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3 rd Annual Postdoctoral Science Symposium August 1, 2013 Organized by the MD Anderson Postdoctoral Association Sponsored by MD Anderson Cancer Center.

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Presentation on theme: "3 rd Annual Postdoctoral Science Symposium August 1, 2013 Organized by the MD Anderson Postdoctoral Association Sponsored by MD Anderson Cancer Center."— Presentation transcript:

1 3 rd Annual Postdoctoral Science Symposium August 1, 2013 Organized by the MD Anderson Postdoctoral Association Sponsored by MD Anderson Cancer Center Alumni & Faculty Associations and the Department of Trainee & Alumni Affairs

2 Symposium Agenda August 1Morning Sessions 9:00 – 9:15Welcome Address APSS Organizing Committee 9:15 – 10:15Combinatorial mapping of the human vasculature: towards ligand-directed therapies and imaging agents Renata Pasqualini, Ph.D., Professor, Department of Genitourinary Medical Oncology, MD Anderson Cancer Center 10:15 – 10:35Personalized canine cancer therapy Colleen O’Connor, Ph.D., Postdoctoral Fellow, Department of Pediatrics Research, MD Anderson Cancer Center 10:35 – 10:55Mesenchymal stem cells promote skin invasion and metastasis in inflammatory breast cancer through an EGFR dependent mechanism Lara C. Alvarez de Lacerda, Ph.D., Postdoctoral Fellow, Department of Radiation Oncology, MD Anderson Cancer Center 10:55 – 11:15Integrated analyses identify a master microRNA regulatory network for the mesenchymal subtype in serous ovarian cancer Da Yang, Ph.D. Postdoctoral Fellow, Department of Pathology, MD Anderson Center 11:15 – 12:30Lunch/Poster Session 12:30 – 1:30Breakout SessionsClassroom 1.Reverse Phase Protein Microarrays (RPPA): Yiling Lu, M.D. S1.8331 2.Bioinformatics: Nicholas Navin, Ph.D. Onstead 3.Cytometry by Time-Of-Flight (Cy-TOF): Jared Burks, Ph.D. S3.8003 4.Non-coding RNA: Chang-Gong Liu, Ph.D. S5.8004 5.Small Animal Imaging: James A. Bankson, Ph.D. S5.8005

3 August 1Afternoon Sessions 1:45 – 2:45Oncogenome-selective vulnerabilities in lung adenocarcinoma Michael White, Ph.D., Professor, Department of Cell Biology, UT Southwestern Medical Center 2:45 – 3:05Tobacco-related cancer disparities: the role of health literacy Diana W. Stewart, Ph.D., Instructor Department of Health Disparities Research, MD Anderson Cancer Center 3:05 – 3:25Development of a force assay to monitor the mobility of cancer cells Varun Sreenivasan, Ph.D., Postdoctoral Associate, Department of Otolaryngology, Baylor College of Medicine 3:25 – 3:45Dynamic changes in protein abundance and cell cycle profiles revealed by profiling of human embryonic stem cells during differentiation at the single cell level by mass cytometry Ryan McCarthy, Ph.D. Postdoctoral Fellow, Department of Biochemistry, MD Anderson Cancer Center 3:45 – 4:00Coffee Break 4:00 – 5:00 Keynote Normal and neoplastic stem cells Irving L. Weissman, Professor, Department of Pathology and Developmental Biology, Stanford University 5:00 – 5:05Closing Remarks 5:05 – 6:30Reception

4 Abstracts

5 Buchanan and Seeger Professor of Medicine and Experimental Diagnostic Imaging Department of Genitourinary Medical Oncology MD Anderson Cancer Center Renata Pasqualini, Ph.D. Education: University of São Paulo, BrazilBS1986 University of São Paulo, BrazilPhD1990 The Children’s Hospital Harvard Medical School Postdoc 1991 Dana Farber Cancer InstitutePostdoc1994 The Burnham Institute, La Jolla, CASr. Fellow1996 Notable Honors/Awards: 2006Living Legend Faculty Achievement Award, UTMDACC 2010Marcus Foundation Award, Marcus Foundation 2007The Top 400 Inventors for 99% of patents filed since 1946 2009Potu N. Rao Award for Excellence in Basic Science 2010Distinguished Women in Science, Bio Houston 2011The Lombroso Achievement Award, Weizmann Institute of Science 2012AACR – The Carcinoid Foundation Investigator Award Research Interest: Human Vascular Mapping Project Ligand-directed Targeting, Nanotechnology & Molecular-genetic Imaging Fingerprinting the Repertoire of Patient-derived Antibodies Obesity Reversal through Vascular Targeting Hybridoma and hybridoma-free Generation and Production of Antibodies Email:

6 As a matter of record, Drs. Arap and Pasqualini have a long-standing collaboration and have led a joint laboratory since October 1999. Our research group currently includes Ph.D. or M.D./Ph.D. students, postdoctoral fellows, faculty (assistant and associate professors), research technicians, and administrative staff members. Our central working hypothesis is that differential protein expression in the human vascular endothelium associated with normal or diseased tissues offers the potential for developing novel diagnostic, imaging, and therapeutic strategies. In essence, our research program uses combinatorial library selection (peptide- and antibody-based) to discover, validate, and exploit the vascular biochemical diversity of endothelial cell surfaces that can be subsequently exploited towards a new vascular-targeted pharmacology. Such targeting technologies may lead to the development of ligand-directed, clinically applicable agents for the treatment of cancer patients. Translational applications, such as first-in-man clinical trials, which have now started within MDACC, will ultimately determine the value of this strategy. Indeed, the Food and Drug Administration (FDA) granted “safe-to-proceed” status for our first vascular-targeted IND in 2009. A first-in-human study has already been completed with several patients enrolled in this MDACC-sponsored clinical trial. A second IND was filed mid-November 2010; subsequent questions from the FDA were addressed though extensive additional experimentation, and the second Phase I study is now active. Two other drugs are in pre-IND stage, with several others in the pre-clinical laboratory phase. Long-term, the broader vision of our research is to generate a large-scale receptor map of the human vasculature Combinatorial mapping of the human vasculature: towards ligand-directed therapies and imaging agents

