Mentors at the University of Arkansas for Medical Sciences
Click here to visit UAF mentor page
Faculty please note that this list of mentors is not exclusive. There are many more potential mentors on the UAMS campus. You can search at the UAMS web site and contact potential mentors yourself or seek assistance from Drs. Jerry Ware or Samantha Kendrick.
Undergraduate students applying to the INBRE Mentored Summer Research Program, please use the list of mentors below for your application.
| Title | Mentor/ Department | Description | Prerequisite Courses? | Bioinformatics Students? |
|---|---|---|---|---|
| Innate Immune Defense Against Intracellular Pathogens | Youssef Aachoui, PhD, COM, Department of Microbiology and Immunology | We study how the innate immunity detect intracellular pathogens and subsequently orchestrate their elimination. We specifically focus on cytosolic pathogen pattern recognition detectors, inflammasomes, which activate caspase-1. Caspase 1 subsequently activates the processing of the pro-inflammatory cytokines pro-IL-1β and pro-IL-18 and/or promotes a form of programmed cell death termed pyroptosis. Pyroptosis restricts intracellular bacterial growth by lysing infected cells, thereby eliminating the intracellular replication niche, and exposing the bacteria to attack by neutrophils. For instance, we showed that the inflammatory caspase-11 discriminates between cytosolic and vacuolar bacteria, and this detection is necessary for protection against cytosolic pathogens such as Burkhloderiaspecies, and the ΔsifA mutant of Salmonella typhimurium that aberrantly exits the vacuole. We went on to show that caspase-11 is activated in response to cytosolic LPS. Current studies examine the activation of caspase-1 and caspase-11 inflammasones, and investigates their role in infection and inflammatory disorders. | No | No |
| Mechanisms of Chemotherapy-Induced Cognitive Impairment | Antiño R. Allen, PhD, Division of Radiation Health, UAMS | Chemotherapy is commonly used in the management of cancer, but its effectiveness is limited by the potential for injury to normal tissues. Chemotherapy induced cognitive impairment, also Referred to as “chemobrain” or “chemofog,” is experienced by 15 – 80% of cancer patients and survivors. The Allen laboratory is interested in understanding the mechanisms that are responsible for behavioral toxicities after cancer therapy. We currently have two active projects; the first is studying how chemotherapy after breast cancer affects cognition in adult female mice. The second project is investigating the neurocognitive late effects after acute lymphoblastic leukemia chemotherapy in a juvenile mouse model. Trainees in my lab learn and use a variety of techniques including: behavioral studies, molecular biology (PCR), biochemistry (protein expression, Western blots), immunohistochemistry, histology, light/fluorescent microscopy, cell culture and electrophysiology (brain slice recording) in order to answer questions at multiple levels of the investigation. | No | |
| Targeting lipoprotein homeostasis for the treatment of multiple myeloma | Ryan M. Allen, PhD, COM, Department of Physiology and Cell Biology | Lipoproteins are essential for lipid transport between tissues, a process critical for vertebrate development and homeostasis. Imbalances in lipid distribution, particularly between high-density lipoprotein (HDL) and low-density lipoprotein (LDL), are strongly linked to cardiovascular disease, but also some types of cancers. For instance, high HDL-cholesterol levels, often termed ‘good cholesterol,’ correlate with improved survival in multiple myeloma (MM) patients, while statin drugs, which lower LDL-cholesterol, have also been shown to enhance MM patient outcomes. These findings suggest that disrupted lipoprotein homeostasis may play an under-explored role in MM progression. Our research aims to identify novel genes that contribute to dyslipidemias associated with cardiovascular disease and MM, with the goal of developing new targeted therapies for these diverse patient populations. To achieve this, we leverage a comprehensive toolkit of in vitro (cultured cells) and in vivo (mouse models) techniques to manipulate and analyze lipoprotein metabolism, complemented by advanced bioinformatics approaches, including small RNA, bulk RNA, and single-cell RNA sequencing. | No | No |
| Understanding Molecular Mechanisms of Cell Plasticity in Cardiometabolic Diseases | Rushita Bagchi, PhD, COM, Department of Physiology and Cell Biology | Our lab studies the characteristics and regulation of cell states in health and disease. We use human induced pluripotent stem cells (iPSCs), intact human and mouse tissues, pre-clinical rodent models, and omics platforms to understand the molecular pathways that drive cellular plasticity in cardiovascular and metabolic diseases. We also employ genetic and pharmacological manipulations in cells and mice to investigate how specific genes/proteins may cause cell state transitions, thereby contributing to cardiometabolic diseases. Trainees in the lab can learn and master a variety of techniques, including cell culture (2D and 3D), protein and gene expression assays, DNA-protein and protein-protein interaction assays, cell and tissue imaging techniques, cell behavior assays, animal models of diseases, among others. | Cell Biology and/or Biochemistry, Physiology recommended | No |
| Natural Language Processing (NLP) of Clinical Data | Ahmad Baghal, MD, COM, Department of Biomedical Informatics | Secondary use of clinical data for clinical and translational research is instrumental in growing our knowledge of clinical medicine. Unfortunately, not all clinical data are represented as discrete elements. Clinical practices generate enormous amounts of documents that store rich and valuable information that can enhance our knowledge discovery. The goal of the engagement is to perform an evaluation of open source NLP tools that can be suited to UAMS clinical environment, particularly within the Arkansas Clinical Data Repository (AR-CDR) domain. There is also a potential to participate in research work that focuses on developing new NLP pipeline using novel methodologies. | Programming (Python/ knowledge of Databases) | Yes |
| Alzheimer Disease: Connections to Diabetes and Obesity | Steven W. Barger, PhD, Departments of Geriatrics, Neurobiology and Developmental Sciences, and Internal Medicine | The Barger laboratory studies basic elements of cellular neurobiology, particularly as they relate to the development of Alzheimer’s disease. Using cell cultures and transgenic mice, Dr. Barger and coworkers examine the ways in which the Alzheimer amyloid protein perturbs blood glucose levels and other elements of metabolism outside the brain. It is hypothesized that these “peripheral” perturbations, in turn, impair brain function in Alzheimer’s disease. An aspect of the project involves testing new drugs that might alleviate these abnormalities. | None | Yes |
