Research, Research Resources and Publications
Taking a basic science research approach to understanding cancer
Research in the Department of Epigenetics and Molecular Carcinogenesis (EMC) aims to define the mechanisms that control normal cell proliferation, differentiation, survival, and genome maintenance to identify the aberrations in these processes that drive cancer. EMC research focus areas include: Cellular and Molecular Mechanisms of Carcinogenesis; Cancer Genetics and Epigenetics; Genome Integrity - DNA Replication, Recombination and Repair; and Cancer Stem Cells, Apoptosis and Autophagy. EMC hosts research laboratories and research resources on both the North and South MD Anderson campuses in Houston, Texas.
Research
Cellular and Molecular Mechanisms of Carcinogenesis
The overall goal of our carcinogenesis research is to understand the basic cellular and molecular mechanisms that allow the transformation of normal cells into cancer cells. Defining these mechanisms will help identify new cancer targets and novel strategies for identifying, treating, and preventing cancer.
Departmental carcinogenesis research includes:
- Discovering new genetic contributors and drivers of cancers
- Identifying genetic and/or therapeutic vulnerabilities in cancers (e.g. CRISPR screens identifying synthetic lethality)
- Defining genetic, epigenetic, immunologic, and transcriptional alterations accompanying cancer initiation and progression
- Investigating cell signaling pathways involved in cancer induction and progression
Developing novel computational approaches for cancer research
Enormous amounts of data have been generated from high-throughput, genome-wide experimental approaches, thus creating a pressing need for novel computational approaches to mine and interpret complex "-omics" data sets. Understanding these data sets will help define both the players in biological interaction networks and their functions. Research in the department is combining in-silico approaches with wet-lab experiments to identify drivers and attenuators of cancer. Likewise, the development of CRISPR technology has led to new high-throughput approaches such as genome-wide synthetic lethal screens that also benefit from computational approaches, like those being developed in the department to aid the design and interpretation of high-throughput screens.
Implementing cutting-edge animal models?
Our research relies on the development of genetically engineered animal models for investigating the stepwise molecular changes that occur during carcinogenesis, the function of key genes and gene variants in cancer development, and preclinical prevention and therapeutic studies. A number of existing models are being used for these mechanistic studies, including models for skin, mammary gland, prostate, thymus and blood cancers, but we are also creating novel mouse models using modern knockout/knock-in technologies (e.g. CRISPR-Cas9) to study specific genes and pathways involved in cancer induction and progression.?
Making discoveries at the intersection of immunology and tumor biology
Immunotherapy has been hailed as the fourth pillar of cancer therapy joining surgery, chemotherapy, and radiation treatment. Yet, this treatment approach does not work for all patients. Collaborative departmental research has revealed that patients who respond to immunotherapy have antibody responses against their tumors and that the presence of B cells within a tumor may serve as a marker to predict patient immunotherapy response. These findings are leading to new questions about how B cells in tumors affect immunotherapy response.
Examples of faculty members who are defining the Cellular and Molecular Mechanisms of Carcinogenesis:
¡ª Role of WWOX in cancer and disease; genomic determinants controlling development and progression of pre-invasive breast lesions
Shawn Bratton ¡ª Autophagy and prostate cancer; caspase-activating complexes
Charles Ishak ¡ª Repetitive DNA elements and viral mimicry in tumorigenesis and cancer therapy
Kevin McBride ¡ª B cell function and antibody repertoire; B cell lymphoma; role of B cells in immunotherapy response
¡ª Regulation of thymus development and homeostasis; role of thymic epithelial cells in regulating T-cell development and T-cell receptor repertoire selection
Margarida Almeida Santos ¡ª Tumor promoting roles of genome guardians in leukemia
Angela Ting ¡ª Role of microbiome-expressed genes in altering host DNA to drive cancer
Richard Wood ¡ª Role of DNA polymerase theta in genome stability
Han Xu ¡ª Global view of transcriptional and epigenetic regulation using CRISPR screens; machine-learning and statistical algorithms for high-throughput experiments
Cancer Genetics & Epigenetics
Epigenetic factors that regulate DNA methylation, histone modification and chromatin organization can act as either oncogenes or tumor suppressors. Departmental epigenetics research seeks to define both the normal functions of these factors as well as their roles in cancer formation or suppression.
Readers, Writers and Erasers of Epigenetic Marks
Epigenetic marks include cytosine methylation and hydroxymethylation of DNA and methylation, acetylation, phosphorylation, and ubiquitination of histones. These marks are created by enzymes called "writers." Epigenetic "readers" are effector proteins that bear domains that recognize the specific marks left by the "writers," and epigenetic "erasers" can remove these marks. Thus, multiple epigenomes can be created from a single genome.
Uncovering how epigenetic changes and mutations in epigenetic proteins alter gene expression
The major outcome of epigenetic change is alterations in gene expression. Some epigenetic changes are required for normal development and stem cell differentiation, whereas others are aberrant and can lead to diseases, including immunodeficiency, centromeric region instability and facial anomalies syndrome (ICF) and leukemia and other cancers. Importantly, many epigenetic proteins are mutated in human disease, and epigenetic alterations may be just as important as DNA mutations in driving cancer. In addition to controlling gene transcription, these chromatin-modifying enzymes regulate other processes that require access to DNA, including DNA replication and repair.