7 Postdoctoral Fellow Department of Pediatrics Research MD Anderson Cancer Center Colleen O’Connor, Ph.D. Education: University of Kentucky, Lexington, Kentucky PhD: Toxicology with Specialization in Immunology University of Miami, Florida, Coral Gables, Florida BS Double Major: Marine Science and Biology Minor: Chemistry Notable Honors/Awards: The Ben F. Love Fellowship in Innovative Cancer Therapies from the Walter Frank Foundation Trainee of the Quarter Winner (For Meritorious Work) Janice Davis Singletary Lymphoma Fellowship Trainee of the Quarter Nominee University of Texas MD Anderson Cancer Center Immunology Poster Contest Winner University of Texas MD Anderson Cancer Center Immunology Retreat Graduate Academic Year Fellowship University of Kentucky Henry King Stanford Academic Scholarship University of Miami, Florida TV Coverage of Scientific Reports Paper Results ABC World News with Diane Sawyer KPRC NBC Houston Evening News Research Interest: Hematology, Oncology, Cell Therapy, Gene Therapy, Comparative Oncology, Immunology, T cells, Bone Marrow Transplants, Biomarker Development, Nanostring, Single Cell Analysis, MRI Imaging, Clinical Trials (Human and Canine) Email:

8 Personalized cancer therapy has come into focus in recent years with newly developed immunotherapies complementing conventional treatment modalities. However, the transition from bench to bedside still faces significant headwinds. Mouse models often fall short in predicting the efficacies and toxicities associated with T-cell therapy. Thus, new models which more closely mimic the human condition are urgently needed. The companion canine spontaneously develops many of the same cancers found in humans, despite a functionally intact immune system. Canine cancers mirror human malignancies with similarities in mutagenesis, tumorigenic responses to environmental toxins, documented oncogenic predispositions, and intra-species genetic diversity. These parallels, coupled with their relatively large body mass, afford a unique therapeutic model to study human cancers. NHL is the most common malignancy of the domestic dog, accounting for up to 25% of canine neoplasm and is rarely curable. Similar to humans, the majority of NHL (60-80%) in dogs arise from malignant B cells, most commonly diagnosed as Stage III or IV at presentation. New approaches are needed to improve patient survival beyond what combination chemotherapy (CHOP) can currently achieve. Biological therapies, such as CAR + or CAR neg T-cell therapy, can target disease by employing mechanisms independent of chemo-radio-therapies. Clinical observations reveal that an augmented pace of T-cell recovery after chemotherapy correlates with improved tumor-free survival, suggesting the add-back of T cells after chemotherapy may improve outcomes. To evaluate adoptive immunotherapy treatment for B-lineage NHL, we expanded T cells from client-owned canines diagnosed with NHL on artificial antigen presenting cells (aAPC) in the presence of human interleukin (IL)-2 and IL-21. Graded doses of autologous T cells were infused after CHOP chemotherapy and persisted for 49 days, homed to tumor sites, and significantly improved survival. Serum thymidine kinase changes predicted T-cell engraftment, while anti-tumor effects correlated with neutrophil-to-lymphocyte ratios and granzyme B expression in manufactured T cells. Our study supports the use of add-back T cells after chemotherapy in NHL patients to improve prognosis and survival. Personalized Canine cancer therapy

9 Postdoctoral Fellow Department of Radiation Oncology MD Anderson Cancer Center Lara C. Alvarez de Lacerda, Ph.D. Education: University of Coimbra (Portugal) - PharmD in Pharmaceutical Sciences University of London (United Kingdom) – PhD in Nanotechnology/Drug Delivery Systems Notable Honors/Awards: Postdoctoral Fellowship - Susan G. Komen for the Cure ® Research Program, USA Postdoctoral Fellowship - Foundation for Science and Technology, Ministry of Science and Education, Portugal PhD Studentship - Foundation for Science and Technology, Ministry of Science and Education, Portugal AACR Scholar-In-Training Award - 2012 CTRC-AACR San Antonio Breast Cancer Symposium, Susan G. Komen for the Cure®, USA Trainee of the Quarter Award - Department of Trainee and Alumni Affairs, University of Texas MD Anderson Cancer Center, USA Research Interest: My research project focuses on the role of the tumor microenvironment in regulating the equilibrium among breast cancer stem cells, progenitors, and differentiated cells. Additionally, I also have interest in new approaches to better understand and treat inflammatory breast cancer. My long-term career goal is to develop targeted therapeutic strategies that are specifically designed to overcome disease recurrence by effectively treating breast cancer stem cell populations. Email:

10 Inflammatory breast cancer (IBC) is an aggressive variant of breast cancer characterized by blocked breast lymphatics and clinically apparent involvement of the skin resulting in erythema, swelling and a high rate of resistance to therapy. Tumor-skin invasion in IBC patients, despite being a rare event, is an event that develops very rapidly, can spread throughout the upper body and ultimately results in breast cancer death. Very little is known about this event and how to prevent it. Mesenchymal stem cells (MSC) are multipotent progenitor cells which are found in normal tissues, including the bone marrow and adipose tissue. We hypothesized that MSC are critical mediators of IBC clinical phenotype and represent targets for treatment. Our data shows a significant difference in the tumor-skin invasion, between groups of mice injected with IBC cells SUM149 with or without MSC. Furthermore, co-injection of MSC with IBC cells significantly increased the spontaneous development of metastasis after primary tumor resection. In vitro, MSC co-culture was associated with increased EGFR signaling, and tumors in MSC co- injected animals had increased p-EGFR staining by IHC. Remarkably, we found that Erlotinib inhibited the rapid development of metastasis promoted by MSC co-injection, independently of primary tumor growth rate. In conclusion, MSC increased tumor-skin invasion and metastasis development in an IBC pre-clinical model independent of growth rate. This mechanism was due to increased EGFR signaling promoted by MSC. Thus MSC-cancer cells interaction can be abolished by Erlotinib. Further studies are needed to understand the role of MSC on the IBC cell involvement in skin contributing to the aggressiveness of this deadly disease. Mesenchymal stem cells promote skin invasion and metastasis in inflammatory breast cancer through an EGFR dependent mechanism

11 Postdoctoral Fellow Department of Pathology MD Anderson Cancer Center Da Yang, Ph.D. Education: Harbin Medical UniversityBachelor in Medicine 2005 Harbin Medical UniversityPh.D. 2009 Bioinformatics and Pharmacology Notable Honors/Awards: Odyssey Fellowship of The University of Texas MD Anderson Cancer Center (2011) Best Publication Award of The University of Texas MD Anderson Cancer Center (2012) The Diane Denson Tobola Fellowship in Ovarian Cancer Research (2012) The Harold C. and Mary L. Daily Endowment Fund Fellowship (2012) The Diane Denson Tobola Fellowship in Ovarian Cancer Research (2013) Bristol-Myers Squibb Award in Clinical/Translational Research (2013) Research Interest: Cancer Genomics Next generation sequencing analysis miRNA network analysis Personalized Medicine Email:

12 Epithelial ovarian cancer (OvCa) is one of the most lethal malignancies in women. Identification of molecular subtypes and corresponding molecular driver events is critical for the development of new therapies for OvCa patients. Here, we develop a computational pipeline (Master mIRna Analysis for Cancer moLecular subtype, MIRACLE) that aims to delineate the driver events, especially driver miRNAs. Applying the MIRACLE pipeline to 459 serous OvCa cases in TCGA database revealed a core miRNA- regulatory network for mesenchymal phenotype of OvCa. Using genes in the regulatory network, we further characterized a robust OvCa mesenchymal subtype significantly associated with poor survival in 459 serous OvCa cases from TCGA and 560 cases from three independent patient cohorts. In the miRNA-regulatory network, eight key miRNAs were predicted to regulate 89% of the targets. Among them are well- established EMT inhibitors, such as miR-200 family. In the follow-up in vitro and in vivo experiments, we further demonstrated that miR- 506, whose function was previously uncharacterized, as a novel EMT inhibitor by targeting SNAI2. Transfection of miR-506 augmented E- cadherin expression, inhibited cell migration and invasion, and prevented TGFβ-induced EMT, while force expression of SNAI2 can abolish miR-506’s effect. In human OvCa tissue, miR-506 expression was correlated with decreased SNAI2, elevated E-cadherin, and beneficial prognosis. To further explore the therapeutic efficacy of miR-506 in OvCa, we treated OvCa orthotopic mouse models with nanoparticle-incorporated miR-506. MiR-506 delivery can suppress EMT and tumor growth in vivo, suggesting miR-506 may serve as a potential therapeutic tool for OvCa patients. Integrated analyses identify a master microRNA regulatory network for the mesenchymal subtype in serous ovarian cancer

13 Professor, Cell Biology Associate Director, Basic Science, Simmons Cancer Center Michael White, Ph.D. Education: U. of North Carolina Chapel Hill Ph.D. 1989-1992 CSHL Postdoctoral Fellow 1992-1995 Notable Honors/Awards: Hortense and Morton Sanger Professorship in Oncology The Sherry Wigley Crow Cancer Research Endowed Chair in Honor of Robert Lewis Kirby, M.D. Grant A. Dove Chair for Research in Oncology Research Interest: Cancer cell biology Signal transduction Email:

14 Diversity in the genetic lesions that drive cancer initiation and progression is extreme. This diversity exists not only among tumors from different patients, but also among cancer cells within the same patient. This nefarious complexity is, in large measure, responsible for the capacity of this disease to evade current best efforts for effective therapy. “Personalized medicine” has been proposed in response to this conundrum as a mechanism to tailor cancer treatment to a specific tumor’s genetic and epigenetic characteristics. However, selection of appropriate treatment is dramatically limited by the paucity of appropriate drugs and by the difficulty of linking treatment options to the appropriate patients. The challenge is to identify authentic intervention targets for development of an appropriately diverse cohort of therapies to contend with disease heterogeneity. We are addressing this challenge by a focused investigation of common vulnerabilities that arise as a consequence of oncogene expression and tumor evolution. Here we will describe a cancer intervention discovery pipeline using parallel genetic and chemical perturbations within an extensive panel of cell lines representative of the molecular lesions detected in lung cancer by national and international cancer genome sequencing efforts. We have found that current first line targeted therapies are discoverable within this panel together with the enrollment biomarkers required to stratify patient treatment regimens. Further, we have found that new genetic and chemical vulnerabilities can be revealed that are linked to recurrent mutations in lung cancer patients that are not currently “actionable”. We are leveraging this approach to stratify lung cancer subtypes and elaborate intervention targets that are linked to those subtypes by robust molecular discriminators. Oncogenome-selective vulnerabilities in lung adenocarcinoma

15 Instructor Department of Health Disparities Research MD Anderson Cancer Center Diana W. Stewart, Ph.D. Education: 2005 The University of Kansas, Lawrence, KS, B.A., Psychology, English 2008 Louisiana State University, Baton Rouge, LA, M.A., Clinical Psychology 2011 Louisiana State University, Baton Rouge, LA, Ph.D., Clinical Psychology, Minor in Behavioral Medicine 2010-2011 Clinical Internship, Behavioral Medicine Track, Alpert Medical School at Brown University, Providence, RI 2011-2013 Cancer Prevention Research Postdoctoral Fellowship (NCI R25T CA57730), Department of Health Disparities Research, University of Texas MD Anderson Cancer Center, Houston, TX Notable Honors/Awards: 2011-present Platinum-level Trainee, Community Based Participatory Research Trainee, Latinos Contra el Cancer Community Networks Program Center, National Cancer Institute 2011-2013 Recipient, Competitive R25-T Postdoctoral Fellowship in Cancer Prevention Research, NCI R25-T CA57730 2012-2014 Recipient, National Institutes of Health, Health Disparities Research Loan Repayment Program 2013 Recipient, Mentored Faculty Fellowship, Duncan Family Institute for Cancer Prevention and Risk Assessment Research Interests: My research program focuses on cancer prevention and health promotion in underserved populations. My specific interests and expertise are in tobacco cessation for marginalized populations. Email:

16 Compared to individuals in the general population, racial/ethnic minorities and individuals with low socioeconomic status (SES) have higher smoking rates and greater difficulty quitting smoking. Thus, smoking has a striking impact on cancer disparities and mortality for individuals from these populations. Low health literacy is one factor that may be uniquely associated with poor cessation outcomes. This presentation will describe three studies investigating relations between health literacy and tobacco use and cessation, and potential mechanisms of this association, among low-SES, racially/ethnically diverse smokers. Implications and specific aims for future research will be discussed. Tobacco-related cancer disparities: The role of health literacy

17 Postdoctoral Associate Department of Otolaryngology Baylor College of Medicine Varun Sreenivasan, Ph.D. Education: Macquarie University, Australia. Ph.D. Physics 2012 Cochin University of Science and Technology, India. M.Sc. Photonics 2008 Notable Honors/Awards: 2012MQ BioFocus vacation scholarship, Sydney 2011Macquarie university post-graduate funding with Vice Chancellor's commendation, Sydney 2008-2012Macquarie postgraduate research scholarship, Sydney 2007Summer research fellowship, Indian academy of sciences, Chennai Research Interests: Molecular & cellular biophysics, cell signaling and motility, biological & biomedical imaging, high resolution & single molecule optical microscopy and nanoparticles. Email:

18 Cancer cells acquire motility by remodeling their cytoskeleton to form migratory structures (e.g., filopodia). Such transformations are dominated by F-actin re-assembly within the cytoplasm. These processes produce protrusive forces (~1 pN) allowing cells to migrate from their primary tumor site into surrounding stroma. Our goal is to elucidate the motility of cancer cells in vitro, by developing an assay to measure the protrusive forces and their time course. An optical trap-based biosensor with a stiffness of 9.2×10 -4 pN.nm - 1.mW -1 and time constant of 23 s -1.mW -1 is built. The trap levitates a 2-μm polystyrene bead 7 μm above the substrate. The bead undergoes a displacement from its equilibrium position in proportion to the force acting. The bead also serves as a handle to initiate the formation of the filopodium-like structure. We use a metastatic squamous cell carcinoma (HN31) of the pharynx, because they exhibit constitutively active Rho-GTPases and can sustain actin remodeling. The experiment involves bringing a cell in contact with the bead to facilitate membrane adhesion and then pulling it apart to rupture membrane-cytoskeletal bonds to initiate the formation of the filopodium-like structure. Results show the maximum force required for bond rupture is 70 pN, and decreases to 25 pN as the formed structure reaches a stationary state. Riding upon the stationary value are force fluctuations, which we associate with F-actin dynamics occurring within the cytoplasm near the tip of the structure. We suggest filopodium-like structures do form and we can monitor F- actin dynamics at its leading edge. Development of a force assay to monitor the mobility of cancer cells

19 Postdoctoral Fellow Department of Biochemistry MD Anderson Cancer Center Ryan McCarthy, Ph.D. Education: Harvey Mudd CollegeB.S. Mathematical Biology2007 University of GeorgiaPh.D. Plant Biology 2012 MD AndersonPostdoctoral FellowPresent Notable Honors/Awards: 2013 Molecular Genetics of Cancer Training Program 2008/2010 Postdoctoral Fellowship, University of Georgia Plant Biology Department Palfrey Grant, Harvey Mudd 2007 College Graduated with Distinction, 2007Sigma Xi Inductee 2003-2007 National Merit Four Year Undergraduate Scholarship Research Interest: My research interests focus on the regulation of differentiation and cell identity of human embryonic stem cells. I am particularly interested in investigating the multiple roles of p53 as a regulator of cell cycle, repressor of pluripotency factors and promoter of differentiation. To better understand this process I utilize mass cytometry for highly parametric profiling of cell populations undergoing differentiation. Email:

20 Development hinges on the capability of pluripotent embryonic stem cells (ESCs) to continuously self-renew and provide a source of somatic cells through differentiation. ESCs are held in a pluripotent state by core transcription factors including OCT4 and SOX2. During early differentiation of human ESCs (hESCs) p53 actively promotes differentiation by inducing cell cycle arrest, repressing pluripotency factors and activating lineage-specific developmental genes. Our understanding of the changes hESCs undergo during differentiation is limited by the inherent heterogeneity of cellular states. To overcome this we employed cytometry by time of flight mass spectrometry (CyTOF) to quantify 30+ distinct protein abundances at the single cell level, changing the heterogeneity of differentiation from an impediment into an asset. Using CyTOF to quantify changes in cell cycle distribution, histone modifications, pluripotency and lineage- specific marker proteins during differentiation we performed novel computational analyses to define a continuum of cell states present during differentiation and pinpointed key regulatory events. Upon differentiation to either ectodermal or endodermal/mesodermal lineages we observed p53 induction and accumulation of cells in G1 phase followed by the appearance of lineage-specific markers. p53 depletion increased proliferation and pluripotency factor abundance in self-renewing hESCs and delayed but did not prevent differentiation of hESCs. Additionally, G1 arrest was diminished but not abolished during differentiation indicating compensation, potentially by p53 homologs p63 and p73 or through p53 independent ERK-mediated cell cycle arrest pathways. Our findings improve our understanding of p53’s non-apoptotic role in differentiation and establish a unique system for further investigating hESC differentiation. Dynamic changes in protein abundance and cell cycle profiles revealed by profiling of human embryonic stem cells during differentiation at the single cell level by mass cytometry

21 Keynote Speaker Professor Stanford University School of Medicine Irving Weissman, M.D. Education: Montana State College (now University)B.S.1961 Stanford UniversityM.D.1965 Notable Honors/Awards: Among others: The Robert Koch Award, Pasarow Award for Outstanding Contribution to Cancer Biology, Election to the National Academy of Sciences; California Scientist of the Year (2001); Jessie Stevenson Kovalenko Medal, National Academy of Sciences Council; Max Delbruck Award; Honorary Doctorates, from Montana State University, Columbia University, Mt. Sinai School of Medicine. Research Interest: Dr. Weissman is an expert in the field of hematopoiesis (blood- formation), leukemia, and hematopoietic stem cells. The main focus of his work for many years has been the purification, biology, transplantation, and evolution of stem cells. His laboratory was first to identify and isolate the blood-forming stem cell (hematopoietic stem cell) in mice and humans, and to define many of the stages of development between these stem cells and their differentiated progeny. In recent years, Dr. Weissman has studied the potential of CD47 as a therapeutic target in multiple cancers and identified cancer stem cells in various hematologic and solid-tumor cancers. Email:

22 Following embryonic development, most of our tissues and organs are continuously regenerated from tissue/organ specific stem cells. The principal property that distinguishes such stem cells from their daughter cells is self-renewal; when stem cells divide they give rise to stem cells (by self-renewal) and progenitors (by differentiation). In most tissues only the primitive stem cells self-renew. Stem cell isolation and transplantation is the basis for regenerative medicine. Self-renewal is dangerous, and therefore strictly regulated. Poorly regulated self-renewal can lead to the genesis of cancer stem cells, the only self-renewing cells in the cancerous tumor. The Weissman lab has followed the progression from hematopoietic stem cells to myelogenous leukemias. They have found that the developing cancer clones progress at the stage of hematopoietic stem cells, until they become fully malignant. At this point, the ‘leukemia’ stem cell moves to a stage of a downstream oligolineage or multilineage progenitor that has evaded programmed cell death and programmed cell removal, while acquiring or keeping self-renewal. While there are many ways to defeat programmed cell death and senescence, there appears to be one dominant method to avoid programmed cell removal—the expression of the cell surface ‘don’t eat me’ protein CD47, the ligand for macrophage SIRP-alpha. All cancers tested express CD47 to overcome expression of ‘eat me’ signals such as calreticulin and asialogylycoproteins. Antibodies that block the CD47– SIRP-alpha interaction enable phagocytosis and killing of the tumor cells in vitro and in vivo. We expect to have the anti-CD47 therapies in phase 1 trials in early 2014. Normal and neoplastic stem cells

