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Computational Genomics

Research using computational genomics approaches or development of computational tools for use in biomedical research.

Labs in This Area

 Mohamed Abazeed Lab

Individualize cancer care (radiotherapy) by helping physicians recommend treatments based on the genetic and imaging features of individual tumors.

Research Description

Mohamed E Abazeed, MD, PhD
Mohamed E Abazeed, MD, PhD

Precision oncology facilitates individualized treatment decisions on the basis of patient and tumor specific factors for an increasing proportion of cancer patients. Despite growing evidence that inter-patient variation affects treatment responses after radiotherapy, patients receiving these treatments continue to be treated with the same or similar doses. We seek to develop an information capability at the forefront of personalized radiotherapy treatments. We achieve this through the assembly of experimental scaffolds that span the translational research spectrum and help us understand tumor complexity and predict clinical outcomes.

Briefly, we conduct large-scale projects that capture the diversity of our patients and provide a rich substrate for computational and mathematical models of cancer’s propensity to resist our treatments. Three large-scale projects have been completed or are currently in progress including: 1) The X-ray Target Discovery and Development (XTD2) project, which profiled 533 cancer cell line survival  comprising 26 cancer types to ionizing radiation. This project represented the largest profiling effort of cancer cell line survival after irradiation ever conducted. 2) The Pan-cancer Radiogenomic Atlas is a gene variant profiling project that interrogated >1000 common and rare genetic variants for response to ionizing radiation in immortalized human cells (non-cancer cells). Current work is building on the unary profiling methodology to study the interaction between varied gene variants, thus building toward greater complexity. 3) The 10,000 Avatar Project was inaugurated by our group in 2019. This will be the largest patient-derived xenograft (PDX) mouse experiment conducted to date by any group. ~10,000 mice engrafted with ~500 genetically annotated PDXs will be irradiated using a singular experimental platform. This work will correlate genetic and other omic (e.g. transcriptomic, metabolomic, et cetera) alterations with the likelihood of response to radiotherapy and matched recurrent tumors.

Concurrent with the large-scale biological profiling approaches described above, we have developed a clinomic dataset that integrates clinical information (e.g. demographics, treatments, outcomes) and patient avatar models (patient-derived xenografts) with omic outputs for individual patients. The latter include radiomics (embedded quantitative data derived from imaging modalities like computed tomography), genomics (genetic information derived from the patient’s tumor or germline), transcriptomics (gene expression), and others. Using this information, we seek to design and implement tools that can augment the physician’s ability to estimate the probability of treatment failures and modulate failure by individualized treatment recommendations.

For lab information and more, see Mohamed Abazeed's, MD,PhD, faculty profile.

Publications

See Dr. Abazeed's publications in PubMed.

Contact

Contact the Abazeed Lab at 312-503-2195. You may also contact Dr. Abazeed directly via email.

Post-doctoral Fellows

Priyanka Gopal, Rohan Bareja

Students

Alexandru Buhimschi

Technical Staff

Titas Bera, Dylan Schellenberg, Trung Hoang

 Mazhar Adli Lab

Studying how to prevent cancer development and chemotherapy resistance using genomic and epigenomic approaches

Research Description

I am interested in understanding the key drivers of cancer and identifying novel therapeutic drug combinations to prevent cancer development and chemotherapy resistance. To achieve these goals, our lab is using and developing genomic and epigenomic mapping, editing and imaging approach to understand genome regulation in normal and malignant settings. We integrate experimental approaches with large-scale computational data analysis to verify our experimental observations and come up with new testable hypotheses.  Our laboratory is utilizing and also developing cutting-edge functional genomics strategies and developing novel CRISPR based manipulation tools to understand dynamic gene regulation and 3D genome organization in normal and malignant settings. These efforts are based on our previous expertise in genome-wide approaches and development of novel technologies for cancer research. Our lab has developed particular expertise in utilizing and developing CRISPR based technologies.

For more information, see Dr. Adli's faculty profile or the Adli lab website.

Publications

See Dr. Adli's publications in PubMed.

 

Contact Us

Dr. Adli

 Daniel Arango Lab

Post-transcriptional RNA modifications in protein synthesis, proliferative disorders and stress conditions

 

Research Description

Our laboratory investigates the mechanisms by which post-transcriptional modifications of RNA, also known as the epitranscriptome, regulate protein synthesis and how these mechanisms go awry in proliferative disorders and stress conditions. By integrating RNA biology, genomics, cell biology, and animal models, our research program will potentially uncover novel mechanisms of gene expression regulation and their contributions to disease as well as generate new tools and methods that can be harnessed for therapeutic means. 

For more information, see Dr. Arango's faculty profile.

Publications

See Dr. Arango's publications in PubMed.

Contact

Dr. Arango

 Daniel Brat Lab

Mechanisms Underlying Glioblastoma Progression and Regulators of Asymmetric Cellular Division in Glioblastoma Stem Cells

Research Description

Mechanisms Underlying Glioblastoma Progression
We investigate mechanisms of progression to glioblastoma (GBM), the highest grade astrocytoma, including genetics, hypoxia, and angiogenesis. Progression is characterized by tumor necrosis, severe hypoxia and microvascular hyperplasia, a type of angiogenesis. We propose that vaso-occlusion and intravascular thrombosis within a high grade glioma results in hypoxia, necrosis and hypoxia-induced microvascular hyperplasia in the tumor periphery, leading to neoplastic expansion outward. Since the pro-thrombotic protein tissue factor is upregulated in gliomas, we investigate mechanisms of increased expression and pro-coagulant effects.

In Silico Brain Tumor Research
We initiated an In Silico Center for Brain Tumor Research to investigate the molecular correlates of pathologic, radiologic and clinical features of gliomas using pre-existing databases, including as TCGA and Rembrandt. Using datasets and image analysis algorithms, we study whether elements of the tumor micro-environment, such as tumor necrosis, angiogenesis, inflammatory infiltrates and thrombosis, may correlate with gene expression subtypes in TCGA gliomas. We also have demonstrated the clinical relevance of TCGA subclasses within the lower grade gliomas using the Rembrandt dataset.

Regulators of Asymmetric Cellular Division in Glioblastoma Stem Cells
We study mechanisms that confer specialized biologic properties to glioma stem cells (GSC) in GBM. The Drosophila brain tumor (brat) gene normally regulates asymmetric cellular division and neural progenitor differentiation in the CNS of flies and, when mutated, leads to a massive brain containing only neuroblastic cells with tumor-like properties. We study the human homolog of Drosophila brat, Trim3, for its role in regulating asymmetric cell division and stem-like properties in GSCs. Trim3 may elicit its effects is through repression of c-Myc.

For more information, visit the faculty profile of Daniel Brat, MD, PhD or the Brat Lab website.

Publications

See Dr. Brat's publications in PubMed.