| DNase Inhibitors: Universal Anti-Disease Drugs of the Future | Alexei G. Basnakian, MD, PhD, DSc, COM, Department of Pharmacology and Toxicology | All human diseases are associated with a tissue injury by a direct physical impact, infection, inflammation, hypoxia, or poisoning. All of those induce cell death, which is a multi-step process. However, independently of the cause and mechanism of cell death, all they end up with DNA fragmentation by cellular endonucleases, including deoxyribonuclease I, deoxyribonuclease II, caspase-activated DNase, endonuclease G, DNase gamma, and a few other enzymes. Sometimes these enzymes are called “apoptotic endonucleases,” however they participate in all cell death mechanisms: necrosis, necroptosis, ferroptosis, mitotic catastrophe, anoikis, and dysregulated autophagy. Our studies showed that genetic inactivation or inhibition of these enzymes universally protects cells from death in different models of cell or organ injuries in vitro and in vivo. We have recently discovered several specific chemical inhibitors of endonucleases and now test if they can be applied as drugs to protect healthy tissues against various types of tissue injury (diseases). Our first results in this direction are very encouraging. | None | Yes |
Computational Multi-Omics & Cancer Biology Research | Michael A. Bauer, PhD, COM, Department of Biomedical Informatics, UAMS | The Bauer lab integrates computational methods with multi-omic technologies to investigate the molecular drivers of cancer and to identify biomarkers that can inform precision oncology. We analyze genomic, transcriptomic, epigenomic, and proteomic data, including single-cell, and long-read sequencing technologies, using statistical and machine-learning approaches. Current research areas include multiple myeloma, liver and other solid tumors, blood-based biomarkers for early cancer detection, and cancer health disparities in diverse populations. Summer students will join an ongoing project and complete a defined analysis during the program. Example projects include: — Identifying and validating molecular biomarkers of cancer using proteomic or genomic data— Testing whether findings replicate in large public datasets such as TCGA and GEO — Analyzing single-cell data to understand how tumor cells and their microenvironment change during disease progression and treatment — Applying machine-learning methods to classify disease states or predict outcomes Students will gain hands-on experience in R programming, reproducible analysis workflows, high-performance computing, statistical analysis of high-dimensional data, and scientific data visualization. | ||
| Control of Bone and Muscle Weakness by Hormones, Cancer, and Nutrition | Teresita Bellido, PhD, COM, Department of Physiology and Cell Biology | Research projects in the Bellido lab center on understanding physiological and pathophysiological mechanisms that govern the function of bone and muscle in health and disease, and developing genetic and pharmacological approaches to promote musculoskeletal health. Particular emphasis is placed on the role of osteocytes, the most abundant cells of bone, in driving the bone remodeling process in response to mechanical and hormonal cues, as well as in the role of these cells in cancer in bone and in multiple myeloma bone disease. Current projects in the lab are: 1. Mechanism of action of glucocorticoids in the musculoskeletal system 2. Parathyroid hormone (PTH), osteocytes, and diabetes-induced bone disease 3. Role of Osteocytes in cancer in bone in multiple myeloma 4. Nutrition, bone, and the microbiome The laboratory receives funding from the National Institutes of health (NIH), the Veteran Administration (VA), and the biopharmaceutical industry. | None | No |
| Using Molecular Genetics to Study Virulence in Pathogenic Borrelia | Jon Blevins, PhD, COM, Department of Microbiology and Immunology | Pathogens of the genus Borrelia are spirochetal bacteria transmitted to humans via the bite of an infected arthropod. There are two diseases, Lyme disease and relapsing fever, which are commonly associated with Borrelia infection in humans. Despite intensive research efforts studying the Borrelia bacteria that cause Lyme disease and relapsing fever, there is still significant progress to be made toward understanding the pathogenic mechanisms that these bacteria utilize to cause disease, colonize tick vectors, and transmit during tick feeding. Specifically, we are working to determine how Borrelia controls the expression of its genes as it moves between tick and mammal and define the contributions of individual Borrelia genes to bacterial virulence and tick colonization. One of the most direct approaches to demonstrate a causal relationship between a bacterial gene, its cognate gene product, and a requirement during the bacterial lifecycle is to create Borrelia mutants in which specific genes of interest have been inactivated. The abilities of these mutant strains to colonize animals and ticks can then be assessed experimentally to determine whether a given mutant is no longer competent for infection. Once bacterial factors required for Borrelia infection or tick transmission have been identified, we can begin to study their physiological contributions to these bacterial processes. In addition, since these factors are known to be essential during the bacterial lifecycle, they also represent viable targets against which therapies could be developed to prevent or treat disease. | Microbiology (Preferred) | |
| Understanding Lung Cancer Metabolism | Gunnar Boysen, PhD, Department of Occupational Health and Safety | The Boysen lab interested in understanding the interplay between chemical exposure and nutritional or lifestyle habits, such as diet selection and physical activity. To achieve this we utilize DNA and protein adducts to study carcinogen metabolism, how it is modified by nutritional components and the underlying mechanisms regulating corresponding enzyme activities. In addition studies investigate exposures related changes in common metabolic pathways, using targeted and un- targeted mass spectrometry based metabolomic approaches. The long term goal is to improve our understanding of lung carcinogens and to improve lung cancer therapy. | None | Yes |
| Molecular mechanisms of maintenance of genomic stability to aid in development of new cancer therapeutics | Alicia Byrd, PhD, COM, Department of Biochemistry and Molecular Biology | Our lab investigates the molecular and cellular mechanisms that allow the cell to survive DNA damage and DNA replication stress. These pathways are critical for maintaining genome stability, and defects in these pathways result in a predisposition to many types of cancer. One major focus in the lab is how DNA helicase B promotes survival from DNA replication stress and maintains treatment efficacy in BRCA1 and BRCA2 mutant tumors. We use a variety of in vitro and cellular models; cellular techniques include immunoblots, microscopy, CRISPR knockouts, and flow cytometry. In vitro, we use purified proteins to measure helicase activity characterize protein-DNA and protein-protein interactions by electrophoresis and fluorescence spectroscopy. The goal of our research is to define the molecular mechanisms that enable timely DNA replication and repair. This will enhance our understanding of the fundamental molecular processes essential for normal growth and reproduction that also contribute to the development of cancer. Increased understanding these DNA repair processes could ultimately lead to the design of better cancer therapies. | None | No |