23 Breakout Sessions

24 Associate Professor Department of Systems Biology MD Anderson Cancer Center Yiling Lu, M.D. Education: M.D. degree from Shanghai Jiao Tong University, College of Medicine (Major in Medicine) M. Med. from Shanghai Jiao Tong University, College of Medicine (Major in Immunology and Microbiology) Postdoctoral Training in Texas Tech University, HSC (Immunology, Biochemistry and Molecular Biology) Notable Honors/Awards: The Susan Komen Breast Cancer Foundation: Rational design of combinational targeted therapeutics in breast cancer: Towards improving patient outcomes NIH Roadmap Molecular Libraries Initiative: Reverse Phase Protein Microarrays (RPPA) as a High Throughput Assay for Molecular Screening Breast SPORE Career Development Award: Identification of synthetic lethal targets interacting with mTOR inhibition in breast cancer cells expressing activated PI3K signaling network Ovarian SPORE Development Research Award: Identification of therapeutic targets interacting with autophagy in ovarian cancer Research Interest: My research focuses on identifying and characterizing novel cellular targets for cancer therapy by Systems Biology approach, which represents a paradigm shift from an in-depth study of one molecule or a few molecules at a time to a study of systemic integrated and interacting molecules. Cancer systems biology demonstrates that multiple genomic aberrations in cancer cells integrate to alter cellular functions at the level of protein. Email:

25 The Functional Proteomics Reverse Phase Protein Array (RPPA) provides investigators with a powerful high throughput, quantitative, cost-effective technology for functional proteomics studies. The RPPA technology complements Mass Spectroscopy and tissue microarray approaches to measure total and phospho- or cleaved- protein levels. RPPA represents an antibody-based functional proteomics analysis for both tumor tissue and cultured cells. Protein extracts denatured by SDS followed by serial dilution (in order to define antigen-antibody reaction in a linear range for accurate quantification) are arrayed on nitrocellulose-coated slides and probed with validated antibodies that recognize signaling molecules in their functional state. Signals are captured by tyramide dye deposition and a DAB colorimetric reaction. Data are collected and quantified using custom software developed for this purpose. The values derived from the slope and intercept are expressed relative to standard control cell lysates or control peptides on the array. These values indicate the levels of protein expression and modification. The sensitivity of RPPA technology can detect signals at the concentration of a femtogram from micrograms of starting materials. It characterizes, across large numbers of tumor samples or cell lines, the basal protein expression levels, growth factor- or ligand-induced effects, and time-resolved responses appropriate for systems biology analysis. It provides information to integrate the consequence of genetic aberrations in cancer, to validate therapeutic targets, to demonstrate on- and off- target activity of drugs, and to evaluate drug pharmacodynamics. We have defined a set of standard lysates to be used in each array for quality control of data generation and analysis. Functional Proteomics by Reverse Phase Protein Array (RPPA) and its application in cancer biology Session 1. Reverse Phase Protein Array (RPPA)

26 Assistant Professor Department of Genetics MD Anderson Cancer Center Nicholas Navin, Ph.D. Education: Skidmore College.B.S.2002 Stony Brook University & Cold Spring Harbor LaboratoryPh.D. 2010 Cold Spring Harbor LaboratoryPostdoc 2011 Notable Honors/Awards: 2005 Lindasy-Goldberg Fellowship 2008 King & Miller Fellowship 2009 NCI T32 Fellowship 2010 James Watson Suzhou Symposium Speaker 2012 AACR Princess Takamatsu Symposium Speaker 2012 Damon-Runyon Rachleff Innovation Award Research Interest: Single Cell Sequencing Intratumor Heterogeneity Genome Evolution Cancer Genetics & Genomics Email:

27 The objective of this workshop is to provide a basic overview of the tools and methods used by computational biologists to analyze large- scale genomic datasets from human cancer patients. We will discuss next-generation sequencing methods including genome sequencing(DNA-seq) and transcriptome sequencing (RNA-seq). Next we will cover tools used for detecting structural variants, copy number changes and somatic mutations. We will then provide an overview of the ongoing large-scale genomic sequencing projects such as the Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC) and how to access data from these projects using COSMIC and cBIO. We will also discuss how to distinguish driver from passenger mutations using prediction algorithms and mutation frequency. The topic of intratumor heterogeneity will also be discussed and how clonal diversity can affect the analysis of next-generation sequencing data. We will also cover data visualization tools including the Integrated Genome Viewer (IGV) and basic bioinformatics methods in multivariate statistics. Common programming languages and operating systems used by computational biologists will also be covered. Finally, we will discuss advanced courses offered at different institution that can be used to seek further training in computational biology, including the Cold Spring Harbor Laboratory (CSHL), the European Molecular Biology Laboratory (EMBL) and the Sanger Institute. Bioinformatics for cancer biologists Session 2. Bioinformatics

28 Assistant Professor and Co-Director Flow Cytometry & Cell Imaging Core Facility MD Anderson Cancer Center Jared K. Burks, Ph.D. Education: Degree-Granting Education Florida Institute of Technology, Melbourne, FL, BS, 1995, Molecular Biology Florida Institute of Technology, Melbourne, FL, BS, 1995, Pre- Professional Biology Texas A&M University, College Station, TX, PHD, 2005, Biology Postgraduate Training Postdoctoral Associate, Baylor College of Medicine, Houston, TX, 1/2006-7/2007 Notable Honors/Awards: 2003Entomology Graduate Student Forum Presentation Award, Texas A&M University 2004 American Society of Virology 2004 Annual Meeting, McGill University, Montreal, Canada Research Interest: As a member of the Flow Cytometry and Cellular Imaging Core Facility I get to contribute to research across the spectrum here at MD Anderson. I specifically enjoy applying imaging techniques to solve problems. Specifically, my interest is protein trafficking. Email:

29 Mass Cytometry is a burgeoning field where two very different technologies meet, Flow Cytometry and ICP-Mass Spec. DVS Sciences has developed an instrument based on an ICP-Mass Spec capable of performing flow cytometry measurements in an environment without spectral overlap and autofluorescence, thus removing the need for compensation. As such this new system alleviates the limitations of fluorescent based flow cytometry creating a paradigm shifting new instrument capable of up to 100 parameters per cell. Current limitations are ~35 parameters per cell. This instrument, called a CyTOF, utilizes unique metal isotopes (non-radioactive) as tags attached to antibodies to label your favorite proteins of interest. This results in Massively High Parametric data per cell which is then analyzed with SPADE Analysis. The limitations and benefits of the instrumentation will be discussed with some example preliminary datasets. Mass cytometry Session 3. Cytometry by Time-of-Flight (Cy-TOF)