Contact

Email Dr. Brat

 Gemma Carvill Lab

Genetic causes and pathogenic mechanism that underlie epilepsy

Research Description

The primary goal of our research is to use gene discovery and molecular biology approaches to identify new treatments for epilepsy. We aim to 1) identify the genetic causes of epilepsy, 2) use stem cell models to understand how genetic mutations can cause epilepsy, 3) develop and test new therapeutics for this condition. Our work is based on the promise of precision medicine where knowledge of an individual’s genetic makeup shapes a personalized approach to care and management of epilepsy.

Current Projects

  • Next generation sequencing in patients with epilepsy
  • Alternative exon usage during neuronal development
  • Identify the regulatory elements that control expression of known epilepsy genes
  • Stem cell genetic models for studying the epigenetic basis of epilepsy

For more information, see Dr. Carvill's faculty profile or the Carvill Lab Website.

Publications

Please see Dr. Caraveo Piso's publications on PubMed.

Contact Information

Gemma L. Carvill, PhD

 Rex Chisholm Lab

Studying molecular motors and cell motility

Research Description

Movement is a fundamental characteristic of life. Cell movement is critical for normal embryogenesis, tissue formation, wound healing and defense against infection. It is also an important factor in diseases such as cancer metastasis and birth defects. Movement of components within cells is necessary for mitosis, hormone secretion, phagocytosis and endocytosis. Molecular motors that move along microfilaments (myosin) and microtubules (dynein) power these movements. Our goal is to understand how these motors produce movement and are regulated. We wish to define their involvement in intracellular, cellular and tissue function and disease—with the long-term goal of developing therapies for the treatment of diseases caused by defects in these molecular motors.

Our work involves the manipulation of myosin and dynein function in the single celled eukaryote Dictyostelium, cultured mammalian cells and transgenic and knockout mice. Yeast two-hybrid screens to identify proteins that interact with or regulate myosin and dynein and characterization of gene expression are being used to define the pathways regulating myosin and dynein. To analyze the biological significance of myosin and dynein, we use confocal and digital microscopy of living cells, analysis of cell movement, vesicle transport and cell division. We employ biochemical techniques including heterologous expression, enzyme purification and characterization and analysis of how phosphorylation state affects physiological function. We are pursuing signal transduction studies to understand the physiologically important pathways that regulate cell motility and biophysical studies such as in vitro motility assays to understand how these molecular motors function at the molecular level.

For lab information and more, see Dr. Chisholm's faculty profile.

Publications

See Dr. Chisholm's publications on PubMed.

Contact

Contact Dr. Chisholm at 312-503-3209.

 Jaehyuk Choi Lab

Genetic basis of inherited and acquired immunological disorders and skin cancer.

Research Description

We employ cutting-edge genomics approaches to identify the genetic basis of inherited and acquired immunological disorders and skin cancer.

As an example, we have recently identified the genes and mutations underlying cutaneous T cell lymphoma, an incurable non-Hodgkin lymphoma of skin-homing T cells. The genes are components of the DNA damage, chromatin modifying, NF-kB and the T cell receptor signaling pathways. We are currently employing a comprehensive approach using human tissues and animal models to investigate the functions of these genes. We are confident these studies will allow us to elucidate the pathophysiology of this cancer and lead to the identification of novel therapeutic targets.

Work in the lab is funded by National Cancer Institute, Dermatology Foundation, American Skin Association and American Cancer Society. For further information, please also see Dr. Choi's faculty profile.

Publications

See Dr. Choi's publications on PubMed.

Contact

Contact Dr. Choi.

 Lee Cooper Lab

Developing software algorithms and research infrastructure for computational pathology

Our research develops computational approaches to analyze data generated in the pathology lab. Our goal is to improve diagnostics, to advance clinical translation of computational pathology research, and to provide investigators with tools to generate new insights from complex data. To accomplish these goals we focus on:

  1. Fundamental research in machine-learning and artificial intelligence
  2. Development of software infrastructure for computational pathology
  3. Generating annotated datasets for training and validation of computational pathology algorithms

We apply these techniques to a number of problems including:

  1. Measuring immune response in cancer and development of immuno-oncology biomarkers
  2. Prediction of clinical outcomes from genomic and digital pathology data
  3. Classification of hematologic malignancies

 Richard Gershon Lab

Health care outcome assessments

Research Description

Dr. Gershon is a leading expert in the application of Item Response Theory (IRT) in individualized and large scale assessments. He has developed item banks and Computerized Adaptive Testing (CAT) for educational, clinical, and health applications - including cognitive, emotional, and motor applications. He is currently principal investigator on these projects with the NIH: NIH Toolbox for the Assessment of Neurological Function and Behavior, the NIH Roadmap Patient – Reporting Outcomes Measurement Information System (PROMIS) Technical Center, the National Institutes on Aging Genetic Norming project, and the National Children's Study: Vanguard Study(South ROC). He is also co-investigator and measurement development expert on numerous smaller projects including the NINDS sponsored project “Quality of Life Outcomes in Neurological Disorders” (Neuro-QOL), and the cancer-specific supplement to PROMIS.

For more information visit the faculty profile of Rich Gershon, PhD.

Publications

See Dr. Gershon's publications in PubMed.

Contact

Dr. Gershon

 Jeffrey Goldstein Lab

Placental diagnosis and deep phenotyping using machine learning and artificial intelligence.

Research Description

Area: Placenta diagnosis and deep phenotyping by machine learning:
Diagnosis of placental abnormalities relies on microscopic examination of glass slides. Digitizing the slides to form whole slide images opens several avenues for applying machine learning techniques. Avenues of research include studies to improve interobserver reliability, decrease vulnerability to artifacts, aid humans in diagnosing, and produce explainable predictions. Machine learning techniques can be used to probe basic problems in placental biology and pathophysiology, quantifying changes that evade routine human detection.
Area: Placental diagnosis using AI on placental photographs:
 Placental examination can provide insight into future maternal and child health, but preparation of slides and expert examination are expensive and time consuming. Many diagnoses can be made in whole or in part from the photographic appearance of the placentas. An AI algorithm, installed on smart phones, could make placental examination feasible for all births, everywhere. Bioinformatic studies of electronic health records can identify new associations between placental features and outcomes.

For lab information and more, see Jeffrey Goldstein, MD,PhD, faculty profile.

Publications

See Dr. Goldstein's publications

Contact

Email Dr. Goldstein

 

 Richard Green Lab

The Green Lab investigates the genetics and molecular biology of cholestatic liver diseases and fatty liver disorders. The major current focus is on the role of ER Stress and the Unfolded Protein Response (UPR) in the pathogenesis of these hepatic diseases.

Dr. Green’s laboratory investigates the mechanisms of cholestatic liver injury and the molecular regulation of hepatocellular transport. Current studies are investigating the role of the UPR in the pathogenesis and regulation of hepatic organic anion transport and other liver-specific metabolic functions. We employ genetically modified mice and other in vivo and in vitro models of bile salt liver injury in order to better define the relevant pathways of liver injury and repair; and to identify proteins and genes in these pathways that may serve as therapeutic targets for cholestatic liver disorders.