Departmental epigenetic research areas include:
- Uncovering epigenetic factors controlling developmental reprogramming
- Discovering biological roles of histone and non-histone lysine and arginine methylation
- Defining the structure and function of epigenetic proteins and epigenetic marks
- Finding new cellular functions for ATP-dependent chromatin remodelers
- Identifying and characterizing ¡°readers¡± of epigenetic marks
- Understanding the role of histone modifications in DNA repair
- Deciphering crosstalk between: histone modifications; histone modifications and DNA methylation; and histone modifications and post-translational modifications of non-histone substrates
- Developing technical and computational tools for genome-wide DNA methylation assessment
- Defining the functions of DNA methylases and DNA methylation in both normal development and cancer
- Understanding the role of DNA methylation-regulated alternative polyadenylation in human health and disease
- Defining the contributions of repetitive DNA elements and viral mimicry to cancer initiation and progression and patient therapy response
Epigenetics research provides new avenues for cancer treatment
Epimutations, unlike genetic mutations, can be reversed by chemotherapeutic intervention, which makes epigenetic therapy conceptually appealing. Researchers in the department are screening and identifying small-molecule regulators of epigenetic modifiers and evaluating their potential as anti-cancer drugs, providing clear translational relevance to this research.
Making foundational protein arginine methyltransferase inhibitor discoveries
EMC department members worked with Experimental Radiation Oncology to show that the protein arginine methyltransferase CARM1 might be a useful therapeutic target for small cell lung cancer (SCLC) by demonstrating that both CARM1 and its target nuclear factor I B (NFIB) are required for the rapid onset of cancer in a preclinical SCLC model. Further, they showed that CARM1 inhibition combined with etoposide and cisplatin (EP - the current standard of care treatment) led to partial tumor regression in SCLC patient-derived xenograft models, which was superior to that of either CARM1 inhibition or EP alone.
In another example, departmental researchers combined their expertise to use cell culture experiments, computational approaches evaluating cancer cell line RNAi screens, and animal xenograft models to show that small molecule inhibition of CARM1 in CREBBP/EP300-mutated diffuse large B-cell lymphomas (DLBCLs) reduces histone acetyltransferase activity and causes synthetic lethality through downregulation of CBP-target genes. This synthetic interaction reveals the possibility that combination therapy using CARM1 inhibitors with CBP/p300 inhibitors may be useful for treating DLBCLs and other cancers with non-mutated CREBBP/EP300.
Examples of faculty engaged in epigenetics research:
Blaine Bartholomew ¡ª ATP-dependent chromatin remodelers influence on chromatin dynamics and non-coding RNA transcription
Mark Bedford ¡ª Arginine methylation in cellular processes; development of technologies to identify readers of proteins bearing specific epigenetic marks
Taiping Chen ¡ª Biological function of histone methylases and demethylases in development and disease
Xiaodong Cheng ¡ª Structure and function of readers, writers, and erasers of DNA modifications and their associated histone modifications
Francesca Cole ¡ª Epigenetic regulation of meiotic chromosome organization & pairing
Charles Ishak ¡ª DNA repetitive elements in cancer initiation, development and therapeutic response
Margarida Almeida Santos ¡ª Epigenetic regulators affecting hematopoietic stem cells
Angela Ting ¡ª Defining novel, clinically relevant functions for DNA methylation and the mechanics of DNA methylation in cancer
DNA Replication, Recombination & Repair - Genomic Stability
Understanding how DNA is damaged and repaired is fundamental to cancer research
DNA breaks can result from molecularly programmed, intentional DNA damage or non-programmed, incidental DNA damage. Intentional breaks results from specialized cellular processes such as those needed for accurate segregation of chromosomes during meiosis and for creating immune system diversity. In contrast, incidental DNA damage results from exposure to DNA damaging agents from both external and internal sources. External sources include ultraviolet radiation from the sun and chemicals in the environment. Internal sources include reactive chemical species, such as oxygen and water as well as accidental DNA breaks formed during DNA replication. Moreover, many cancer therapies induce irreparable DNA damage leading to cell death. Therefore, investigating how cells respond to and repair DNA damage is important for understanding the causes of cancer and developing new treatments. Research in this area employs a broad range of approaches including protein biochemistry, single-cell genomics, high-resolution microscopy, and genetically engineered mouse models.
Departmental research related to genomic stability includes:
- Defining molecular mechanisms of DNA double-strand break repair
- Discovering new DNA repair pathways and proteins
- Defining the functions of DNA polymerases in DNA repair
- Characterizing DNA damage and repair processes in normal cell function and in carcinogenesis
- Learning how DNA damage and repair contribute to immune system diversity
- Unraveling the relationships between DNA damage, chromatin remodeling and DNA repair
- Understanding how DNA methylation influences DNA mutation and repair
When DNA damage causes cells to go awry
Department investigators are studying the protein machinery involved in several DNA repair pathways, including homologous recombination and DNA end-joining processes for the repair of DNA double-strand breaks, and nucleotide excision repair for the repair of ultraviolet radiation-induced DNA damage and other strand-distorting lesions.
First mammalian HR precursors identified
EMC members uncovered the first evidence of homologous recombination (HR) precursors in mammals. Through molecular and cellular characterizations of >1 million haploid genome equivalents from 13 independent mouse single and double mutant conditions, two distinct recombination precursors were identified that form during mouse meiosis including a double Holliday junction (dHJ) that requires the MutL homolog MLH3, but not its nuclease activity, to form.
Faculty are also uncovering how programmed DNA damage and repair are involved in normal cellular processes, such as meiosis and immune system B cell development, as well as how these normal processes go awry and contribute to cancer and disease.
Other active areas of research include investigations into the actions of DNA polymerases at repair sites, how chromatin-modifying proteins cooperate with the DNA repair machinery to facilitate repair in the context of chromatin, the mechanisms underlying the conversion of DNA damage into the mutations that cause cancer, and the mechanisms that allow cells to tolerate and survive DNA damage.