30 Professor and Director Sequencing & Non-coding RNA Program Department of Experimental Therapeutics MD Anderson Cancer Center Chang-Gong Liu, Ph.D. Education: Ph.D. in Biochemistry-Molecular/Cellular Biology, 1995, University of Vienna, Austria. M. S. in Developmental Biology, 1989, Shandong University, Jinan, P.R. China. B. S. in Embryological Biology, 1982, Shandong University, Jinan, P.R. China. Notable Honors/Awards: 2000-Present Guest Professorship, Shandong University 1992-1995Pre-Doctoral Fellowship, Austria National Science Foundation Research Interest: Our research interest is to identify ncRNA biomarkers for cancer early stage detection and diagnosis, later stage prognosis and therapeutic targets collaboratively using ultra-throughput and cutting-edge genomic technologies of microarray and next generation sequencing. As a centralized sequencing and ncRNA Core services, our primary responsibility is to provide NGS sequencing and ncRNA services support to Investigators and facilitate cancer research. In addition, we do collaboration with investigator for in-house developments of new methodology and applications using in-house existing technology and expertise. Our previous collaborative efforts of microRNA in cancer have resulted in over hundreds of scientific research papers. Email:

31 The technologies of microarray and next generation sequencing enable us to analyze the changes of entire human genome and transcriptome in one single experiment. Data analysis has indicated more than 80% of human non-coding genome is transcribed into non- coding RNA (ncRNA). ncRNA includes large and small ncRNA that transcribed from the genomic regions of intronic, intergenic, antisense, interleaved, and overlapping with protein-coding genes. Given evidences have revealed the crucial and critical rules of miRNA, one class of ncRNA, expression in regulation of crucial processes of normal development, cell proliferation, apoptosis, differentiation and metabolism. Recent studies have identified different miRNA expression signature patterns, by miRNA expression profiling, associate with diagnosis and prognosis in human cancers and revealed abnormal miRNA expression modulates a wide array of growth and differentiation processes in human cancers. To explore more about non-coding RNAs involved in cancer and expand our concept in cancer genomic research, we have established a complete and comprehensive analytical system to study ncRNA in cancers at MD Anderson Cancer Center. This system includes 1) SOLiD™5500XL ultra-throughput genome system for novel ncRNA discovery and global profiling; 2) Ion Torrent PGM for targeted cancer related genes; 3) in-house custom miRNA/ncRNA expression array for all known targeted ncRNA expression profiling in cancer; 4) identification of miRNA/ncRNA and target mRNA interaction experimentally using NGS and Affymetrix mRNA profiling system besides computing prediction and 5) the correlation studies of differentially expressed ncRNA to it genomic copy number change by using NGS and array CGH assays. These combined approaches will allow us to gain full picture of cancer genomics and its differentially expressed noncoding RNA as biomarkers. An integrated platform facilitate comprehensive genomic and transcriptomic research in cancer Session 4. Non-coding RNA

32 Associate Professor Department of Imaging Physics, MD Anderson Cancer Center James A. Bankson, Ph.D. Education: 1994 Texas A&M UniversityBS, Electrical Engineering 2000 Texas A&M UniversityPhD, Electrical Engineering 2002 UT MDACCPostdoctoral Fellowship, Imaging Physics Notable Honors/Awards: 2003-2011Assistant Professor 2006-PresentDeputy Director, Small Animal Imaging Facility 2007-PresentAd hoc member, various NIH grant review panels 2011-PresentAssociate Professor, with award of Tenure 2011-2013Associate Editor, IEEE Transactions on Biomedical Engineering, Medical Physics 2013Graduate, UT MDACC Faculty Leadership Academy Research Interests: Imaging science Advanced biomedical imaging Magnetic resonance imaging and spectroscopy Signal and image processing RF and systems engineering Cancer imaging Metabolic imaging with hyperpolarized tracers Email:

33 The Small Animal Imaging Facility (SAIF) is an core resource at The University of Texas MD Anderson Cancer Center. It was established to ensure that cancer researchers, regardless of their academic training, have access to cutting-edge imaging technologies and to the expertise that is necessary for their successful integration into routine cancer research. SAIF consists of instrumentation, specially trained staff, faculty affiliates with academic focus in imaging sciences, and infrastructure that facilitates data management and scheduling of services. Services include magnetic resonance imaging and spectroscopy, nuclear imaging, x-ray computed tomography, image-guided radiation therapy, ultrasound, photoacoustic, and optical (fluorescence/bioluminescence) imaging. Faculty and staff are available for consultation through all phases of research, from preliminary estimation of feasibility, through experiment design, data acquisition, analysis, and interpretation, and summary of results in grants, manuscripts, progress reports, and other media. SAIF is a fee- for-service facility with fees that compare favorably with similar preclinical/translational imaging cores at other institutions. Dedicated staff can carry out all aspects of imaging experiments, or users can be trained to operate SAIF instrumentation for self-directed imaging services. Recent advances in imaging technologies inform on the structure, function, and composition of tissue and disease with unprecedented specificity and resolution, and the Small Animal Imaging Facility is an efficient conduit for the integration of emerging imaging sciences into cancer research. The small animal imaging facility Session 5. Small Animal Imaging

34 Poster Presentations

35 NoNameInstitutionTitle 1Alexander, AngelaMDACCTargeting Deregulated Cyclin E in Inflammatory Breast Cancer via Sequential Combination Therapy With CDK Inhibitors 2Appikonda, SrikanthMDACCHistone acetylation recruits TRIM24 to wrestle SUMO 3Au Yeung, Chi LamMDACCLeptin up-regulates matrix metalloproteinase-1 in metastatic ovarian cancer cells in the omental tumor microenvironment 4Bhadane, MinalUTHSCEvaluating severity of post- stroke spasticity through resting joint angle measurement 5Bird, Kathleen N.UTHSCReal-time Sonographic Measurements at the Bedside can Evaluate Sarcopenia in the Elderly Traumatized Patient 6Brugmann, WilliamMDACCNK cells exhibit cytotoxic activity against medulloblastoma cells in vitro and in vivo 7Wang, ChaoMDACCThe role of Numb expression and nuclear translocation in endometrial cancer 8Chen, JixinRiceMulti-Loop DNA Hairpin Folding/Unfolding