| Dynamics of Regulation and Function of Diverse Subsets of Anterior Pituitary Cells | Gwen V. Childs, PhD, COM, Department of Neurobiology and Developmental Sciences | Classical studies of the anterior pituitary have shown 6 major cell types with unique neuropeptide releasing hormones as regulators from the brain. However, sensitive molecular assays show that pituitary cells are much more diverse than previously believed. Currently the funded projects in Childs laboratory focus on two examples of this diversity. The first study focuses on the significance and regulation of leptin by specific pituitary cells. Leptin is an appetite regulatory peptide normally produced by adipose cells. However, it might also be a cytokine in the pituitary, working locally to regulate pituitary cells. One project even looks at the possibility that it might be an endocrine factor, produced by gonadotropes to help regulate the reproductive system. The second study focuses on how pituitary cells integrate responses so that a cocktail of hormones is released to meet the needs of a particular physiologic state. Co-expression of multiple neuropeptide receptors is one of the ways the cells can meet these needs and this is regulated by gonadal steroids. The studies use molecular cytochemistry and cytophysiology with a focus on the analysis of individual cells. | Cell Biology | No |
| Investigating the epigenetic regulatory mechanisms and therapeutic interventions in Acute Myeloid Leukemia | Samrat Roy Choudhury, PhD, Arkansas Children’s Research Institute (ACRI), COM Department of Pediatrics | Our laboratory investigates the epigenetic mechanisms at the regulatory regions (enhancers and promoters) of critical oncogenes and tumor suppressors that drive malignant proliferation and tumor infiltration of the leukemic cells. Using multi-omics platform, the laboratory studies alterations in DNA-methylation, histone modifications and binding of the transcription factors to the aberrantly expressed genes. We use bioinformatic tools to integrate epigenomic and transcriptomic data to determine the epigenetically dysregulated pathways in the disease. The laboratory also uses a combination of in vitro and in vivo mouse models to screen small molecule-based chemotherapies to reverse the dysfunctional epigenetic states and overall malignant growth. | None | Yes |
| Tumor Microenvironment | Jesús Delgado-Calle, PhD, COM, Department of Physiology and Cell Biology | The Delgado-Calle laboratory investigates the mechanisms by which cancer cells alter the biology of other cells in the tumor niche with the final goal of identifying new targets to treat cancer. We employ a combination of bioinformatics, imaging, and in vivo mouse models to study the crosstalk between tumor cells and host cells. Current projects in the laboratory investigate the effects of Notch and FGF23 signaling, as well as cellular senescence, on tumor growth and cancer cell dormancy. | None | No |
| Computational Multi-Omics, Cancer Genomics & AI-Driven Bioinformatics | Kalyani Dhusia, PhD, Department of Physiology & Cell Biology; Data Science, Arkansas INBRE | The Dhusia research program applies computational biology, machine learning, reproducible workflow development, and multi-omics integration to biomedical and translational research. Projects span cancer genomics, proteomics, transcriptomics, clinical data integration, AI-assisted scientific workflows, and development of reusable computational tools. Current research and development areas include: (1) proteogenomics and multi-omics workflow development, including ProteoVar and reproducible Nextflow-based pipelines; (2) analysis of RNA-seq, WES/WGS, single-cell, and proteomics(DDA/DIA) datasets for tumor biology, treatment response, and biomarker discovery. (3) machine-learning and AI/LLM-assisted approaches for biological knowledge extraction, annotation, and data integration; (4) integration of clinical and molecular data using SQL-based databases and reproducible statistical frameworks; and (5) development of translational computational tools, including AI-enabled decision-support systems for biomedical research and oncology. I am developing a student onboarding and training pathway with introductory materials in Linux, Git/GitHub, Python/R, biomedical data analysis, reproducibility, and responsible use of AI in research so that incoming students can begin contributing to projects more quickly. For faculty collaborators: I welcome collaborations with faculty at Arkansas PUIs who need support with bioinformatics, genomics, proteomics, multi-omics integration, machine learning, AI-enabled research tools, reproducible workflow development, or preliminary data analysis for grants and manuscripts. Faculty considering an AR INBRE Developmental Research Project/Pilot Project and AR INBRE Research Technology Core vouchers can contact me early during project development. Visit: https://kalyanidhusia.github.io/faculty_collaboration/ For undergraduate students: Students can participate in computational research projects involving real biomedical datasets and gain hands-on experience with Python, R, Git/GitHub, Linux, Nextflow, machine learning, RNA-seq, proteomics, genomics, scientific visualization, and reproducible research practices. Students interested in the Arkansas INBRE Mentored Summer Research Program or Professional Research Opportunity program are encouraged to contact me about potential computational biology/data-science projects. These programs specifically support undergraduate STEM students interested in biomedical research. Visit: https://kalyanidhusia.github.io/student_training/ Website: kalyanidhusia.github.io GitHub: github.com/kdhusia Contact: KDhusia@uams.edu | No | Yes |
| The Role of Tumor Vasculature in Carcinogenesis and Treatment | Ruud P.M. Dings, PhD, MSc, COM, Department of Radiation Oncology | The primary goal of our lab is to enhance our understanding of vascular biology to discover and develop improved methods for cancer treatment. Our major research interest is the tumor microenvironment, with emphasis on the crosstalk between the immune system and the tumor vasculature. Our objective is to identify and delineate unexplored mechanisms to positively contribute to the vascular biology field and improve treatment strategies. We use multi-disciplinary techniques that include cellular and molecular biology approaches (e.g. aseptic techniques, flow cytometry, PCR, ELISA and others) using patient samples and mouse models to decipher cancer initiation and progression, and the treatment thereof. Lab Website: Ruud P.M. Dings lab website | No, but Biology, Immunology, and/or Chemistry is desired | Yes |
| Molecular Mechanisms of DNA Damage Tolerance | Robert L. Eoff, PhD, COM, Department of Biochemistry and Molecular Biology | The Eoff laboratory uses a variety of approaches to investigate the molecular and cellular mechanisms that facilitate the bypass of DNA damage and other barriers to accurate and timely duplication of the genome. Studying the relationship between DNA replication stress response pathways and adverse outcomes for cancer patients (e.g., pro-malignant tumor properties and resistance to therapy) is a central theme in the laboratory. One major area of interest is focused on understanding how DNA polymerase kappa supports the replication stress response in malignant brain tumors. We are also collaborating with Dr. Julie Gunderson (Hendrix College) to explore the molecular features and protein-protein interactions involved in the replication of four-stranded G-quadruplex DNA. Through our research, we hope to contribute new insights into mechanisms that are central to mutagenesis, genome stability, cancer biology, therapy resistance, and biological evolution. | None | No |
| Virus-Host Interactions in Gammaherpesvirus Infections | J. Craig Forrest, PhD, COM, Department of Microbiology and Immunology | Virology, cancer biology, immunology! Gammaherpesviruses, such as Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus, are cancer-causing viruses that infect the majority of humans. We are working to define functions of viral proteins in infection and disease, identify host factors that block viral infection and prevent virus-driven cancers, and understand immune responses to chronic viral infections. We use a multi-disciplinary approach that includes basic cell biology, molecular genetics, global proteomics, and mouse models of infection to accomplish our major goal of defining the complex relationship between gammaherpesviruses and their hosts. PLUS, we get to do cool science and figure out how stuff works! | Biology and Chemistry | No |
