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Faculty Profile Last Modified Time: 12:16:11 PM Wed, 18 Jul 2018   Contact Information Xiaodong Cheng Associated Profiles  Professor, Epigenetics and Molecular Carcinogenesis, UT MD Anderson Cancer Center   Mitchell Basic Sciences Research Building, Room No.: S9.8336    xcheng5@mdanderson.org     713.834.6274    Web Link    Lab Webpage    Methyltransferases, DNA, Methylation, DNA Methylation, Histones, Lysine, Cytosine, Proteins    Associated Profiles Professional Preparation Research and Expertise Affiliations Appointments  Professional Preparation  Degree Major Institution Year  PhD Protein Crystallography State University of New York at Stony Brook 1989  BS Physics Fudan University 1982  Research and Expertise Research Interests   My current primary research interests are: 1. How are the patterns of mammalian epigenetic DNA modifications generated, recognized and erased, and 2. What are the associated histone modifications, and how are they generated, recognized and erased? In mammalian DNA, cytosine exists in at least five chemical forms: unmodified (C), 5-methylated (5mC), 5-hydroxymethylated (5hmC), 5-formylated (5fC), and 5-carboxylated (5caC). These five forms exhibit base-pairing and protein-coding, but differ in their interactions with transcription factors and strongly influence gene expression. DNA methyltransferases convert specific cytosines to 5mC, and a subset of the 5mC residues is then converted to 5hmC, 5fC, and 5caC consecutively by ten-eleven translocation (Tet) dioxygenases. Mammalian DNA methylation is intricately connected to histone modifications, such as the methylation status of lysine 4 in histone H3 (H3K4). Cancer is associated with an altered 'epigenome', with widespread changes in DNA and histone modifications reprogramming gene expression and affecting genome stability. Many epigenetic regulators, including the DNA modifiers (DNMT3A, TET2), histone modifiers (EZH2, MLL1/2/3) or demodifiers (UTX, JARID1), undergo mutation or are misexpressed in human cancers. This raises the possibility that epigenetic dysregulation is causally associated with the development and progression of the disease. As a result, there is great interest in targeting epigenetic regulators by small molecule inhibitors with the goal of returning the cancer epigenome to a normal state.  Publications/Creative Works Click here to search for this faculty member's publications on PubMed.  Affiliations  Research Consortia GCC Cluster for Cellular and Molecular Biophysics  Training Grants Training in Precision Environmental Health Sciences (TPEHS) Houston Area Molecular Biophysics Training Program  Appointments Title Department / School Institution Professor Molecular & Cellular Oncology MD Anderson Cancer Center

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