Examples of faculty members leading the way in DNA Replication, Recombination, and Repair :
Xiaodong Cheng ¡ª Role of DNA methylation in DNA mutation and repair
Francesca Cole ¡ª DSB repair by homologous recombination during meiosis
Kevin McBride ¡ª Role of programmed DNA damage in creating antibody diversity and leading to lymphomagenesis
Margarida Almeida Santos ¡ª DNA damage-induced differentiation of stem-like cancer cells
Richard Wood ¡ª Nucleotide excision repair, DNA crosslink repair, role of polymerases in DNA damage tolerance
Cancer Stem Cells & Programmed Cell Death
Stem cells are undifferentiated cells that are unique in their ability to self-renew to create more stem cells while also being able to create daughter cells that can differentiate into other cell types. Most, if not all, cancerous states reflect inappropriate or incomplete cellular differentiation. Aggressive, therapy resistant cancer cells often resemble stem cells in terms of their transcription profiles and self-renewal capacities. Likewise, unregulated growth, abnormal cell division, and defective apoptotic?cell death pathways are hallmark features of tumors.
The goal of research in this area is to define normal stem cell biology and developmental pathways as well as to define genetic, molecular, and biochemical mechanisms that regulate cell proliferation, apoptosis and autophagy and relate these pathways to carcinogenesis.
Specific research in this area includes:
- Defining pathways that govern stem cell biology and embryo development
- Understanding DNA damage response in cancer stem cells
- Epigenetic modifications in embryonic, adult, and cancer stem cells
- Epigenetic mechanisms in early embryos and germ cells
- Role of caspases in apoptosis
- Apoptosis and autophagy in normal and disease processes
Using stem cells to learn about cancer
Our research using mouse embryonic and adult stem cells has led to several foundational discoveries. For example, research centered on GCN5, a histone acetyltransferase component of the SAGA complex, uncovered a Myc-SAGA axis that is critical for driving stem cells to pluripotency and is essential for the expression of cell-cycle genes driven by MYC overexpression in a mouse model of B cell lymphoma. Studies of SETDB1, a lysine methyltransferase that deposits the repressive H3K9me3 mark, revealed that SETDB1-dependent gene repression is essential for preserving intestinal stem cell identity by modulating the Wnt and Notch signaling pathways. Other research using mouse models of MLL-rearranged acute myeloid leukemia showed that protein arginine methyltransferase 5 (PRMT5) is essential for the initiation and maintenance of MLL-AF9-mediated leukemia and that inhibiting PRMT5 restores normal differentiation to hematopoietic stem cells.
Apoptosis and autophagy: cancer inhibitors and facilitators
Autophagy (self-cannibalism) and apoptosis (programmed cell death) are fundamental cellular processes that provide mechanisms for cell survival (autophagy) and cell death (apoptosis). Autophagy provides cells with means not only to survive cellular stress and to recycle cellular materials and organelles but also to rid themselves of damaged, malformed, or foreign material. Although autophagy helps suppress carcinogenesis, it can also promote tumor progression, metastasis, and cancer therapy resistance. Apoptosis is required for normal organismal development, but also provides a mechanism to stop cells with DNA damage from dividing. Many chemotherapeutics work by causing DNA damage and inducing apoptosis; however, defects in apoptosis contribute to both tumorigenesis and resistance to cancer treatment. Therefore, defining the molecular mechanisms guiding autophagy and apoptosis, and the pathways allowing cross-talk between them, will provide insights into how cells evade and succumb to cancer treatments.
Faculty with research interests in Cancer Stem Cells and Programmed Cell Death:
Blaine Bartholomew ¡ª Chromatin remodelers in pluripotency and development
Shawn Bratton ¡ª Heat shock- and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis; caspase-activating complexes and the apoptosome; structure and function of autophagosomes; role of autophagy in prostate cancer
Taiping Chen ¡ª Epigenetic regulation of embryonic and adult stem cell behavior and function
Margarida Almeida Santos ¡ª Epigenetic regulation of cancer stem cells
EMC Research Resources
Flow Cytometry - EMC
Flow Cytometry-EMC provides cutting-edge resources to dissect the cellular and molecular mechanisms of developmental and disease processes, by aiding researchers in identifying, isolating and quantifying cell types and/or cell subsets, while also offering individualized training on specific instruments and assisting with data analysis and experimental design.
Although Flow Cytometry-EMC focuses on EMC users, non-departmental users may also be accommodated, as time and resources permit.
For microscopy services formerly provided by the Flow Cytometry and Cellular Imaging Core-EMC, please see the Advanced Microscopy Core. Please also see the MD Anderson, CCSG-supported, full-service Flow Cytometry and Cellular Imaging Core Facility, directed by Michael Andreeff, M.D., Ph.D.
Flow Cytometry-EMC, located in South Campus Research Building 4, provides assisted use services (hourly fee) to researchers for analytical flow cytometry on all instruments, including the BD LSR Fortessa, BD FACSAria? Fusion SORP, BD FACSAria? Fusion and BDAccuri C6PlusTM. Assisted cell sorts are also available on the BD FACSAria? Fusion SORP and BD FACSAria? Fusion. Instrument training is mandatory for users wishing to perform unassisted analyses. The fee schedule is listed in . Please contact Pam Whitney (pjwhitney@mdanderson.org) prior to scheduling initial services.
Analytical Flow Cytometry
Flow cytometry is used broadly in cell biological research. Protein expression or specific indicators of cell status can be measured simultaneously for individual cells within a larger, heterogeneous population. Flow Cytometry-EMC provides access to both to advanced instruments and expert staff to meet researcher needs, while specializing in developing complex assays to quantitatively examine cell surface and cytoplasmic antigens, cell cycle, apoptosis, "side populations" and fluorescent transgene expression (e.g. GFP, YFP, RFP and BFP).