| Development of Precision Medicine for Oncology | Brendan Frett, PhD, COP, Department of Pharmaceutical Sciences | Drug development is largely target-driven, where drugs are developed to modulate a pharmacologically, relevant target in a given disease state. This type of drug development has been heavily utilized for oncology to improve effectiveness and reduce toxicity to chemotherapy. The Frett laboratory is interested in further improving target-based drug discovery in oncology. We have numerous, active projects which aim to uncover next-generation strategies to target malignant disease. Trainees in my laboratory learn a variety of techniques including organic chemistry (drug synthesis), analytical chemistry, biochemistry (drug/target studies), and cell culture all in the context of drug discovery and development. | No | Yes |
| Liposomal Drug Delivery | Robert J. Griffin, PhD, COM, Department of Radiation Oncology | Nanotechnology has shown considerable potential for cancer treatment, particularly through combination therapies that integrate two or more therapeutic mechanisms within a single platform. Our group has established an ionic material (IM)-based approach to develop economical combination anticancer drugs with enhanced antitumor activity in vitro and in vivo. However, the long-term stability of these IMs at high concentration remains a significant challenge for their further development and potential clinical translation. To overcome this limitation, we propose, for the first time, to incorporate IM-based combination drugs into a liposomal drug-delivery platform. Liposomes are biocompatible and biodegradable nanocarriers capable of accommodating therapeutic compounds with different physicochemical properties and have been successfully translated to the clinic, as an example, FDA-approved liposomal doxorubicin (Doxil) as well as lipid particle-based agents such as the hugely successful COVID vaccines. Our overall goal is to develop liposome-encapsulated combination ionic materials (Lipo-IMs) with improved long-term stability, cellular uptake, and selective anticancer activity. IM-based combination drugs will be prepared by pairing oppositely charged therapeutic ions with complementary mechanisms of action. Specifically, the chemotherapeutic cation doxorubicin (DOX) will be paired with negatively charged indocyanine green (ICG) to integrate chemotherapy with NIR-mediated phototherapy along with bioimaging potential. | Cell Biology and/or Biochemistry, Physiology recommended | Yes |
| Precision Environmental Health to Tackle High Rates of Early-Onset Breast Cancer in Arkansas Rural Community Health Study (ARCH) | Ping-Ching Hsu, PhD, MSc, Department of Environmental Health Sciences | Residents in Arkansas face high risks in generational exposure to pesticides and fertilizers from agricultural production; heavy metals such as arsenic found in the soil, water, air; and aromatic hydrocarbons (benzene, benzo[a]pyrene) from frequent burning of trash, crop and timber residues, and high-temperature cooking. Arkansas Rural Community Health Study (ARCH) is the first and the largest epidemiologic cohort of adult women in AR to examine the effects of both genetic and environmental exposures on an individual’s risk of developing breast cancer (BC) and predicted response to treatment. In total, the institutional-supported ARCH cohort has 26,375 women from all 75 AR counties. In contrast to most cohorts conducted among populations well below average risk, ARCH is enriched with a high rate of early-onset breast cancer (EOBC) cases among all BC prevalent cases at baseline and incident cases when linked with the Arkansas Cancer Registry. Given the increasing incidence of EOBC nationwide, it is crucial to invest in an understudied rural population with generations of exposure to identify factors responsible for increasing risk and the mechanisms underlying EOBC etiology. Our goal is to maintain, enrich, and enable a broader use of data and sample resources for the ARCH cohort by facilitating longitudinal follow-up since the baseline recruitment in 2007. Students will be involved in cohort data (from cancer registry, residential address, follow-up survey) cleaning, support optimizing, and documenting the protocol for the detection of environmental chemicals using Inductively-coupled plasma mass spectrometry (ICP-MS), conducting pilot projects comparing trace metals from different bio-specimen (saliva, urine, blood, toenails) using ICP-MS, and to support data analysis on genome-wide DNA methylation profiling. https://uams.info/ARCH. | No, but Biology, Epidemiology, and Chemistry are desired. | Yes |
| Deciphering host-pathogen interactions underlying Acinetobacter baumannii ventilator-associated pneumonia | Clay D. Jackson-Litteken, PhD, MPH, COM, Department of Microbiology and Immunology | Ventilator-associated pneumonia (VAP) is a leading nosocomial infection, and the bacterium Acinetobacter baumannii is a predominant cause of VAP. Concerningly, A. baumannii has the highest rate of multi-drug resistance of any pathogen, leading the CDC and WHO to classify the bacterium at its highest priority for development of novel therapeutics and preventative measures. The Jackson-Litteken laboratory has recently developed the only longer-term murine VAP model that can be used to study bacterial pathogenesis. Using this model, we have acquired preliminary data suggesting that bacteria exploit host proteins coating the endotracheal tube deposited as part of the immune response to intubation to bind, form biofilm, and subsequently exacerbate VAP. An INBRE participant will have the project of defining bacterial adhesins (i.e., surface proteins which bind to specific biotic or abiotic surfaces) required for VAP establishment and progression. Additionally, the INBRE participant will define the specific molecules bound by these adhesins. | None | No |
| Pharmacological Modulation of Poly(ADP-ribose) Metabolism | Darin E. Jones, PhD, COP, Department of Pharmaceutical Sciences | Molecularly-targeted cancer therapies have revolutionized the treatment of this heterogeneous and increasingly prevalent disease. Genetic instability is a hallmark of many cancers that generates mutations to support uncontrolled tumor growth and resistance to chemotherapies. The underlying DNA repair defects in these tumors can be exploited in tumor-selective therapies that block critical remaining DNA repair functions to trigger catastrophic damage and cell death. This idea is borne out by the clinical successes of inhibitors of poly(ADP-ribose) polymerase 1 (PARP1) to treat breast and ovarian cancers with mutations in BRCA1 or BRCA2. However, these BRCA-deficient tumors account for a minority of cancers so it is important to identify other physiological defects of tumors that are synthetically lethal in combination with molecularly targeted therapies. Additionally, the current PARP inhibitors suffer from dose-limiting toxicities, which may result from off-target effects on other members of the large PARP superfamily. As an alternative to PARP inhibitors, we used high-throughput screening to identify selective inhibitors of the human poly(ADP-ribose) glycohydrolase PARG. PARG is a monogenic enzyme that removes the poly(ADP-ribose) posttranslational modification of proteins modified by PARP1. A genetic knockdown of PARG sensitizes cancer cells to DNA damaging agents and radiation and phenocopies the tumor-specific killing effects of PARP1 enzymatic inhibitors in BRCA- deficient cancer cells. We utilize structure-guided chemical synthesis and in vitro testing, to improve the potency and selectivity of small molecule PARG inhibitors. Selected compounds are advanced to preclinical trials of tumor killing activity in cultured cells and xenograft models of breast cancer. We design and synthesize focused libraries of analogs that exploit unique features of the PARG active site and screen small molecule fragment library to identify new chemotypes and interactions that are incorporated into our inhibitor design strategy. Selective inhibitors of PARG will be useful probes of cellular responses to cancer chemotherapeutics that damage DNA, and may be useful cancer therapies in their own right by exploiting the genomic instability phenotype of many tumors. | Organic Chemistry | Yes |