The laboratory also investigates the mechanisms of liver injury in fatty liver disorders and the molecular regulation of hepatic metabolic pathways. The current focus of these studies includes investigations on the role of the UPR in the pathogenesis of non-alcoholic steatohepatitis and progressive fatty liver disease. We employ several genetically modified mice and other in vivo and in vitro models of fatty liver injury and lipotoxicity. Additional studies include the application of high-throughput techniques and murine Quantitative Trait Locus (QTL) analysis in order to identify novel regulators of the UPR in these disease models.  

Publications

See Dr. Green's publications in PubMed.

For more information, please see Dr. Green's faculty profile.

Contact

Contact Dr. Green at 312-503-1812 or the Green Lab at 312-503-0089

 Alan Hauser Lab

Pathogenesis of Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae infections

Research Description

Our laboratory investigates the pathogenesis of the gram-negative bacteria Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae. We focus on virulence factors such as the type III secretion, an apparatus that injects toxins directly into host cells. A second interest is the use of genomic approaches for the identification of novel virulence determinants. Our studies utilize a broad range of techniques, including molecular and cellular assays as well as animal models and epidemiologic studies on human populations.

For lab information and more, see Dr. Hauser's faculty profile and lab website.

Publications

See Dr. Hauser's publications on PubMed.

Contact

Contact Dr. Hauser at 312-503-1044 or the lab at 312-503-1081.

Lab Staff

Postdoctoral Fellows

Kelly Bachta, Travis Kochan, Sumitra Mitra, Timothy Turner

Graduate Students

Bettina Cheung, Marine Lebrun Corbin, Nathan Pincus

Lab Manager

Shradha Rao

Technical Staff

Sophia Nozick

 Lifang Hou Lab

Environmental, genetic and epigenetic risk factors for disease

Research Description

Dr. Hou’s research interest lies in integrating traditional epidemiologic methods with the ever-advancing molecular techniques in multi-disciplinary research focusing on identifying key molecular markers and understanding their potential impact on disease etiology, detection and prevention.

Dr. Hou’s major research efforts to date have focused on two areas: 1) identification of risk factors that may cause chronic diseases; and 2) identification of biomarkers that serve as indicators of an individual’s past exposure to disease risk factors and/or predict future disease risks and/or prognosis. The environmental/lifestyle risk factors that Dr. Hou has studied include air pollution, pesticides, overweight, physical inactivity and reproductive factors in relation to chronic diseases. The biomarkers that Dr. Hou has investigated include genetic factors (i.e., polymorphisms, telomere length shortening, mitochondria DNA copy number variations) and epigenetic factors (i.e., DNA methylation, histone modifications and microRNA profiling). Her over-arching research goal is to understand the biological mechanisms linking environmental risk factors with subclinical or clinical disease development to ultimately lead to development of effective strategies for prevention of chronic diseases.

In addition to being a PI of several NIH funded grants, Dr. Hou is the co-director and Co-PI of the Northwestern Consortium for Early Phase Cancer Prevention Trials of the Division of Cancer Prevention (DCP) Consortia, National Cancer Institute.

For more information visit the faculty profile of Lifang Hou, MD, PhD.

Publications

See Dr. Hou's publications in PubMed.

Contact

Dr. Hou

 Zhe Ji Lab

Dissecting the regulation of gene transcription and RNA translation underlying oncogenic processes.

Research Description

Cancer happens through accumulated genetic mutations and epigenetic alternation in normal cells. With the advances of genomic technologies, we now can precisely characterize the genome-wide alternations of gene expression underlying oncogenic processes in a cost-effective and unbiased manner. My lab will use the combined experimental genomic technologies and computational modeling to examine the regulation of gene transcription and RNA translation during steps of oncogenesis. We aim at revealing novel cancer therapeutic targets and strategies for precision medicine and immunotherapy.

Current Projects

Currently, we are working on the following projects.

  • Characterizing the transcriptional regulatory circuits mediating inflammation in the cancer microenvironment.
  • Examining the genome-wide regulation of RNA translation in cancers.
  • Defining the functional roles of non-canonical translation in lncRNAs, pseudogenes and 5’UTRs in cancers.

For lab information and more, see Dr. Ji's faculty profile.

Publications

See Dr. Ji's publications on PubMed.

Contact

Contact Dr. Ji at 312-503-2187.

Lab Staff

Postdoctoral Fellows

Qianru Li, Haiwang Yang

Graduate Students

Emily Stroup, Sheng Wang

 Jennie Lin Lab

The Lin lab studies the functional significance of human-based genomic and transcriptomic discoveries in cardiometabolic and kidney diseases.

Research Description

Elucidating How Genotype Lease to Phenotype in Cardiometabolic and Renal Disease

Unbiased human-based discovery efforts, such as genome-wide and exome-wide association studies, have identified many genetic loci for complex, disease-relevant traits. These genetics studies have provided invaluable data implicating novel loci in disease development and progression, but require functional follow-up to elucidate the mechanistic underpinnings driving the associated findings. A focus of the lab is to interrogate, through experimental wet-bench approaches, the functional significance of novel loci for blood lipids levels and measurements of renal function in the hopes of gaining new insights into pathways relevant to cardiometabolic and renal disease, respectively.

In particular, we are studying the role of A1CF, a gene encoding the RNA-binding protein APOBEC1 complementation factor and recently implicated as a locus for (1) elevated plasma triglycerides (Liu et al., Nature Genetics 2017), (2) estimated glomerular filtration fraction in non-diabetic individuals (Pattaro et al., Nature Communications 2016) and (3) serum urate (Kottgen et al., Nature Genetics 2013). We have already discovered that A1CF's actions extend beyond its canonical role of facilitating the editing of APOB mRNA, and we are currently integrating studies using animal and human cellular models to investigate how A1CF contributes to these associated traits.

Using iPSC and Genome Editing Technologies to Study Human Diseases

Although rodent models have contributed greatly to our understanding of human diseases, the genomic and physiologic differences between rodent and human have presented challenges in translating bench-based findings into clinic. To circumvent this roadblock, our lab is using iPSC-derived organoid models to study the effects of DNA variants within the native human genomic context. Using CRISPR-based technology to introduce or correct mutations in human iPSCs, we are modeling the effects of disease-associated mutations on cellular phenotype.

RNA-centric Approach to Studying Kidney Disease

Building upon A1CF-related work and previous experience with long non-coding RNA, we are studying the role of transcriptome-level regulation in the context of kidney disease. We have discovered that A1CF is a novel regulator of alternative splicing in both the liver and kidney, and we are currently working on how A1CF's regulation of splicing may influence intracellular metabolism. We are also studying how human-specific long non-coding RNAs influence gene expression and cellular phenotypes.

For more information, visit the Faculty Profile of Jennie Lin or visit the Lin Lab Website

Publications

See Dr. Lin's publications in PubMed.