Cell Sorting
Flow Cytometry-EMC cell sorting equipment includes a BD FACSAria? Fusion, 17 parameter, high-speed cell sorter for processing of ¡Ü BSL2 samples within a biosafety cabinet and a BD FACSAria? SORP, 18 parameter, high-speed cell sorter. Users can isolate a wide variety of different cell types based on many different combinations of antibody-based stains, fluorescent protein expression, and viability indicators. Cells are detected using BD FACSDiva? software and can be collected from a single heterogeneous sample into 1-4 tubes, simultaneously.
Recent software upgrades allow for index sorting, letting researchers identify the origin of single cells collected from within the population defined by their experimental parameters. The automatic cell-dispensing unit can dispense single cells into 96- or 384-well plates. The sample chamber and collection apparatus are climate controlled and aerosol contained.
Flow Cytometry-EMC also operates a Miltenyi Biotec autoMACS Pro Cell Separator, an immunomagnetic cell separation system that can be used to enrich or deplete a population of cells prior to sorting on one of our BD instruments.
Other Services
- Multi-parameter analysis and sorting
- Full-spectrum analysis of fluorescent proteins
- autoMACSpro available for depletion/enrichment of cell populations prior to flow experiments
- Sorting cells into a variety of tubes and plates including 96- and 384-well plates
- Index sorting allowing identification of which experimental population a particular cell was derived
- Guidance with experimental design
- Consultation and training
First-Time Users and Training
First-time users should contact Pam Whitney (pjwhitney@mdanderson.org) to schedule a consultation before finalizing any experimental plans. This consultation will aid researchers in optimizing their experimental approach, assay design, and fluorescent panels to ensure recovery of meaningful data, and will define user expectations and service costs for the project. Please schedule your appointment at least one week prior to the anticipated date of service to ensure availability of their chosen instrument. Flow personnel can also assist with data analysis using FlowJo software, or they can perform analysis for a specific project, as time permits, for an additional fee.
Instrument training is mandatory for any user who would perform unassisted flow cytometric analyses. Training is provided by Pam Whitney (pjwhitney@mdanderson.org) and requires uninterrupted blocks of time over multiple days. Please note that all users are responsible for archiving their own data. Flow Cytometry-EMC personnel can assist users in learning this practice.
Additional Information and Resources
Sample Preparation
Experimental Samples
- All samples should be at a concentration of 5.0 x 106 cells/ml in appropriate buffer in 12 x 75 FACS tubes or 15 ml conical tubes depending upon instrument.
- Bring additional buffer for concentration adjustments.
- All samples must be filtered before running on the instruments.
Control Samples
- Each experiment must have proper controls. Biological controls for data samples could include isotype controls for antibody staining or stained normal cycling cells for cell cycle analysis.
- The instrument setup requires additional controls: unstained cells and single-stained color controls.
- Contact Pam Whitney (pjwhitney@mdanderson.org) for more information about the requirements for your experiment.
Spectrum Viewer & Laser Configuration Files
Tissue Culture Hints
BD FACSAria?Fusion SORP
The BD FACSAria?Fusion SORP is a 5-laser, 18-parameter, high-speed cell sorter, with automatic cell-dispensing unit, run by platform personnel. This instrument can be used to isolate and capture viable cell subsets or single cells for molecular, genetic and/or functional analyses. This instrument can distinguish many fluorescent proteins, stem cell and side populations, in addition to fluorescent antibody preparations. Cells are detected by digital BD FACSDiva? software and collected into one or as many as four tubes simultaneously from a single sample. The cell-dispensing unit on this instrument can dispense single cells into 96- or 384-well plates. The sample chamber and collection apparatus are climate-controlled and aerosol-contained. A laser configuration file for this instrument may be downloaded here.
BD FACSAria? Fusion
The BD FACSAria? Fusion is a 5-laser, 17-parameter high-speed cell sorter with biosafety cabinet and automatic cell-dispensing unit. It is the primary flow instrument and is run by platform personnel. It can be used to isolate and capture viable cell subsets or single cells for molecular, genetic, and functional analyses. The instrument provides exceptional sensitivity and resolution for optimal multicolor analysis and cell sorting. It allows users to distinguish many fluorescent proteins, fluorescent antibody preparations, and other markers to identify stem cell and side populations. Cells are detected by digital BD FACSDiva? software and collected into one, or as many as four tubes, simultaneously. The automatic cell-dispensing unit deposits single cells into 96- or 384-well plates. The enhanced stream stability increases sorting purity and efficiency to help isolate minor subsets of cells (e.g. stem cells) for subsequent in vitro and in vivo experiments. This instrument is contained in a bio-safety cabinet permitting analysis of human specimens while ensuring user protection. A laser configuration file for this instrument may be downloaded here.
BD LSRFortessa?
The BD LSRFortessa? is a 4-laser, 15-parameter cell analyzer equipped with digital BD FACSDiva? software. It can be used for quantification of cellular subsets based on the expression of surface or intracellular antigens, analysis of apoptosis and cell cycle parameters, and multiparameter analyses. Individualized training on the BD LSRFortessa? for unassisted operation is available. A laser configuration file for this instrument may be downloaded here.
Miltenyi autoMACS? Pro Separator
The autoMACS? Pro Separator by Miltenyi is an automated high-speed immunomagnetic cell separation system that can process multiple samples at a time. Many cell and tissue types, including whole blood, can be processed with the use of immunomagnetic beads. Cells can be separated using positive selection, depletion, or untouched isolation programs. It can sort more than 10 million cells per second from samples of up to 4¡Á109 total cells. The system reduces manual sample handling and increases reproducibility.