| Real-Time Pathogen Surveillance for Infection Prevention and Antibiotic Stewardship | Se-Ran Jun, PhD, COM, Department of Biomedical Informatics | Antibiotic resistance (AR) ranks today as one of the most significant global health concerns, presenting challenges that affect not only individual clinics and hospitals, but also threaten worldwide public health. Hospital-acquired infections by antibiotic resistant pathogens are a significant cause of morbidity and mortality, particularly in immunocompromised patients. With a major driver of AR being antibiotic misuse, this practice both increases the rate of AR and fuels the course of transmission of these infectious agents within and between hospitals. Dr. Jun’s lab has a particular focus on genomic pathogen surveillance for infection prevention and antibiotic stewardship with goals of development of a system with 1) fast enough turnaround time and 2) discriminatory power to impact antibiotic stewardship decision and to assist in breaking transmission routes to improve interventions made by infection prevention teams. | None | Yes |
| Exploring the Role of DNA Secondary Structures in Lymphoma | Samantha Kendrick, PhD, COM, Department of Biochemistry and Molecular Biology | Our overall research goal is to identify the molecular mechanisms behind the genomic instability at critical oncogenes in lymphoma and the role DNA secondary structures may play in facilitating these genomic alterations. To address these important questions, we integrate basic and translational science using in silico, ex vivo, cell-based, and tissue-based genomic and proteomic approaches. | None | Yes |
| Preclinical modeling of cancer immunotherapy | Brian S. Koss, PhD, COM, Department of Biochemistry and Molecular Biology | The Koss lab is dedicated to unraveling the intricacies of T cell biology within the context of solid tumors. Our primary focus is on understanding the factors driving T cell dysfunction within the solid tumor environment. Our ongoing projects center around T cell metabolism, DNA repair, and protein turnover, aiming to shed light on critical aspects of T cell function. To bridge the gap between research and application, we are actively engaged in developing new immune monitoring methodologies and engineering cellular T-cell therapies. A cornerstone of our approach involves leveraging proteomics to explore the depths of T cell biology, and we offer support and training in this specialized field. Our work spans both human and mouse primary cell culture, as well as pre-clinical mouse models of cancer immunotherapy, enabling comprehensive training opportunities. Lab website: https://thekosslab.com/ | No, but Biology, Immunology, and/or Chemistry is desired. | Yes |
| The impact of diet and lifestyle on cognitive function in children | Linda J. Larson-Prior, PhD, COM, Departments of Neuroscience, Neurology, Psychiatry, Pediatrics, Biomedical Informatics, UAMS, ACNC | My laboratory is interested in better understanding the dynamic neural network re-configurations that occur as the brain develops over the lifespan, including the impact of diet, physical activity, and sleep on cognitive performance from infancy through advanced age. The laboratory uses multimodal neuroimaging methods, including electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) to help us better understand changes in brain connectivity and function over development. Connectomics and biomedical informatics approaches to the analysis of large, multi-modal datasets is an area my laboratory is actively pursuing to better understand the role of behavioral and neural state on function across the lifespan. This project focuses on understanding the neurobiological mechanisms that underlie changes in cognitive performance in children with different levels of adiposity from the perspective of body composition, physical activity and socioecomonic status. In addition to my research focus, I have a strong commitment to mentoring of students at all levels, from undergraduates (INBRE, REU programs) to graduate students and faculty. | None | Yes |
| Host Immunity to Bacterial Infections | Lin-Xi Li, PhD, COM, Department of Microbiology and Immunology | Research in my laboratory focus on understanding the protective T cell and antibody responses against Chlamydia female reproductive tract infection. To track Chlamydia-specific CD4 T cells in vivo, we developed new tools called Chlamydia-specific MHC Class II tetramers that allow for the first time direct visualization of endogenous, antigen-specific CD4 T cells during Chlamydia infection in the mouse FRT. We are also employing a variety of immunological methods, including flow cytometry and immunofluorescence imaging, in conjunction with cellular approaches and gene ablation mouse models to characterize the memory CD4 T cell responses in the FRT during Chlamydia reinfection. In addition, we recently showed that mice lacking B cells experience disseminated Chlamydia infection and develop ascites during Chlamydia primary infection. These unexpected observations lead us to actively seek the precise effector function of host B cells during initial encounter of Chlamydia at the FRT mucosa. We hope that improved understanding of host adaptive immune responses to Chlamydia infection will provide important insights into the rational design of an urgently needed Chlamydia vaccine. Li Lab Website | No | Yes |
| Virus-Host Interactions during Poxvirus Infections and Immunotherapeutics Using Poxviruses | Jia Liu, PhD, COM, Department of Microbiology and Immunology | Join us to learn about virology, Immunology, and cell biology! We use large DNA viruses, called poxviruses, to investigate how host immune response work. These powerful viruses can also effectively inhibit host responses and we study how they do that, so that we can develop ways to prevent disastrous infectious diseases caused by them. Poxviruses are also fantastic tools to study evolution on virus-host interactions. You can examine millions of years long evolution process under your eyes in short a few weeks! More importantly, by genetic manipulation we can engineer viruses to treat cancer! We learn the tricks from viruses and use them to kill cancer cells! We adopted multidisciplinary approaches for our work, which include proteomics, cell biology, molecular virology, and animal models (mouse and rabbit) to test our hypotheses and to confirm treatment effectiveness. There are so much more to learn about the host and the cool viruses. Join us, you can make differences in science and therapy! | Biology, Chemistry, or Genetics | Yes |