Contact

Email Dr. Lin

Phone 312-503-1892

 Yuan Luo Lab

Machine learning, natural language processing, time series analysis, integrative genomic analysis and big data analytics, with a focus on medical and clinical applications

Research Description

Dr. Luo is the Chief AI Scientist at Northwestern University Clinical and Translational Sciences Institute (NUCATS).

For more information visit Dr. Luo's faculty profile page

Contact

Email Dr. Luo

Phone 312-908-7914

 Yong-Chao Ma Lab

Regulation of Motor Neuron and Dopaminergic Neuron Function in Development and Disease

Postdoctoral fellow jobs and graduate student rotation projects are available.

Research Description

Spinal Motor Neurons and Spinal Muscular Atrophy (SMA)

SMA is characterized by the selective degeneration of spinal motor neurons. As the leading genetic cause of infant mortality, SMA affects one in every eight thousand live births. Our group is interested in studying mechanism regulating motor neuron development and function, as well as why motor neurons specifically degenerate in SMA. To address these questions, we use a combination of genetic, biochemical and cell biological approaches and utilize genetically modified mice, induced pluripotent stem (iPS) cells reprogrammed from fibroblasts and zebrafish as model systems. We focus on the regulation of mitochondrial functions in SMA pathogenesis. Based on our findings, we hope to develop new therapeutic strategies for treating SMA.

 
Dopaminergic Neurons and Parkinson's Disease

Dopaminergic neurons located in the ventral midbrain control movement, emotional behavior and reward mechanisms. Dysfunction of these neurons is implicated in Parkinson’s disease, drug addiction, depression and schizophrenia. Our group is interested in the genetic and epigenetic mechanisms regulating dopaminergic neuron functions in disease and aging conditions. We are particularly interested in how aging and mitochondrial oxidative stress contribute to dopaminergic neuron degeneration in Parkinson's disease through transcriptional and epigenetic regulations. We use mouse models, cultured neurons and iPS cells for these studies.

For more information visit Dr. Ma's faculty profile and Dr. Ma's lab website within the Children's Hospital Research Center.

Publications

View Dr. Ma's publications at PubMed

Contact

Email Dr. Ma

Phone 773-755-6339

Lab Staff

Nimrod Miller, PhD, Postdoctoral Fellow

Han Shi, Graduate Student

Brittany Edens, Graduate Student

Kevin Park, Graduate Student

Monica Yang, Undergraduate Student

Aaron Zelikovich, Undergraduate Student

 Aline Martin Lab

The Martin Lab investigates the role of the skeleton in the endocrine regulation of mineral metabolism and the cardiovascular complications of mineral and bone diseases.

Our research program focuses on the contribution of the skeleton to the mineral balance in the body.  Bone produces a hormone, Fibroblast Growth Factor (FGF)-23, that participates in this balance.  However in mineral metabolism disorders, such as in chronic kidney disease, the massive production of FGF23 is associated with negative outcomes and mortality.  By understanding the mechanisms that control the production of FGF23, our goal is to develop new therapeutic strategies and improve outcomes in mineral metabolism disorders.  To this goal, we perform basic and translational research using a combination of genetics, molecular biology, proteomics, histology and advanced imaging techniques. 

A major focus of the lab is to investigate the transcriptional and post-translational regulation of FGF23 within the bone cells.  In particular, we study the specific role of a known regulator of FGF23, Dentin Matrix Protein 1 (DMP1), on these regulations and on osteocyte biology in the context of diseases associated with FGF23 excess (chronic kidney disease, hypophosphatemic rickets …).  A second focus is to investigate the mechanisms involved in negative outcomes associated with FGF23 excess, including bone mineralization defects, cardiac hypertrophy and cognitive defects.  Our team works in collaboration with the Center for Translational Metabolism and Health and the Division of Cardiology at Northwestern, and with multiple additional collaborators and partnerships around the world.

The Martin Lab is sponsored by the National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and by the Northwestern Women’s Health Research Institute.

Publications

For more information view Dr. Martin's Faculty Profile or  view publications by PubMed

Contact Us

Contact Dr. Martin at 312-503-4160 or the Martin Lab at 312-503-4805, or by email.

 Elizabeth McNally Lab

Genetic mechanisms responsible for inherited human diseases

Research Description

My laboratory studies genetic mechanisms responsible for inherited human diseases including heart failure, cardiomyopathy, muscular dystrophy, arrhythmias, aortic aneurysms. Working with individuals and families, we are defining the genetic mutations that cause these disorders. By establishing models for these disorders, we can now begin to develop and test new therapies, including genetic correction and gene editing.


For lab information and more, see Dr. McNally's faculty profile or visit the McNally Laboratory site.

Publications

See Dr. McNally's publications on PubMed.

Contact

Email Dr. McNally

Phone  312-503-5600

 Joshua Meeks Lab

Investigating genetic and epigenetic changes in bladder cancer, as well as immuno-oncology in bladder cancer

Research Description

The Meeks lab is investigating the epigenetics and genetic mutations associated with cancer biology. Specifically, he is studying how chromatin remodeling genes play a role in bladder cancer. In addition, he is investigating the “driver mutations found in bladder cancer. In the future, he hopes to develop novel systemic and intravesical therapies to improve survival of patients with bladder cancer.

In the United States, there are an estimated 72,570 new cases of bladder cancer each year. Dr. Meeks is conducting innovative research to increase our understanding of the biology of bladder cancer and to identify new therapies and technologies for bladder cancer in order to improve quality of life for our patients. In this podcast, Joshua Meeks, MD, PhD, shares how his team of scientists are involved in three active trials focused on genetic and epigenetic changes in bladder cancer, as well as immuno-oncology in bladder cancer. Listen here>>

Dr. Meeks is investigating the gender disparities in bladder cancer by dissecting the tumor and immune mechanisms of resistance to chemotherapy and immunotherapy. This research may translate into novel pathways and potential therapeutic targets to improve outcomes and reduce gender disparities in bladder cancer. In this video, Meeks shares details about his work. Watch here>>

Select Publications

Meeks JJ, Robertson AG. Immune Signatures Dominate Molecular Subtyping to Predict Response to Neoadjuvant Immunotherapy. European Urology. June 2020.

Robertson AG, Groeneveld CS, Jordan B, Lin X, McLaughlin KA, Das A, Fall LA, Fantini D, Taxter TJ, Mogil LS, Lindskrog SV, Dyrskjøt L, McConkey DJ, Svatek RS, de Reyniès A, Castro MAA, Meeks JJ. Identification of Differential Tumor Subtypes of T1 Bladder Cancer. European Urology. January 2020.

Fantini D, Glaser AP, Rimar KJ, Wang Y, Schipma M, Varghese N, Rademaker A, Behdad A, Yellapa A, Yu Y, Sze CC, Wang L, Zhao Z, Crawford SE, Hu D, Licht JD, Collings CK, Bartom E, Theodorescu D, Shilatifard A, Meeks JJ. A Carcinogen-induced mouse model recapitulates the molecular alterations of human muscle invasive bladder cancer. Oncogene. April 2018.