BD Accuri C6Plus? Cell Analyzer
The newest Flow Cytometry-EMC instrument is a compact, easy-to-use, BD Accuri C6PlusTM 2 laser, 4-parameter cell analyzer. It is optimized for fluorchromes such as FITC, PE, PerCP-Cy?5.5, APC, and BD Horizon Brilliant? Blue 515 and can analyze fluorescent proteins such as GFP, YFP, and mCherry.
Bioinformatics and Biostatistics Services - EMC
Bioinformatics
EMC Bioinformatics faculty members work collaboratively with investigators to provide novel computational methods, tools and algorithms for the advancement of cancer disease research. Our bioinformatics faculty engage in collaborative research in the areas of bioinformatics, statistical genetics and systems biology to retrieve and analyze various kinds of biological data including DNA/RNA sequences, protein sequences and structures, microarray data and RT-PCR data for the purpose of facilitating biological discovery. Special emphasis is placed on next-generation sequencing data analysis.
Biostatistics
Biostatistics services are augmented with additional support from faculty in the Quantitative Sciences division. Many modern research projects generate data sets that require statistical analyses. Biostatistics staff members provide expertise for such projects and can aid in early project conception, helping develop a fully elaborated study design, and aiding with data collection and analysis. Early statistical planning and incorporating power calculations into study design can help researchers implement more cost-effective projects by helping determine the appropriate size and scope of a study as well as aiding with approaches for more meaningful data collection and analysis.
Research Areas & Projects
- Developing working relationships with MD Anderson research faculty and external collaborators to expand the use of advanced computational techniques and statistical analyses, especially as related to next-generation sequencing (e.g. RNA-Seq, DNA-Seq, ChIP-Seq) and DNA methylation analysis
- Providing guidance to faculty, students and coworkers in the use of specialized applications, programming, computation and statistical analysis techniques for interpretation of biological data
- Conducting computational biology and bioinformatics/biostatistics seminars and workshops for researchers and students
- Co-developing or contributing to grant proposals with research faculty, professional colleagues and external collaborators to apply advanced computing and related bioinformatics research to the study of human cancers and disease
- Maintaining awareness of emerging computational technologies and new statistical methods, especially to work with large data sets
Recombinant Antibody Creation and Production Platform
The McBride Lab hosts the Recombinant Antibody Production and Creation Platform (RAPCP). The platform is used to develop custom, recombinant, monoclonal antibodies using a propriety method for isolating single-antigen-specific plasma cells, following inoculation into mice.
Curated antibody-encoding genes are cloned into expression vectors for recombinant antibody production and purification. The antibodies can then be tested in collaboration with the end-user, using a number of assays based on user priorities. The process results in sequence-defined, recombinant antibodies in as few as 30-90 days. For more information, please see the McBride Lab Research page.
Epigenomics Profiling Core (EpiCore)
The Epigenomics Profiling Core (EpiCore) is an institutional resource for epigenomics research that brings scientific expertise, advanced assays, and specialized equipment not otherwise readily available to MD Anderson Cancer Center researchers. The core offers cost-effective, full-service protocols to investigate DNA methylation (Pyrosequencing Methylation Analysis, RRBS, cfMeDIP-seq, WGBS), chromatin accessibility (ATAC-Seq), and DNA-protein interactions (ChIP-Seq and CUT&RUN). This core facilitates researchers¡¯ efforts to define epigenetic mechanisms that alter chromatin and regulate transcription in normal and disease conditions. To learn more, please see the Epigenomics Profiling Core website.
Advanced Microscopy Core (AMC)
The Advanced Microscopy Core enables any number of studies including those centered on cellular protein distribution, cell fate, tumor heterogeneity, drug delivery and tumoricidal activity, DNA damage repair, development, neurodegeneration, cell migration/invasion, angiogenesis and cancer-stroma interactions. Staff can guide users through tissue fixation, permeabilization, vibratome sectioning, and tissue clearing to optimize specific imaging needs and develop pilot applications for investigators. Staff will assist in selecting the optimal instrument, fuorophores, and fluorophore combinations for a user¡¯s particular study, as well as helping users apply image processing software, such as the IMARIS 4-D Image Analysis and Tracking software, for their downstream analyses.
Please see the Advanced Microscopy Core website for more information.
AMC Instruments include:
- DeltaVision OMX Blaze V4 Super-Resolution Microscope
- Leica TCS SP8 Confocal Microscope with Environmental Chamber
- Zeiss LSM880 Confocal Microscope with Airyscan
- Leica SP8 DIVE Multiphoton (2-Photon) Microscope
- Zeiss Gaussian Lightsheet 7 (LS7) Microscope
- LifeCanvas SmartSPIM Lightsheet Microscope
- Zeiss Axio Observer Z1
- INCell Analyzer 6500 HS Slide/Plate Scanner
Selected Publications
2025
Ishak CA, Marhon SA, Tchrakian N, Hodgson A, Loo Yau H, Gonzaga IM, Peralta M, Lungu IM, Gomez S, Liang SB, Shen SY, Chen R, Chen J, Chatterjee B, Wanniarachchi KN, Lee J, Zehrbach N, Hosseini A, Mehdipour P, Sun S, Solovyov A, Ettayebi I, Francis KE, He A, Wu T, Feng S, da Silva Medina T, Campos de Almeida F, Bayani J, Li J, MacDonald S, Wang Y, Garcia SS, Arthofer E, Diab N, Srivastava A, Austin PT, Sabatini PJB, Greenbaum BD, O'Brien CA, Shepherd TG, Tsao MS, Chiappinelli KB, Oza AM, Clarke BA, Rottapel R, Lheureux S, De Carvalho DD. Cancer Discov. 2025 Jan 7. doi: 10.1158/2159-8290.CD-24-0094. Online ahead of print. PMID: 39776167
2024
Carvajal-Maldonado D, Li Y, Returan M, Averill AM, Doubli¨¦ S, Wood RD. J Biol Chem. 2024 Jul;300(7):107461.