| Molecular Mechanisms of Intracellular Membrane Trafficking | Vladimir Lupashin, PhD, COM, Departments of Physiology and Cell Biology | How do cells deliver proteins to the right destinations—and what happens when this delivery system fails? The Lupashin Laboratory investigates the molecular machinery that organizes traffic inside human cells. We focus on the Golgi apparatus, the cell’s processing and shipping center, and the transport vesicles that carry cargo between cellular compartments. Our research examines how the Conserved Oligomeric Golgi (COG) and GARP complexes help vesicles reach their destinations and how SNARE proteins drive membrane fusion to deliver their cargo. Students can explore these questions using CRISPR/Cas9 gene editing, super-resolution microscopy, biochemical approaches, and human cell culture, including induced pluripotent stem cells. Projects connect fundamental cell biology to human health by investigating how trafficking defects disrupt protein glycosylation – the addition and processing of sugar chains essential for protein function – and contribute to inherited disorders. We also study how pathogens and toxins exploit cellular transport pathways. In our lab, students can gain hands-on research experience while investigating questions such as: How does a disease-associated mutation change the organization of the Golgi? What happens to cargo when a trafficking protein is missing? Through designing experiments, visualizing cellular structures, and interpreting results, students develop practical laboratory skills and scientific reasoning while contributing to ongoing research. Our goal is to help students experience the excitement of discovery and build a strong foundation for future careers in biomedical research and medicine. | None | Yes |
| Integrating data-mining, modeling and experimental approaches to develop safer targeted cancer therapeutics | Grover Paul Miller, PhD, COM, Department of Biochemistry and Molecular Biology | Recent advances in targeted cancer therapeutics boast superior health outcomes relative to traditional chemotherapy drugs; however, hepatotoxicity poses a major clinical concern for patients undergoing treatment with these revolutionary drugs. Drug metabolism plays a central role in toxicological mechanisms and thus, my research focuses on assessing clearance and bioactivation of drugs and subsequent biological, pharmacological and toxicological impacts on human health. In practice, my group integrates and leverages powerful analytical, biochemical, and computational tools to identify and quantitate small molecules including drugs, pollutants, and food additives during metabolism and correlate findings to biological activity and in vivo outcomes such as liver toxicity. Specific projects involve targeting drug classes prone to bioactivation for establishing a mechanism(s) to interpret and explain observed toxicity. We will assess oxidative steady-state metabolism including bioactivation of drugs using human liver microsomes as a model for the liver. This work will rely on HPLC coupled to UV/Vis, fluorescence and MS detection for quantitating metabolites and translating the data into reaction kinetics to assess metabolic fluxes down bioactivation and detoxification pathways. In subsequent studies, we will employ inhibitor phenotyping to identify potential cytochrome P450 isozymes responsible for metabolism and then carry out steady-state metabolic studies with recombinant forms of those enzymes. As an alternate, faster analysis of drug metabolism and bioactivation, we will employ deep neural network models to predict the sites and likelihood for metabolism, and then compare those findings to results from experimental studies. Knowledge gained from these studies will aid in the design and use of safer targeted cancer therapeutics by minimizing associated toxicities that limit their use in the clinic. | None | Yes |
| Investigating antidiabetic drugs as anticancer agents in colorectal cancer | Isabelle R. Miousse, PhD, COM, Department of Biochemistry and Molecular Biology | Cancer cells sense and respond to nutrients such as glucose and amino acids, using these signals to decide whether to grow and divide. Decreasing nutrient availability or blocking these nutrient-sensing pathways can slow tumor growth and improve responses to therapy. In our lab, we study how FDA-approved antidiabetic drugs (metformin, SGLT2 inhibitors, and GLP-1 receptor agonists) alter glucose signaling and colorectal tumor proliferation in mouse models of normal weight and diet-induced obesity. Our long-term goal is to repurpose safe, commonly used drugs to enhance the effectiveness of standard treatments for colorectal cancer. Students will gain hands-on experience with techniques such as RNA and protein expression analyses, as well as data analysis. Students will also participate in experimental design discussions, weekly lab meetings, and the preparation of scientific figures and presentations. This position is well suited for motivated students interested in cancer biology, metabolism, or medicine. | No | No |
| Structural and chemical biology of programmed cell death in cancer biology | Tudor Moldoveanu, PhD, COM, Department of Biochemistry and Molecular Biology | INBRE summer training program opportunities in the Moldoveanu lab: 1. Structural biology of programmed cell death proteins and their complexes. To prepare samples suitable for mechanistic investigations of our apoptotic, necroptotic, ferroptotic, and other targets of interest trainees will learn to clone, express, and purify the targets. As time permits trainees will use purified samples to perform functional biochemistry, biophysical characterization, and structural analysis using cryo-electron microscopy and X-ray crystallography. 2. Chemical biology of programmed cell death. Trainees will access the Screening and Drug Discovery Resource at UAMS Cancer Institute to perform small molecule drug discovery. Trainees will use our established workflows for early-stage drug discovery involving assay optimization for high-throughput screening (HTS), primary screening, orthogonal validation, and initial optimization of hits to identify modulators of our targets of interest. 3. Structure-guided drug discovery of programmed cell death. Trainees will learn to use cryo-EM, X-ray crystallography, and/or NMR spectroscopy to map binding and determine the structures of complexes of small molecules modulators bound to our targets of interest. Trainees will work with chemists in Dr. Darin Jones laboratory to perform cycles of structure activity relationship (SAR) involving structure elucidation–rational design–chemical synthesis to optimize small molecule modulators into preclinical therapeutic candidates. Trainees may also design proteolysis targeting chimeras (PROTACs), which link a targeted drug to an E3 ligase ligand for targeted protein degradation (TPD) of the target of interest. 4. Probing programmed cell death in cancer biology. Trainees will use cancer cell models relevant to the UAMS Cancer Institute cancer catchment area, including multiple myeloma and breast cancer cells, to probe the engagement of programmed cell death pathways using genetic engineering (e.g., CRISPR/Cas9) and targeted small molecules. Trainees will seek to identify combination strategies for effective and selective tumor killing based on established cell death assays available in the Moldoveanu lab. Genomic and proteomic profiling of successful combinations will also be pursued as time permits. | None | No |