Refer to PubMed for a full list of publications. 

Email Dr Meeks

Phone 312-695-8146

 Marc Mendillo Lab

Cellular stress response systems in malignancies

Research Description

The cellular stress response systems guard the proteome from diverse endogenous and environmental insults to maintain the fitness of the organism. Ironically, this pro-survival system can act to the detriment of the host to enable tumor cells accommodate to the myriad stresses associated with malignancy. Our long-term goals are to identify and characterize the systems that promote protein homeostasis, understand how these systems are co-opted and perturbed in malignancy, and ultimately identify means to manipulate them for therapeutic benefit. To accomplish these goals our group bridges biochemical, genetic and chemical biology approaches with systematic high-throughput and genomic methods.

For lab information, publications and more, see Dr. Mendillo’s faculty profile.

Publications

View Dr. Mendillo's publications at PubMed

Contact

Email Dr. Mendillo

Phone 312-503-5685

 David C. Mohr Lab

Design, developing, evaluating, and implementing technology-assisted behavioral and psychological interventions.

Research Description

David C. Mohr, PhD, is the Director of the Northwestern University Center for Behavioral Intervention Technologies (CBITs).   Dr. Mohr’s expertise is in the design, development, evaluation, and implementation of technology-assisted behavioral and psychological interventions. These technologies use mobile phones, tablets, computers, and sensors to support patient behaviors related to health, mental health, and wellness.  In the area of development, Dr. Mohr’s primary expertise is in designing applications that can be deployed to phones and desktop computers aimed at treating mental health disorders. While many of these have been relatively standard applications, he is also developing methods of harnessing sensor data from the phone to identify user states that are relevant to the treatment of depression.  A second area of development focuses on developing applications aimed at improving adherence to medications and medical regimens. These applications are being deployed in General Internal Medicine, Community Health Centers, and Psychiatry.  Finally, Dr. Mohr examines methods of implementing behavioral intervention technologies in the healthcare settings.  In general, behavioral intervention technologies are not effective in improving symptoms when delivered as standalone treatments. Dr. Mohr has developed and evaluated methods of providing low intensity coaching support to enhance the use and effectiveness of behavioral intervention technologies. These coaching models can use health professionals, lay people, and  peers. 

He is also interested in the relationship between stress, depression and inflammation, particularly in multiple sclerosis.

For more information visit the faculty profile of David Mohr, PhD.

Publications

See Dr. Mohr's publications in PubMed.

Contact

Dr. Mohr

 Andrew Naidech Lab

Clinical and translational research of life-threatening neurological diseases, particularly brain hemorrhage.

Research Description

Intensive monitoring is a core function of an intensive care unit, and generates large amounts of data. In a neurologic unit, surveillance neuromonitoring is as important as vital signs and cardiac rhythm, yet there has been less clarity as to precisely what should be measured (biomarkers, imaging markers, serial examination scores) and its impact on complications and outcomes. We have established methods and models for the retrieval and analysis of data from the electronic health record for patients with stroke for a large registry that I have maintained over 10 years (Northwestern University Brain Attack Registry, NUBAR), which now includes >1,000 patients.

Research to improve patient outcomes is limited to endpoints we can reliably measure. Collaborating with Neuro-QOL, a platform for measuring Quality Of Life in neurological disorders, and the NIH Patient Reported Outcomes Measurement Information System (PROMIS) Statistical Center, we have shown web-based computer-adaptive testing by study staff, patients or family members are valid compared to the usual standard of a validated interview, have increased statistical power, and highlight aspects of HRQoL, such as cognitive function, that would otherwise be undetectable (supported by K23 HS023437). Further, these measures improve our statistical power to perform research that measurably improves patient-centered outcomes.

In a continuing project with Preventive Medicine faculty, we are using network analytic techniques to identify high-performing teams. Previous publications have established methods to identify which members of the health care team (e.g., physicians, pharmacists, nurses) interacted with the patient in the electronic health record. Then, a quantitative measure of the success of interactions is calculated on an outcome. In past research, likelihood to recommend scores were the outcome. Here, we used NUBAR’s recorded functional outcomes (e.g., independence, dependence, death), and established that the interactions of team members are an independent predictor of patient outcome after accounting for severity of injury. This research opens up new lines of research on how to design high-performing teams.

In short, the lab collaborates widely to leverage innovative techniques to improve treatments for patients with life-threatening neurologic injury.

Contact Information

Andrew Naidech, MD, MSPH, FANA

Professor of Neurology

 Panagiotis Ntziachristos Lab

Studying Molecular Mechanisms of Oncogenesis In Acute Leukemia

Research Description

This is an exciting time for cancer biology especially with the advent of epigenetics and chromatin biology. New molecules with tumor suppressive or oncogenic roles are currently identified and characterized paving the way for new therapeutic ways but at the same time, posing new challenges for researchers. This area of cancer epigenetics is my personal and laboratory's focus. To study this perplexing biology we use patient samples and disease-relevant mouse models.

The Ntziachristos laboratory studies the mechanistic aspects of oncogenesis with an emphasis on transcriptional and epigenetic regulation of acute leukemia. Important questions are related to how oncogenes interact with each other and with epigenetic modulators to influence gene expression programs as well as how their function is related to tri- dimensional (3D) structure of the nucleus and other biological aspects of cancer cells, like metabolism. To address these questions we use high-throughput molecular and cell biology techniques like ChIP-Seq, RNA-Seq, 4C-Seq and HiC, fluorescent in situ hybridization and biochemical analysis in cell lines and primary cells of human origin and tissues of mouse models of disease. In addition to understanding cancer biology these finding help us design and test targeted therapies in preclinical models of leukemia.

For lab information and more, see Dr. Ntziachristos's faculty profile and lab website.

Publications

See Dr. Ntziachristos's publications at PubMed.

Contact

Contact Dr. Ntziachristos at 312-503-5225 or Searle 6-523

 Pembe Hande Ozdinler Lab

Understanding the cortical component of motor neuron circuitry degeneration in ALS and other related disorders.

The Les Turner ALS Laboratory II at Northwestern

Research Description

We are interested in the cellular and molecular mechanisms that are responsible for selective neuronal vulnerability and degeneration in motor neuron diseases. Our laboratory especially focuses on the corticospinal motor neurons (CSMN) which are unique in their ability to collect, integrate, translate and transmit cerebral cortex's input toward spinal cord targets. Their degeneration leads to numerous motor neuron diseases, including amyotrophic lateral sclerosis, hereditary spastic paraplegia and primary lateral sclerosis.

Investigation of CSMN require their visualization and cellular analysis. We therefore, generated reporter lines in which upper motor neurons are intrinsically labeled with eGFP expression. We also characterized progressive CSMN degeneration in various mouse models of motor neuron diseases and continue to generate reporter lines of disease models, in which the upper motor neurons express eGFP.