36 Poster Presentations NoNameInstitutionTitle 9Cobanoglu, ZehraMDACCSNDX-275 IS A POTENTIAL IMMUNOMODULATOR FOR NK CELL IMMUNOTHERAPY OF MEDULLOBLASTOMA 10Correa-Fernández, Virmarie MDACCSimultaneous Treatment of At- Risk Drinking and Tobacco Dependence among Puerto Ricans 11Cox, AaronBaylorExtreme obesity induces massive β-cell expansion through self- renewal and does not alter cell fate 12Datar, VrushaliMDACCStudy of Histone Methyl Transferase G9a Inhibition in ATRT and Medulloblastoma 13Fan, XiaozhouMDACCEngagement of the ICOS pathway markedly enhances efficacy of CTLA-4 blockade in cancer immunotherapy 14Forget, Marie- Andree MDACCGenetically modified artificial antigen-presenting cells (aAPC) to improve expansion, phenotype and function of tumor infiltrating cells for adoptive cell therapy in melanoma 15Gehlot, PrashasnikaMDACCBio-mathematical modeling of Yucatan pigs – a pilot report

37 Poster Presentations NoNameInstitutionTitle 16Sim, Geok ChooMDACCImmunotherapy with High Dose IL-2 in Metastatic Melanoma Patients Induces Dramatic Changes in an Activated ICOS+ T- regulatory Cell Subset that is Associated with Clinical Response 17Haymaker, CaraMDACCEnhanced functional and survival properties of a CD8 + BTLA + T-cell subset from human metastatic melanoma 18Hossain, Mohammad MDACCThe tyrosine kinase receptor Tie2 plays a significant role in the radioresistance of malignant gliomas and DNA repair 19Hu, ZhengMDACCGENOME-WIDE ANALYSIS OF REPLICATIVE LIFE SPAN EXTENSION MEDIATED VIA ALTERING HISTONE LEVELS IN YEAST S. CEREVISIAE 20Hylin, MichaelUTHSCCharacterization of the severity of neurocognitive and histopathological deficits following a mild fluid percussion injury 21Irwin, MaryMDACCThe Antioxidant Heme Oxygenase 1 Promotes Proliferation and Survival of Flt3- ITD-positive AML

38 Poster Presentations NoNameInstitutionTitle 22Carey, JasonMDACCDinaciclib a potent CDK inhibitor, abrogates cell cycle response in TNBC cells and induces susceptibility to PARP inhibition 23Taube, JosephMDACCEpigenetic silencing of microRNA-203 is required for EMT and cancer stem cell properties 24Jung, Su YonMDACCAssociations Between Sedentary Behavior And Cancer-Related Biomarkers 25Kota, DanielUTHSCMesenchymal Stem/Progenitor cell pre-conditioning with Poly I:C Increases monocytic leukemia cell line binding through Hyaluronic acid 26Krukowski, KarenMDACCContribution of Peripheral Immune Cells to Chemotherapy- Induced Neuropathy 27Kumar, VivekRiceMonocyte/ Macrophage Response to Nanofibrous Multidomain Peptide Hydrogels 28Lee, HyunUTHSCYAP is activated by shear stress to promote metastatic behavior in prostate cancer cells 29Lee, YoungbokMDACCReal Time In Vivo Metabolic Profiling of Cancer Using Hyperpolarized Imaging Agents

39 Poster Presentations NoNameInstitutionTitle 30Liu, ChenUTHSCPathogenic tissue transglutaminase stabilizes placental AT1 receptor by ubiquitination-preventing isopeptide modification in preeclampsia 31Liu, KevinRicePleiotropy and Polygenes in Adaptive Hybridized Gene Clusters in Mice 32Li, XuMDACCTargeting Myc-overexpressed difficult-to-treat cancers 33Low, Kwang HueiMDACCLMWE induced genomic instability via mis-regulated DNA replication licensing machinery 34McCullough, Christopher MDACCMetabolic Biomarker for Ovarian Cancer Determined by High Field Nuclear Magnetic Resonance Spectroscopy 35Morcos, FaruckRiceConformational changes leave an evolutionary footprint across protein lineages 36Morelli, M. PiaMDACCHeterogeneity of acquired KRAS and EGFR mutations in colorectal cancer patients treated with anti-EGFR monoclonal antibodies 37Moss, TylerMDACCmiR365-1 upregulates ERα and HER2 and is associated with poor outcome in patients

40 Poster Presentations NoNameInstitutionTitle 38Ornelas, ArgentinaMDACCImaging Cell Death Through Minimalist Molecular Probes 39Pradeep, SunilaMDACCHematogenous metastasis of ovarian cancer: rethinking mode of spread 40Purwaha, PreetiMDACCTargeted LC-MS/MS metabolomics for quantitation of amino acids with application to studies of L-asparaginase treatment 41Riquelme, ErickMDACCVEGF/VEGFR-2 upregulates EZH2 expression and EZH2 depletion reduce promotion of the malignant phenotype in lung adenocarcinoma cells, enhancing the response to platinum-based and VEGFR-2–targeted therapy 42Say, AmandaMDACCGeneration of LMW-E knock-in human mammary epithelial cells and mice 43Sehgal, LalitMDACCEZH2 and RBM5 cooperate to mediate resistance to FAS mediated apoptosis by regulating the function of FAS Natural Antisense Transcript in B cell Lymphoma 44Sehgal, VasudhaMDACCIdentification of candidate miRNA Associated with Survival for Breast Cancer Patients

41 Poster Presentations NoNameInstitutionTitle 45Seviour, ElenaMDACC 46Shao, Long JiangBaylorHighly Specific Targeting of the TMPRSS2/ERG Fusion Gene in Prostate Cancer Using Liposomal Nanotechnology 47Shirazi, FazalMDACCDiet modification and metformin (MET) have a beneficial effect in a fly model of obesity and disseminated mucormycosis 48Singhmar, PoojaMDACCGRK2-kinase activity inhibits Epac-Rap1 signaling to prevent transition from acute to chronic pain 49Sorokin, AlexeyMDACCAberrant expression of proPTPRN2 confers resistance to apoptosis in breast tumors 50Sreenivasan, VarunBaylorSilent membrane potential and voltage at maximum amplification: Are they coincident in outer hair cells of the mammalian cochlea? 51Srivastava, PriyankaUTHSCSimulating membrane binding of K-Ras monomers and dimers 52Sun, HongqiangBaylorEpidemiological trends and the advances of Treatments of Amphetamine-type Stimulants (ATS) in China