| Bone Biology and Disease Mechanisms in Osteogenesis Imperfecta (Brittle Bone Disease) | Roy Morello, PhD, COM, Department of Physiology and Cell Biology | In my laboratory we study the function of novel genes, in particular those involved in connective tissue formation, development, homeostasis and disease, with an emphasis on the skeleton. We utilize the power of mouse gene targeting and conditional gene-inactivation techniques to generate ubiquitous or tissue-specific mutations in the mouse. With the use of cell biology, biochemistry, cell microscopy, proteomics, transcriptomics and genetic approaches we characterize the phenotype of genetically-modified mice to understand the underlying gene function. The objective is to learn from the animal model and make correlations with relevant aspects of human disease and hence gain mechanistic insights of biological function. Of particular interest is the study of the disease osteogenesis imperfecta (also known as brittle bone disease), which is most often caused by alterations in type I collagen. We aim to understand the underlying pathogenetic mechanisms that lead to low bone mass, also respiratory impairment and skeletal muscle weakness. | ||
| Skeletal Aging: Role of Autophagy and Osteocytes in age-associated bone loss | Melda Onal, PhD, COM, Department of Physiology and Cell Biology | Osteoporosis is a common bone disease in which bones become weak and brittle to a point that falls or even mild stressors such as coughing can cause fractures. Old age is the most significant risk factor for the development of osteoporosis. Several mechanisms have been proposed to contribute to age-related pathologies in various tissues. Autophagy is a proteostasis mechanism in which cellular components are recycled in lysosomes to adapt to changing nutrient conditions or clear damaged/malfunctioning/ excess cytoplasmic contents in order to maintain cellular homeostasis. A decline/dysfunction in different types of autophagy has been proposed to be a contributor of age-associated pathologies in several tissues, in particular in long-lived cell types. In our laboratory, we use a combination of in vivo and in vitro molecular and cell biology techniques to examine the contribution of different types of autophagy to age-related bone loss. In addition, as part of our quest to address mechanisms underlying age-related bone loss, we are utilizing CRISPR interference technology to develop murine loss of function models that are specific to osteocytes, the long-lived cells of bone. | None | No |
| The Role of the Mitochondrion in the Metabolic Stress Response to Burn Trauma | Craig Porter, Ph.D. COM, Department of Pediatrics | Trauma is the principle cause of unexpected death in people aged 1 to 46 years in the U.S. The annual cost of treating trauma patients exceeds the combined cost of treating cancer and heart disease patients. Burns are a leading cause of non-fatal trauma in the US. Severe burns result in a devastating metabolic stress response that causes long-term morbidity and reduced quality of life in burn survivors. Hypermetabolism (increased energy expenditure), cachexia, hepatomegaly, and immune dysfunction are all hallmarks of the metabolic stress response to burns. Recent evidence suggests a central role of the mitochondrion in this stress. The goal of this research program is to advance our understanding of the role of the mitochondrion in the metabolic stress response to burn trauma. By leveraging innovative animal models and studying patients, our long-term objective is to generate new knowledge that will aid in the development of strategies that reduce suffering and promote the recovery of burn survivors. | None | No |
| Mechanisms of Action of DNA and RNA Helicases | Kevin D. Raney, PhD, COM, Department of Biochemistry and Molecular Biology | The Raney laboratory is studying the mechanisms of action of DNA and RNA helicases in work that is funded by the National Institutes of Health. These enzymes manipulate DNA and RNA and enable replication and repair of genomes. Another project is focused on non-canonical forms of DNA, such as quadruplex DNA. Biochemical and molecular biological techniques are used for in vitro and cellular experiments. | General Chemistry, Organic Chemistry | No |
| Genetic and Metabolomic Predictors of Longevity and Age-Associated Diseases | Robert J. S. Reis, DPhil, Departments of Geriatrics and Biochemistry & Molecular Biology at UAMS and the McClellan Veterans Medical Center (CAVHS) | We have an NIH Program Project grant to quantitate metabolite levels and measures of metabolic activity and damage, as well as the status of antioxidant defenses. We will use these to formulate robust predictors of future longevity in young adults, for a variety of model systems in which life span can be extended markedly by genetic or dietary means. We will then seek common “fingerprints” indicative of future survival that may extrapolate to humans. A database will be developed and a variety of means of data mining will be employed to interrogate it. In the near future, we also plan to develop databases comprising a panel of measures (both those of known clinical prognostic value, and some of the novel markers developed in our model systems), monitored in healthy human subjects. We can thus look for new markers that correlate well with established biomarkers, and evaluate the application of these metabolic profiles to predicting susceptibility to common diseases and conditions associated with reduced fitness (e.g., obesity, diabetes/impaired glucose tolerance, cancer, high blood pressure, and cardiovascular impairment). | None. Prior courses and/or experience with databases and/or data mining are desirable but not essential. | Yes |
| Translational Brain Tumor Research | Analiz Rodriguez, MD, PhD, COM, Department of Neurosurgery | My laboratory focuses on the development of therapeutics for brain tumor treatment. We have integrated multiple omics platforms (i.e. genomics, transcriptomic, and proteomics) to identify therapeutic targets. I established a precision medicine platform in our department in which all patients receive prospective sequencing of their brain tumor. I am also developing patient derived organoid modeling to test therapeutics. | No | No |
| Role of Rho GTPases in cell migration and invasion | Katie R. Ryan, PhD, COM, Department of Biochemistry and Molecular Biology | Our laboratory focuses on the identification of molecular mechanisms and signaling pathways involved in Rho GTPase signaling. Rho family GTPases act as ‘molecular switches’ and are master regulators of many aspects of cellular behavior including regulation of the actin cytoskeleton, gene expression, cell cycle, cell migration, and apoptosis. Many cellular processes regulated by Rho GTPases, are commonly dysregulated in cancer. We are currently focusing on the role of Rho GTPases in cell migration and invasion in several in vitro cancer models including breast and lung cancer. We utilize common molecular and cellular biology techniques as well as proteomic approaches to identify novel therapeutic targets of metastasis. | None | Yes |