The overall goal in our investigation, is to develop effective treatment strategies for ALS and other related motor neuron diseases. We appreciate the complexity of the disease and try to focus the problem from three different angles. In one set of studies, we try to reveal the intrinsic factors that could contribute to CSMN vulnerability by investigating the expression profile of more than 40,000 genes and their splice variations at different stages of the disease. In another set of studies, we try to understand the role of non-neuronal cells on motor neuron vulnerability and degeneration, using a triple transgenic mouse model, in which the cells that initiate innate immunity are genetically labeled with fluorescence in an ALS mouse model. These studies will not only reveal the genes that show alternative splice variations, but also inform us on the canonical pathway and networks that are altered with respect to disease initiation and progression.

Even though the above mentioned studies, which use pure populations of neurons and cells isolated by FACS mediated approaches, will reveal the potential mechanisms that are important for CSMN vulnerability, it is important to develop therapeutic interventions. One of the approach we develop is the AAV-mediated gene delivery directly into the CSMN via retrograde transduction. Currently, we are trying to improve CSMN transduction upon direct cortex injection.

Identification of compounds that support CSMN survival is an important component of pre-clinical testing. We develop both in vitro and in vivo compound screening and verification platforms that inform us on the efficiency of compounds for the improvement of CSMN survival.

In summary, we generate new tools and reagents to study the biology of CSMN and to investigate both the intrinsic and extrinsic factors that contribute to their vulnerability and progressive degeneration. We develop compound screening and verification platforms to test their potency on CSMN and develop AAV-mediated gene delivery approaches. Our research will help understand the cellular basis of CSMN degeneration and will help develop novel therapeutic approaches.

For more information see the faculty profile of Pembe Hande Ozdinler, PhD or the Ozdinler Lab website.

Publications

View Dr. Ozdinler's full list of publications at PubMed

Contact

Hande Ozdinler, PhD at 312-503-2774

 Clara Peek Lab

Circadian clock control of fuel selection and response to nutrient stress

Research Description

The Peek Lab is focused on understanding the interplay between hypoxic and circadian transcriptional pathways both at the genomic and nutrient signaling levels. Peek aims to uncover novel mechanisms linking circadian clocks to the control of metabolic function and disease, such as type 2 diabetes and cancer. The lab utilizes metabolic flux analyses, in vivo metabolic and behavior monitoring, and next-generation sequencing in their research.

For lab information and more, see Dr. Peek's faculty profile and lab website.

Publications

See Dr. Peek's publications on PubMed.

Contact

Contact Dr. Peek at 312-503-6973.

Lab Staff

Technical Staff

Noah Hamlish

 Minoli Perera Lab

Pharmacogenomics research in minority patient populations

Perera Lab

Research Description

The Perera laboratory focuses on pharmacogenomics (using a patient's genome to predict drug response) in minority populations. Working in this translation research space requires both clinical expertise as well as the use of high-throughput basic science approaches. Our goal is to bring the benefits of precision medicine to all US populations.

The Perera lab has recruited patient populations from around the world. The data collection includes genomic (DNA), transcriptomic (mRNA), pharmacokinetic and clinical data. We then integrate these different data sources to understand genetic drivers of drug response (e.g. genetic predictors of adverse events) as well as disease. By studying minority populations the lab has discovered genetic risk variants that may benefit the implementation of precision medicine in African Americans and others.

Recent Findings

  • Warfarin Bleeding Risk Association study
    We recently discovered a genetic variant that predispose African Americans to bleeding complications while on anticoagulant drugs. These bleeds occurred even when the patient was within the therapeutic window for the medication. We hope that this new data will help to identify high risk individuals prior to therapy.
  • Novel African-specific genetic polymorphisms predict the risk of venous thromboembolism
    We discovered a new genetic variant associated with a 2.5 fold increase in risk of developing a blood clot. We went on to show that this SNP significantly affects the expression of a key protein in the coagulation cascade. View article on PubMed.
  • Common genetic variant is predictive of warfarin metabolism and gene expression in African Americans
    We tested the association of a SNP, previously shown to effect gene expression CYP2C9, for association with warfarin drug clearance (pharmacokinetics). This SNP increased the expression of CYP2C9 (enzyme that metabolized warfarin), hence causing fast clearance of the drug. This African American-specific SNP may help to explain the higher warfarin dose required by African Americans in general. View article on PubMed.

Current Projects

  • Genomics of Drug Metabolism
    We are using African America primary hepatocytes to understand the genetic regulation of drug metabolizing enzymes that are involved in a majority of drug used in the US.
  • Anticoagulant Pharmacogenomics
    We are conducting several genetic association studies to understand both the genetic drivers and the biological mechanisms behind response and adverse effect to anticoagulant medications.
  • Pharmacogenomics of Inflammatory Bowel disease
    We are investigating the genetic predictors of primary non-response to biologic therapies used in inflammatory bowel disease. Studies have implication for other autoimmune disorders that target the same pathways.
  • eMERGE
    We are involved in analyzing the GWAS and sequencing data specifically for genomics variation affect key pharmacogenomics gene in African Americans.

For lab information and more, see Dr. Perera's faculty profile and lab website.

Publications

See Dr. Perera's publications on PubMed.

Contact

Contact Dr. Perera at 312-503-6188 or the lab at 312-503-4119.

Lab Staff

Lab Manager

Cristina Alarcon

Postdoctoral Fellows

Paula Friedman, Guang Yang

Graduate Student

Carolina Clark

 Steven J. Schwulst Lab

 Monocyte and microglia interaction in the etiology and evolution of traumatic brain injury-induced neurodegeneration

 

Dr. Schwulst is an Assistant Professor of Surgery and attending Trauma and Critical Care Surgeon at Northwestern University and Northwestern Memorial Hospital. His primary research interests are in traumatic brain injury and post-injury immune dysfunction.  To date, his research has centered on three facets of TBI and immune dysfunction: the role of constitutive microglial activation in the etiology and evolution of chronic neurodegeneration after TBI (the focus of his current R01 award); the role of macrophage heterogeneity in the direction of TBI-induced immune dysfunction (the focus of his prior NIH K08 award); and understanding common molecular pathways between TBI-associated neurodegeneration and chronic neurodegenerative diseases such as Alzheimer’s Disease (the focus of an upcoming  NIH R21).

 

 Hank Seifert Lab

Bacterial pathogenesis, DNA recombination mechanisms, epithelial cell adherence

Research Description

Our laboratory studies the pathogenesis of Neisseria gonorrhoeae, the causative agent of the sexually transmitted disease gonorrhea. This gram-negative bacterium is an obligate human pathogen that has existed within human populations throughout recorded history. We are using a variety of molecular biological, genetic, cell biological and biochemical techniques to investigate the molecular mechanisms controlling gonococcal infection, define mechanisms and pathways of DNA recombination, replication and repair in this human specific pathogen, study the interactions between gonococci and human cells, tissues and the innate immune system and determine how the pilus functions to help mediate genetic transfer and pathogenesis. Our goal is to discover new mechanisms important for the continued existence of this microbe in the human population to further our understanding of how infectious agents have evolved to specifically infect humans.