42 Poster Presentations NoNameInstitutionTitle 53Tang, HongweiMDACCGene-environment interactions in smoking-associated pancreatic cancer: A GWAS data analysis 54Vichaya, ElisabethMDACCEvaluating the role of neuroinflammation in head and neck cancer-related symptoms 55von Maltzan, Kristine MDACCMelanocyte Activation by UVR- induced Calprotectin 56Wadhwa, RoopmaMDACCIncidence of brain metastases following trimodality therapy (TMT) in patients with esophageal and gastroesophageal cancer 57Wang, WenqiMDACCDefining New Regulators for Hippo Pathway 58Watson, IanMDACCComprehensive Molecular Characterization of Regional Metastatic Melanoma 59Whiting, NicholasMDACCTowards the Implementation of Hyperpolarized, Functionalized Silicon Nanoparticles as In Vivo Molecular Imaging Agents for the Early Detection of Cancer by MRI 60Zhou, WenjunMDACCIndoleamine 2,3 dioxygenase (IDO1) is a Key Regulator of Depressive-like Behavior but not of Mechanical Hyperalgesia in the Spared Nerve Injury Model of Neuropathic Pain

43 All postdoctoral fellows in MD Anderson Cancer Center are automatically members of the Postdoctoral Association (PDA). The PDA Executive Committee (PDAEC) strives to improve, enhance, and enrich the postdoctoral fellowship experience at MD Anderson by planning monthly events and fostering interactions between members of the Texas Medical Center (TMC). Ways to contact the PDA and find information: research/education-and-training/schools-and- programs/research-training/postdoctoral-association/index.html!/groups/83955564561/ MDACC Postdoctoral Association

44 PDAEC Co-Chair: Lara Alvarez de Lacerda, Ph.D Lara is a Susan G. Komen Postdoctoral Fellow, training with Dr. Wendy A. Woodward in the Department of Radiation Oncology. Her research focuses on the role of the tumor microenvironment in regulating the equilibrium among breast cancer stem cells, progenitor, and differentiated cells. PDAEC Co-Chair Melissa Singh, Ph.D. Melissa is a postdoctoral fellow in the laboratory of Dr. Joya Chandra in the Department of Pediatrics Research. Her current research focuses on targeting histone deacetylases and demethylases as a rational combination therapy for the treatment of glioblastoma. Secretary and Publicity Co-Chair: Shadia Zaman, Ph.D. Shadia is a postdoctoral fellow in the department of Experimental Therapeutics. She is currently training with Dr. Varsha Gandhi to identify and validate novel therapeutics for the treatment of hematological malignancies such as multiple myeloma. Policy Co-Chair: Haley Peters, Ph.D. MDACC Postdoctoral Association Executive Committee (PDAEC)

45 Speakers Chair Prashasnika Gehlot, Ph.D. Prashasnika is a postdoctoral fellow in the Department of Surgical Oncology under the mentoring of Dr. Steven Curley. She is currently working on hepatocellular cancer and liver cancer stem cells with animal models. International Co-Chairs: Amir Hamdi, M.D. Dong Yang, Ph.D. Events Co-Chair: Becket Hui RCR Seminars Co-Chair: Enrique Fuentes-Mattei, Ph.D. Enrique is currently training in the Department of Molecular and Cellular Oncology under the mentorship of Dr. Mong- Hong Lee and Dr. Sai-Ching Yeung. His main areas of research include toxicology, molecular biology, receptor mechanisms, obesity, diabetes and carcinogenesis South Campus Chair: Diane Scaduto, Ph.D. MDACC Postdoctoral Association Executive Committee (PDAEC)

46 Science Park Chair: Brent Ferguson, Ph.D. Brent is a postdoctoral fellow in the Department of Molecular Carcinogenesis at Science Park in Smithville, TX working under the direction of Dr. Marcelo Aldaz. His research is focused on understanding the function of the putative tumor suppressor gene WWOX in various types of cancer. Postdoc Liaison Chair: Figen Beceren-Braun, Ph.D. Figen is a postdoctoral fellow in the laboratory of Dr. Tomasz Zal in the Department of Immunology. Her research focuses on restoring the anti-tumor immunity of lymphocytes in tumor microenvironment. APSS Working Group: Becket Hui Melissa Singh, Ph.D. Fabiola Gomez, Ph.D. Fabiola is a postdoctoral fellow in the laboratory of Dr. Varsha Gandhi in the Department of Experimental Therapeutics. She is working on developing strategies to combine Pim kinase inhibitors with other agents in chronic lymphocytic leukemia. Associate Director, Research Trainee Programs: Martha Skender, MPH MDACC Postdoctoral Association Executive Committee (PDAEC)

47 Mentor Award Co-Chairs: Rob Cowan, Ph.D. Argentina Ornelas, Ph.D. Qingshan (Carly) Yang, Ph.D. Program Manager, Office of Postdoctoral Affairs: Tracy Jennifer Costello, Ph.D. Tracy is charged with assisting Martha Skender with the planning, organization, direction setting and evaluation of the academic and career development programming for the Institution's research postdoctoral fellow population, including strategic oversight of the MD Anderson Postdoctoral Association. MDACC Postdoctoral Association Executive Committee (PDAEC)

48 Acknowledgements T he MD Anderson PDAEC would like to extend formal gratitude to Dr. Ronald DePhino, MD Anderson President, for his continued support and encouragement of all MD Anderson trainees. Furthermore, we would like to thank Dr. Oliver Bogler, and the MD Anderson Department of Trainee and Alumni Affairs (TAA), as well as the Alumni and Faculty Association (AFA) for their generous sponsorship and assistance with this event. We appreciate the effort it took to secure the funding necessary to help establish and execute this symposium. PDEAC would also like to thank MD Anderson Faculty Advisory Committee for providing endless assistance and mentorship. We would like to especially recognize Martha Skender and Kristina Brown from Office of Trainee and Alumni Affairs, Tracy Costello from Office of Postdoctoral Affairs, and Sandra Craft from Medical Graphics and Photography for their help putting together the symposium. A very special thanks to all the members of PDAEC and former member Chris Vellano, this symposium was made possible by all your hard work, organization, and support. 2013 Working Group Melissa Singh Fabiola Gomez Becket Hui

49 Notes

50 The Mission of APSS The Annual Postdoctoral Science Symposium (APSS) was initiated on August 4 th 2011, by the MD Anderson Postdoctoral Association to provide a platform for talented postdoctoral fellows to present their work to a wider audience. Our ultimate vision is to develop this event into a symposium that incorporates all Texas Medical Center (TMC)-affiliated institutions providing postdocs from a unique opportunity to learn, interact, and foster new collaborations. With your support and participation, we can make this happen.

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