| Epigenetic Mechanisms of pain chronicity | Kimberly E. Stephens, MPH, PhD, COM, Department of Neuroscience | Research in the Stephens laboratory focuses on improving our understanding of the epigenetic basis for inter-individual differences in an individual’s susceptibility to chronic pain. Specifically, we are interested in the identification and functional consequences of changes in chromatin accessibility at cis-regulatory regions promote transcription and cellular response. We use surgical and non-surgical rodent models to study inflammatory and neuropathic pain conditions including cancer-related pain. We assess mechanical and thermal pain behaviors in these models including the evaluation of pharmaceutical and electrophysical treatment to alleviate pain. We routinely use bulk and single sequencing based assays and well-established biostatistical methods to preprocess and comprehensively analyze next-generation sequencing data. We complement these approaches with a variety of molecular biology approaches using in vitro, ex vivo, and in vivo systems and necessary collaborations to comprehensively evaluate phenotypic changes that alter cellular function. | No | Yes |
| Cellular Mechanisms of Antibody-mediated Immunity against Plasmodium Infection | Jason Stumhofer, PhD, COM, Department of Microbiology and Immunology | The Stumhofer laboratory studies basic elements of the immune response against the malaria parasite Plasmodium. Using rodent models of infection we are conducting studies to determine the cellular requirements for the development of antibody-mediated protective immunity to Plasmodium. Also, we are interested in determining how and when memory B cells are formed after Plasmodium infection, and their contribution to protection upon secondary infection. Collectively, our studies will provide valuable information regarding the cellular events that contribute to protective immunity against malaria that will be vital for effective vaccine development. | Microbiology | No |
| Anti-cancer Activity of Derivatives of Natural Products | Alicja Urbaniak, MSc, PhD, COM, Department of Biochemistry and Molecular Biology | Research interests in the Urbaniak Lab lie at the interphase of chemistry and cancer biology. Our Lab intends to tackle the most pressing issues in cancer biology – how to target and therapeutically intervene to disrupt cancer stem cell functionality (self-renewal, drug resistance, tumor recurrence after therapy, and metastatic spread to distant organs). The lab is especially interested in breast cancer biology and discovery of novel small molecules with anti-breast cancer properties. We are particularly focused on the anti-cancer stem cell activity of polyether ionophore antibiotics and their derivatives. currently the lab is developing 3D tumor organoid models to better mimic tumor architecture and to facilitate rapid screening of small molecule drug candidates selectively active against cancer stem cells. | None | No |
| Mechanisms of Intracellular Bacterial Pathogenesis | Daniel E. Voth, PhD, COM, Department of Microbiology and Immunology | The Voth laboratory is focused on understanding mechanisms used by intracellular bacterial pathogens to parasitize host cells and cause pulmonary disease. Specifically, we are studying Coxiella burnetii, which causes human Q fever, an acute debilitating flu-like illness that also presents as life-threatening chronic endocarditis. We are currently studying host signaling pathways manipulated by C. burnetii to generate an intracellular replication compartment with lysosomal features. Additionally, we are characterizing secreted C. burnetii proteins that influence host processes during infection and are predicted to be major virulence factors. We are using a primary human lung infection system to dissect the complex interplay between pulmonary bacterial pathogens and humans. | Cell Biology or Biochemistry | No |
| Understanding and overcoming gastrointestinal bacterial infections | Miranda Wallace, PhD, COM, Department of Microbiology and Immunology | The Wallace Lab is interested in exploring how we can harness bacteria and yeast to better understand and overcome antibiotic-resistant infections that occur within or arise from the gastrointestinal (GI) tract. We have two major research areas. The first research area explores how we can genetically engineer probiotic yeast to deliver protein-based therapeutics to the GI tract to treat bacterial GI infections. The second research area is focused on uncovering mechanisms of antibiotic resistance in Bacteroides fragilis group bacteria using a functional genomics screen. Trainees will have the opportunity to learn a wide variety of techniques including molecular biology, anaerobic microbiology, tissue culture assays, animal models of disease, and microbial genomics. | No | Yes |
| The Platelet Paradigm in Thrombosis, Inflammation and Cancer | Jerry Ware, PhD, Department of Physiology and Cell Biology | The Ware laboratory studies fundamental aspects of platelet biology to elucidate their role of in hemostasis, thrombosis, and inflammation. Since platelets are anucleate fragments of cytoplasm, in vivo models are used based on the hypothesis that the unique cellular characteristics of megakaryocytes and platelets require the correct in vivo environment for meaningful assessment of biological properties. Currently, we are characterizing the platelet’s role in modulating the inflammatory processes associated with sepsis. The clinical management of sepsis remains a challenging and difficult problem and the goal of our work is better understand the complex pathophysiology associated with sepsis. | None | Yes |
| Role of Infant Diet in Gastrointestinal Tract Development and Immune Function | V. Laxmi Yeruva, PhD, USDA-ARS, SEA, Microbiome and Metabolism Research Unit (MMRU), Arkansas Children’s Nutrition Center (ACNC) | Gut microbiota has been shown to influence allergies, obesity, gastrointestinal dysbiosis, and immuno-metabolic health outcomes in mothers and children. Recent evidence suggests that maternal factors (i.e., diet quality, stress, lifestyle, obesity, delivery mode), and postnatal factors (i.e., feeding mode, lifestyle) affect gut microbiota and in turn influence infants’ health and risk for non-communicable diseases. However, there is a critical gap in the literature on how these factors might individually or in a synergistic manner work to alter gut microbiota composition and function, and further program physiological systems (i.e., placenta, gut, immune system, liver, bone, and brain) to optimize growth and development in children. In addition, gut microbiota is known to be impacted by dietary intake; however, a knowledge gap exists in understanding complex biological factors/food interactions that influence health outcomes. Our goal is to determine the prenatal and/or early life factors (i.e. diet, physical activity, stress, and environment) impact on gut microbiome composition and function and its impact on maternal-child health outcomes. We leverage clinical studies, animal models (i.e., conventional and germ-free mouse model and rat model) and in vitro tissue culture models to address our research goals. | No | Yes |
| Study of Multiple Myeloma Progression and Bone Metabolism Using Cancer Cells and Animal Models | Donghoon Yoon, PhD, Myeloma Institute | Multiple myeloma (MM) is a B cell cancer characterized by the proliferation of malignant plasma cells in the bone marrow, the presence of monoclonal serum immunoglobulin, and bone lesions. Previous studies demonstrate that bone de-structuring is highly related to Myeloma progression. Our laboratory is studying the effects of various bone-forming factors on bone metabolism and MM progression using cell lines and animal models. Trainees in my laboratory will learn cell culture, cell proliferation assays with drug treatment, monitoring drug-treated mice, and their effects on MM progression using in vivo mouse imaging techniques. | Cell Biology | Yes |