For lab information and more, see Dr. Seifert's faculty profile.

Publications

See Dr. Seifert's publications on PubMed.

Contact

Contact Dr. Seifert at 312-503-9788 or the lab at 312-503-9786.

Lab Staff

Research Faculty

Elizabeth Stohl 

Postdoctoral Fellows

Linda I-Lin Hu, Jayaram Narayana, Ella Rotman

Graduate Students

Wendy Geslewitz

Technical Staff

Shaohui Yin 

 Ali Shilatifard Lab

Studying molecular machinery for histone modifications in yeast, Drosophila and human cells

Research Description

Chromosomal rearrangements resulting in alterations of gene expression are a major cause of hematological malignancies. Our goal is to advance the understanding of the biochemical and molecular mechanisms of rearrangement-based leukemia and to provide insights into how translocations affect cellular division by altering gene expression. Using mammalian model systems such as tissue culture and mouse genetics, we plan to explore the regulation of gene expression via the MLL gene and its translocation partners found in human leukemia. We are currently defining the molecular composition of the MLL complexes and how translocations alter its biochemical function and integrity, resulting in leukemic pathogenesis. We are also planning to define the mechanism of the targeting of the MLL complex and its histone methyltransferase activity to chromatin to determine its normal cellular functions and its mistargeting and dysregulation in leukemogenesis.

One fusion partner of MLL in acute myelogenous leukemia (AML) is the ELL protein. We show that human ELL functions as a transcription elongation factor. We have identified the Drosophila homolog of ELL and demonstrate it to be essential for development.  Drosophila ELL associates with elongating RNA polymerase II in vivo on chromosomes and is a regulator of the Notch signaling pathway.  This has suggested to us that human ELL might also participate in the same process.

For lab information and more, see Dr. Shilatifard's faculty profile or visit the Shilatifard Laboratory site.

Publications

View Dr. Shilatifard's publications on PubMed.

Contact

Email Dr. Shilatifard

Phone 312-503-5223

 Jonathan Silverberg Lab

Dermatoepidemiology

Research Description

Dr. Silverberg specializes in dermatoepidemiology with a focus on comorbidities and quality of life. His research interests include the patient- and population-based burden of inflammatory skin disease, particularly atopic dermatitis (eczema), contact dermatitis and photosensitive disorders.

Goals:

1 - identify novel modifiable risk factors for inflammatory skin diseases and develop clinical and epidemiological interventions to prevent these disorders throughout the US population. This includes improving the understanding of the genetics and gene-environment interactions in adult atopic dermatitis. 

2 - develop improved assessments for patients with chronic itch that can help us understand how best to reduce the itch, which is so life altering for patients. 

3 - work toward improving the understanding of the direct and indirect burden of inflammatory skin diseases, including their relationship with other health conditions, such as cardiovascular disease.

In 2014, Dr. Silverberg founded Northwestern Medicine’s Multidisciplinary Eczema Center, and as its director, he has been able to advance research and test cutting-edge therapeutic approaches.

Publications

See Dr. Silverberg's publications on PubMed.

Contact

Email Dr. Silverberg

312-503-8287

 Bonnie J. Spring Lab

Behavioral risk factors

Research Description

My laboratory conducts research on behavioral risk factors (obesity, poor quality diet, physical inactivity, tobacco use). We also develop cutting-edge technologies that support self-regulation and healthy behavior change. Finally, we create on-line learning tools to support skill mastery in evidence-based practice and team science.

For more information, visit the faculty profile of Bonnie Spring, PhD.

Publications

View Dr. Spring's publications at PubMed.

Contact

Email Dr. Spring

Phone 312-908-2293

 Alexander Stegh Lab

Defining and targeting the oncogenome of Glioblastoma.

Research Description

Our research program is aimed at understanding the genetic program that underlies the pathogenesis of Glioblastoma multiforme (GBM), the most prevalent and malignant form of brain cancer. Applying a combination of cell/molecular biology, oncogenomic and mouse engineering approaches, we are dedicated to systematically characterize novel gliomagenic oncogenes and tumor suppressors. We will functionally delineate and validate these pathways using cell culture and animal models and develop novel nanotechnological approaches to target these aberrations in established tumors.

For more information see the faculty profile of Alexander H Stegh MD, PhD, or visit  the Alexander H. Stegh Lab website.

Recent Publications

View Dr. Stegh's full list of publications at PubMed

Contact

Alexander Stegh, MD, PhD, at 312-503-2879

 Athanassios Vassilopoulos Lab

The main focus of the Laboratory for Molecular Cancer Biology is to unravel the mechanistic link between aging and cancer with a focus on the regulatory role of post-translational modifications directed by sirtuins.

Research Description

Athanasios Vasilopoulos, PhD
Athanasios Vasilopoulos, PhD

One of the fundamental observations in oncology is that increasing age is the strongest statistic variable that predicts for carcinogenesis. A fact that has emerged over the last several years is that aging is a complex process that appears to be regulated, at least in part, by several signaling protein families that have been identified in multiple species, including sirtuins, a relatively new gene family that was initially identified in S. cerevisiae and C. elegans. Sirtuins have been found to both increase life span and decrease spontaneous tumor development suggesting that they may regulate both processes. They appear to function as fidelity proteins and loss or decrease of function, which may occur during aging, creates a cell environment permissive for several age-related illnesses, including cancer. The significant role played by sirtuins can be explained by accumulating evidence establishing their pivotal role in regulating post-translational modifications (PTMs) in both histone and non-histone proteins involved in diverse cellular processes. Despite recent scientific interest in this field, there is still scarcity regarding the functional consequences of the role of these PTMs in cellular homeostasis. Our proposed studies take an integrative approach to current challenges in dissecting the functional role of sirtuin-directed PTMs in tumorigenesis which may bridge the gap between the observation that tumorigenesis increases with age and the limited information regarding the specific mechanisms underlying this phenomenon. By blending classic molecular/cellular biology, biochemistry and mouse genetics with large-scale proteomics, our ultimate research goal is to elucidate the function of sirtuins in maintaining cellular homeostasis which may provide novel mechanistic insights in different aspects of tumorigenesis.

For lab information and more, see Athanasios Vasilopoulos' faculty profile.

Publications

See Dr. Vassilopoulos’ publications in PubMed.

Contact

 Contact Dr. Vassilopoulos directly at 312-503-0727 or via athanasios.vasilopoulos@northwestern.edu.

Postdoctoral Fellows

Mohamed Ahmed, PhD
Yang Guo, MD, PhD
Mingming Zhang, PhD

Students

Yijun Fan, BSc
Elliot Chang
Michael Bofu Li

 Deborah Winter Lab

Computational immunology - Using genomic approaches to study rheumatic disease.

