAPT enables the inference of their gene regulatory networks, protein interactors, and regulation of chromatin accessibility. We applied iDAPT to profile the epigenomic consequences of granulocytic differentiation of acute promyelocytic leukemia, yielding previously undescribed mechanistic insights with potential therapeutic implications. Our findings demonstrate the power of iDAPT as a discovery platform for both the dynamic epigenomic landscapes and their transcription factor components associated with biological phenomena and disease.