Chen YC, Bhaskara GB, Lu Y, Lin K, Dent SYR. Genes Dev. 2024 Sep 19;38(15-16):738-754.
Deogharia M, Venegas-Zamora L, Agrawal A, Shi M, Jain AK, McHugh KJ, Altamirano F, Marian AJ, Gurha P. Cardiovasc Res. 2024 May 7;120(6):630-643.
Du Z, Lin M, Li Q, Guo D, Xue Y, Liu W, Shi H, Chen T, Dan J. J Cell Physiol. 2024 Sep;239(9):e31337.
Fijen C, Drogalis Beckham L, Terino D, Li Y, Ramsden DA, Wood RD, Doubli¨¦ S, Rothenberg E. Mol Cell. 2024 Apr 18;84(8):1460-1474.e6.
Hardikar S, Ren R, Ying Z, Zhou J, Horton JR, Bramble MD, Liu B, Lu Y, Liu B, Coletta LD, Shen J, Dan J, Zhang X, Cheng X, Chen T. Sci Adv. 2024 Aug 23;10(34):eadr0036.
Hogan CH, Owens SM, Reynoso GV, Liao Y, Meyer TJ, Zelazowska MA, Liu B, Li X, Grosskopf AK, Khairallah C, Kirillov V, Reich NC, Sheridan BS, McBride KM, Gewurz BE, Hickman HD, Forrest JC, Krug LT. mBio. 2024 Feb 14;15(2):e0299823.
Kuang X, Salinger A, Benavides F, Muller WJ, Dent SYR*, Koutelou E*. PLoS One. 2024 Jan 18;19(1):e0290837. (*Co-corresponding authors)
Larouche JD, Laumont CM, Trofimov A, Vincent K, Hesnard L, Brochu S, C?t¨¦ C, Humeau JF, Bonneil ?, Lanoix J, Durette C, Gendron P, Laverdure JP, Richie ER, Lemieux S, Thibault P, Perreault C. Elife. 2024 Apr 18;12:RP91037.
Lee J, Chatterjee B, Oh N, Saha D, Lu Y, Bartholomew B, Ishak CA. J Vis Exp. 2024 Dec 13;(214). doi: 10.3791/67359.PMID: 39760380
Malone CF, Mabe NW, Forman AB, Alexe G, Engel KL, Chen YC, Soeung M, Salhotra S, Basanthakumar A, Liu B, Dent SYR, Stegmaier K. Sci Adv. 2024 May 31;10(22):eadm9449.
Marshall VA, Cornejo Castro EM, Goodman CA, Labo N, Liu I, Fisher NC, Moore KN, Nair A, Immonen T, Keele BF, Polizzotto MN, Uldrick TS, Mu Y, Saswat T, Krug LT, McBride KM, Lurain K, Ramaswami R, Yarchoan R, Whitby D. PLoS Pathog. 2024 Jul 15;20(7):e1012338.
Mise K, Long J, Galvan DL, Ye Z, Fan G, Sharma R, Serysheva II, Moore TI, Jeter CR, Anna Zal M, Araki M, Wada J, Schumacker PT, Chang BH, Danesh FR. Nat Commun. 2024 Mar 4;15(1):1965.
Patel B, Zhou Y, Babcock RL, Ma F, Zal MA, Kumar D, Medik YB, Kahn LM, Pineda JE, Park EM, Schneider SM, Tang X, Raso MG, Jeter CR, Zal T, Clise-Dwyer K, Keyomarsi K, Giancotti FG, Colla S, Watowich SS.. Leukemia. 2024 May;38(5):1143-1155.
Pourebrahim R, Montoya RH, Akiyama H, Ostermann L, Khazaei S, Muftuoglu M, Baran N, Zhao R, Lesluyes T, Liu B, Khoury JD, Gagea M, Van Loo P, Andreeff M. Cell Rep Med. 2024 May 21;5(5):101558.
Saha D, Animireddy S, Bartholomew B. Biochem Soc Trans. 2024 Apr 24;52(2):603-616.
Saha D, Animireddy S, Lee J, Thommen A, Murvin MM, Lu Y, Calabrese JM, Bartholomew B. Mol Cell. 2024 May 16;84(10):1855-1869.e5.
Sarkar S, Stitzlein LM, Chandra J. Pediatr Med. 2024 Feb 28;7:3. doi: 10.21037/pm-23-43.
Shanley M, Daher M, Dou J, Li S, Basar R, Rafei H, Dede M, Gumin J, Pantale?n Garc?a J, Nunez Cortes AK, He S, Jones CM, Acharya S, Fowlkes NW, Xiong D, Singh S, Shaim H, Hicks SC, Liu B, Jain A, Zaman MF, Miao Q, Li Y, Uprety N, Liu E, Muniz-Feliciano L, Deyter GM, Mohanty V, Zhang P, Evans SE, Shpall EJ, Lang FF, Chen K, Rezvani K. Cancer Cell. 2024 Aug 12;42(8):1450-1466.e11.
Sharma M, Barravecchia I, Teis R, Cruz J, Mumby R, Ziemke EK, Espinoza CE, Krishnamoorthy V, Magnuson B, Ljungman M, Koschmann C, Chandra J, Whitehead CE, Sebolt-Leopold JS, Galban S. Mol Cancer Ther. 2024 Jan 3;23(1):24-34.