Research Description

The goal of the Winter Lab of Functional Genomics is to apply genomic approaches to study rheumatic disease. Led by Dr. Deborah Winter, a computational immunologist, we employ the latest technologies for assays, such as RNA-seq, ChIP-seq, ATAC-seq and single cell expression, to profile the transcriptional and epigenomic profiles of immune cells in health and disease. Our goal is to define the underlying regulatory networks and understanding how they respond to challenge, illness and injury. We are particularly interested in the role of macrophages in diseases such as scleroderma, rheumatoid arthritis and lupus. Previous research has addressed the impact of the tissue environment on resident macrophages and the role of microglia, CNS-resident macrophages, in brain development. Our research combines molecular and systems biology, biotechnology, clinical applications and computer science. We use both mouse models and patient samples to help us understand and test different systems. We are committed to high standards of analysis and are continually updating and training in innovative computational techniques. We are currently recruiting highly motivated individuals to join the lab.

For more information, visit the faculty profile of Dr. Winter.

Publications

View Dr. Winter's publications at PubMed

Contact Us

Contact Dr. Winter at  312-503-0535 or by email.

 Rui Yi Lab

Investigate mechanisms of skin development, stem cells, aging and cancer at the single-cell level

Research Description

Mammalian skin and its appendages function as the outermost barrier of the body to protect inner organs from environmental hazards and keep essential fluid within. Our research program studies mechanisms that govern cell fate specification, stem cell maintenance and aging as well as initiation and progression of cancer. We use single-cell genomics and computational tools, live animal imaging and genetically engineered mouse models to study gene expression regulation mediated by transcription factors, epigenetic regulators and post-transcriptional mechanisms mediated by miRNAs and RNA binding proteins at the single-cell resolution in mammalian skin. 

Our research aims to address several fundamental questions in stem cell biology: how the developmental potential of embryonic progenitors and adult tissue stem cells is transmitted or restricted in their progenies at the molecular level when they go through critical transitions such as cell fate specification, self-renewal of stem cells as well as stress response, and how these regulatory mechanisms go awry in aging and diseases. Answers to these questions will help to manipulate skin stem cells for regenerative medicine and discover new treatment for human skin diseases.​

View all lab publications via PubMed.

For more information, visit the faculty profile page of Rui Yi, PhD or visit the Yi Laboratory website.

Contact Us

Email Dr. Yi

 

 

 

 Jindan Yu Lab

Understanding the genetic and epigenetic pathways to prostate cancer.

The Yu lab focuses on cancer genomics and translational cancer research.  At the current stage, our primary research interest is to understand aberrant transcriptional and epigenetic regulation of prostate cancer and to translate such knowledge into clinical applications.  We utilize high-throughput genomic techniques in combination with bioinformatics/statistical analysis to generate testable hypothesis.   We then test these hypotheses using traditional molecular and/or cellular biological approaches and examine the functional relevance of these innovative regulatory pathways in vitro and in vivo using cell lines and mouse models.  Based on the genetic and epigenetic underpinning of the disease, we pursue translational research to develop new biomarkers and novel therapeutics strategies for advanced prostate cancer.

Select Publications

Kim J, Lee Y, Lu X, Song B, Fong KW, Cao Q, Licht JD, Zhao JC, Yu J.  Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator.  Cell Reports. 2018 Dec 04. PMID: 30517868

Fong KW, Zhao JC, Song B, Zheng B, Yu J.  TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression.  Nat Commun. 2018 Nov 27. PMID: 30479348

Fong KW, Zhao JC, Kim J, Li S, Yang YA, Song B, Rittie L, Hu M, Yang X, Perbal B, Yu JPolycomb-mediated disruption of an androgen receptor feedback loop drives castration-resistant prostate cancer.  CancerRes. 2016 Nov 4. PMID: 27815387

View all lab publications via PubMed.

For more information, visit the faculty profile page of Jindan Yu, MD/PhD or visit the Yu Laboratory website.

Contact Us

Contact Dr. Yu at 312-503-2980 or the Yu Lab at 312-503-3041.

Lab Staff

Will Ka-Wing Fong
Research Assistant Professor

Jonathan Zhao, MD, MS
Research Associate Professor

Nathan Damaschke, PhD
Postdoctoral Fellow

Yongik Lee, PhD
Postdoctoral Fellow

Xiaodong Lu, PhD
Postdoctoral Fellow

Gang Zhen, PhD
Postdoctoral Fellow

Xiaoyan Zhu, PhD
Postdoctoral Fellow

Galina Gritsina
Graduate Student

Kevin Park
Graduate Student

Rakshitha Jagadish
Masters Student

 

 

 Feng Yue Lab

Genomics, epigenomics, and 3D genome organization of human diseases

Research Description

The long-term goal of Dr. Yue’s group is to use a combination of high throughput genomics, computational modeling, and functional assays to study how genetic variants contribute to the pathogenesis of human cancer. In particular, he is interested to identify the mutations that can disrupt the function of non-coding regulatory elements such as enhancers and further influence the 3D organization of the human genome. He has been actively involved with several large NIH-funded consortia, and lead the overall analysis effort for the mouse ENCODE consortium (Yue et al. Nature 2014).

More recently, his group and their collaborators show that Hi-C can be used as tool for systematic discovery of SVs in the genome and also reported widespread neo-TADs and enhancer hijacking events, which potentially contribute to gene misregulation in cancer cells (Dixon et al. Nature Genetics 2018).

Dr. Yue’s group is well versed in both functional genomics and computational biology. In the past few years, we have developed a series of algorithms on 3D genome organization, such as evaluating Hi-C data reproducibility (HiCRep) and enhance Hi-C data resolution with deep learning (HiCPlus). My lab built the 3D Genome Browser, one of the most popular tools for visualizing chromatin interaction data which has been visited >1,000,000 times by users from over 100 countries.

For more information, please see Dr. Yue's faculty profile or the Yue lab website.

Publications

 See Dr. Yue's publications on PubMed.

Contact

Contact Dr. Yue at 312-503-8248.

Lab Staff

Research Faculty

Hongbo Yang, PhD

Postdoctoral Fellows

Tingting Liu, Yu Luan, Baozhen Zhang

Lab Manager

Qiushi Jin

Graduate Students

Sriranga "TJ" Iyyanki, Fan Song, Jie Xu, Bo Zhang

 Wei Zhang Lab

Genetics and epigenetics of complex traits including risks for common diseases and drug response

Dr. Zhang is particularly interested in using high throughput technologies (e.g., microarray, next generation sequencing) and systems biology approaches to study the genetics of complex traits or phenotypes such as the risks of common diseases (e.g., cancer and lung disease), individual drug response and gene expression. Dr. Zhang is also interested in building bioinformatic databases that aim to provide user friendly access to primary data from pharmacogenomic and genome-wide association studies (GWAS). An on-going research interest of Dr. Zhang’s is the mapping of expression quantitative trait loci (eQTLs) in sarcoidosis and sickle cell disease, as well as the impact of eQTL mapping on the prioritization of GWAS results form these complex diseases.

For more information, visit Dr. Zhang's Faculty Profile page.

Contact

Email Dr. Zhang

Phone 312-503-1040

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