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2023
Beilinson HA, Sevilleja A, Spring J, Benavides F, Beilinson V, Neokosmidis N, Golovkina T. J Virol. 2023 Aug 31;97(8):e0068523.
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2022
Basu S, Dong Y, Kumar R, Jeter C, Tang DG. Semin Cancer Biol. 2022 Jan;78:90-103.
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Fedoriw A#, Shi L#, O'Brien S, Smitheman KN, Wang Y, Hou J, Sherk C, Rajapurkar S, Laraio J, Williams LJ, Xu C, Han G, Feng Q, Bedford MT, Wang L, Barbash O, Kruger RG, Hwu P, Mohammad HP, Peng W. . Cancer Immunol Res. 2022 Apr 1;10(4):420-436. (#equal contribution)
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Horton JR, Pathuri S, Wong K, Ren R, Rueda L, Fosbenner DT, Heerding DA, McCabe MT, Pappalardi MB, Zhang X, King BW, Cheng X. . Structure. 2022 Jun 2;30(6):793-802.e5.
Huang P, Peslak SA, Ren R, Khandros E, Qin K, Keller CA, Giardine B, Bell HW, Lan X, Sharma M, Horton JR, Abdulmalik O, Chou ST, Shi J, Crossley M, Hardison RC, Cheng X, Blobel GA. . Nat Genet. 2022 Sep;54(9):1417-1426
Huang YH, Chen CW, Sundaramurthy V, S?abicki M, Hao D, Watson CJ, Tovy A, Reyes JM, Dakhova O, Crovetti BR, Galonska C, Lee M, Brunetti L, Zhou Y, Tatton-Brown K, Huang Y, Cheng X, Meissner A, Valk PJM, Van Maldergem L, Sanders MA, Blundell JR, Li W, Ebert BL, Goodell MA. Cancer Discov. 2022 Jan;12(1):220-235.
Iannelli G, Milite C, Marechal N, Cura V, Bonnefond L, Troffer-Charlier N, Feoli A, Rescigno D, Wang Y, Cipriano A, Viviano M, Bedford MT, Cavarelli J, Castellano S, Sbardella G. . J Med Chem. 2022 Apr 28. doi: 10.1021/acs.jmedchem.2c00252.
Kannan S, Irwin ME, Herbrich SM, Cheng T, Patterson LL, Aitken MJL, Bhalla K, You MJ, Konopleva M, Zweidler-McKay PA, Chandra J. . Antioxidants (Basel). 2022 Apr 5;11(4):717.
Khan FI, Rehman T, Sameena F, Hussain T*, AlAjmi MF, Lai D, Khan MKA. . J Mol Recognit. 2022 Jul;35(7):e2958. (*postdoctoral fellow with C.M. Aldaz)
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Koutelou E, Dent SYR. . Nat Cell Biol. 2022 Apr;24(4):412-414. (News & Views article)
Lancaster JN, Keatinge-Clay DE, Srinivasan J, Li Y, Selden HJ, Nam S, Richie ER, Ehrlich LIR. . Aging Cell. 2022 Jun;21(6):e13624. PMID: 35561351
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Liu Y, Iqbal A, Li W, Ni Z, Wang Y, Ramprasad J, Abraham KJ, Zhang M, Zhao DY, Qin S, Loppnau P, Jiang H, Guo X, Brown PJ, Zhen X, Xu G, Mekhail K, Ji X, Bedford MT, Greenblatt JF, Min J. . Nat Commun. 2022 Sep 16;13(1):5453.
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Miglioranza Scavuzzi B, van Drongelen V, Kaur B, Fox JC, Liu J, Mesquita-Ferrari RA, Kahlenberg JM, Farkash EA, Benavides F, Miller FW, Sawalha AH, Holoshitz J. . Commun Biol. 2022 Jul 28;5(1):751.
Moyret-Lalle C, Prodhomme MK*, Burlet D, Kashiwagi A, Petrilli V, Puisieux A, Seimiya H, Tissier A. Role of EMT in the DNA damage response, double-strand break repair pathway choice and its implications in cancer treatment. Cancer Sci. 2022 May 9. doi: 10.1111/cas.15389. (*Prodhomme is a postdoc in the Wood lab)
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Wood RD, Doubli¨¦ S. Annu Rev Genet. 2022 Nov 30;56:207-228.
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2021
Abba MC, Fabre ML, Lee J, Tatineni P, Kil H, Aldaz CM. . Front Oncol. 2021 Nov 17;11:783211.
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Carvajal-Maldonado D, Wood RD. . Cancer Res. 2021 Mar 15;81(6):1441-1442.
Chen J, Horton J, Sagum C, Zhou J, Cheng X, Bedford MT. Biochem J. 2021 May 28;478(10):1943-1958.
Chen LM, Chai JC, Liu B, Strutt TM, McKinstry KK, Chai KX. . Biosci Rep. 2021 Jul 30;41(7):BSR20211370.
Cheng T, Kiser K, Grasse L, Iles L, Bartholomeusz G, Samaniego F, Orlowski RZ, Chandra J. . Cancer Drug Resist. 2021;4(4):888-902.
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DiNardo CD, Beird HC, Estecio M, Hardikar S, Takahashi K, Bannon SA, Borthakur G, Jabbour E, Gumbs C, Khoury JD, Routbort M, Gong T, Kondo K, Kantarjian H, Garcia-Manero G, Chen T, Futreal PA. . Epigenetics. 2021 May;16(5):567-576.
Genois MM, Gagn¨¦ JP, Yasuhara T, Jackson J, Saxena S, Langelier MF, Ahel I, Bedford MT, Pascal JM, Vindigni A, Poirier GG, Zou L. . Mol Cell. 2021 Feb 18;81(4):784-800.e8
He W, Wang H, Wei Y, Jiang Z, Tang Y, Chen Y, Xu H. . Bioinformatics. 2021 Jan 4:btaa1068.
Hu X, Estecio MR, Chen R, Reuben A, Wang L, Fujimoto J, Carrot-Zhang J, McGranahan N, Ying L, Fukuoka J, Chow CW, Pham HHN, Godoy MCB, Carter BW, Behrens C, Zhang J, Antonoff MB, Sepesi B, Lu Y, Pass HI, Kadara H, Scheet P, Vaporciyan AA, Heymach JV, Wistuba II, Lee JJ, Futreal PA, Su D, Issa JJ, Zhang J. . Nat Commun. 2021 Jan 29;12(1):687.
Jung YS, Stratton SA, Lee SH, Kim MJ, Jun S, Zhang J, Zheng B, Cervantes CL, Cha JH, Barton MC, Park JI. TMEM9-v-ATPase Activates Wnt/¦Â-Catenin Signaling via APC Lysosomal Degradation for Liver Regeneration and Tumorigenesis. Hepatology. 2021 Feb;73(2):776-794.
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Lan X, Ren R, Feng R, Ly LC, Lan Y, Zhang Z, Aboreden N, Qin K, Horton JR, Grevet JD, Mayuranathan T, Abdulmalik O, Keller CA, Giardine B, Hardison RC, Crossley M, Weiss MJ, Cheng X, Shi J, Blobel GA. . Mol Cell. 2021 Jan 21;81(2):239-254.e8.
Llorens-Agost M, Ensminger M, Le HP, Gawai A, Liu J, Cruz-Garc¨ªa A, Bhetawal S, Wood RD, Heyer WD, L?brich M. . Nat Cell Biol. 2021 Oct;23(10):1095-1104.
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Muradova E, Patel N, Sell B, Bittencourt BB, Ojeda SS, Adelmann CH, Cen L, Cheng CH, Shen J, Davis CM, Ehli EA, Newberg JY, Cherpelis B, Black MA, Mann MB, Mitragotri S, Tsai KY. . J Invest Dermatol. 2021 Jan;141(1):124-131.e2.
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2020
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Turner OC, Aeffner F, Bangari DS, High W, Knight B, Forest T, Cossic B, Himmel LE, Rudmann DG, Bawa B, Muthuswamy A, Aina OH, Edmondson EF, Saravanan C, Brown DL, Sing T, Sebastian MM. . Toxicol Pathol. 2020 Feb;48(2):277-294.
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2019
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2018
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2017
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2009-2016
2016
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2015
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2014
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2013
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2012
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2011
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2010
Alexander A, Cai SL, Kim J, Nanez A, Sahin M, MacLean KH, Inoki K, Guan KL, Shen J, Person MD, Kusewitt D, Mills GB, Kastan MB, Walker CL (2010) . Proc Natl Acad Sci U S A.107:4153-8.
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Kim D, Lee J, Cheng D, Li J, Carter C, Richie E, Bedford MT. (2010) . J Biol Chem. 285(2):1147-52
Guo R, Chen J, Zhu F, Biswas AK, Berton TR, Mitchell DL, Johnson DG (2010) . J Biol Chem. 285:19308-15.
Mitchell DL, Fernandez AA, Nairn RS, Garcia R, Paniker L, Trono D, Thames HD, Gimenez-Conti I (2010) . Proc Natl Acad Sci U S A. 107(20):9329-34.
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2009
Abba MC, Hu Y, Levy CC, Gaddis S, Kittrell FS, Hill J, Bissonnette RP, Brown PH, Medina D, Aldaz CM. (2009) . Cancer Prev Res (Phila). 2(2):175-84.
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Chen X, Schneider-Broussard R, Hollowell D, McArthur M, Jeter CR, Benavides F, DiGiovanni J, Tang DG. (2009) . Differentiation. 77(3):324-34.
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Griffith AV, Cardenas K, Carter C, Gordon J, Iberg A, Engleka K, Epstein JA, Manley NR, Richie ER (2009) . Dev Biol. 327(1):216-27.
Jeter CR, Badeaux M, Choy G, Chandra D, Patrawala L, Liu C, Calhoun-Davis T, Zaehres H, Daley GQ, Tang DG. (2009) . Stem Cells. 2009 May;27(5):993-1005.
Kim DJ, Kataoka K, Sano S, Connolly K, Kiguchi K, DiGiovanni J. (2009) . Mol Carcinog. 48(10):873-85.
Kuang X, Scofield VL, Yan M, Stoica G, Liu N, Wong PK. (2009) Brain Res. 1286:174-84.
Liu B, Zhu F, Xia X, Park E, Hu Y. (2009) Cell Cycle. 8(4):527-31.
Liu Y, Nairn RS, Vasquez KM. (2009) Nucleic Acids Res. 37(19):6378-88.
Ludes-Meyers JH, Kil H, Parker-Thornburg J, Kusewitt DF, Bedford MT, Aldaz CM. (2009) PLoS One. 4(11):e7775.
Repass JF, Laurent MN, Carter C, Reizis B, Bedford MT, Cardenas K, Narang P, Coles M, Richie ER. (2009) Genesis. 47(4):281-7.
Scofield VL, Yan M, Kuang X, Kim SJ, Crunk D, Wong PK. (2009) Immunol Lett. 122(2):159-69.
Shirley SH, Rundhaug JE, Tian J, Cullinan-Ammann N, Lambertz I, Conti CJ, Fuchs-Young R. (2009) s. Cancer Res. 69(8):3405-14.
Zhao J, Jain A, Iyer RR, Modrich PL, Vasquez KM. (2009) . DNA Repair (Amst). ;8(7):865-72.