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Genetics and Epigenetics

Research on the changes in gene expression and regulation that accompany the origin and growth of cancerous cells.

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.


See Dr. Abazeed's publications in PubMed.


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

Post-doctoral Fellows

Priyanka Gopal, Rohan Bareja


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.


See Dr. Adli's publications in PubMed.


Contact Us

Dr. Adli

 Daniel Arango Lab

Investigating the role of post-transcriptional modifications of RNA in the proliferation, differentiation, and survival of cancer cells

Research Description

Translation is the mechanism by which proteins are made from the information stored in the genetic code. This process is achieved with the help of RNA molecules such as ribosomal RNA (rRNA), transfer RNA (tRNA), and messenger RNA (mRNA). While translation is a tightly regulated process, global perturbations in protein synthesis are observed in stress conditions, cancer, and aging, highlighting the regulatory mechanisms of translation as potential targets in cancer and age-related disorders. One poorly characterized layer of translation regulation is the epitranscriptome, defined as the set of more than 140 ribonucleotide modifications that alter the biochemical properties and function of all classes of RNA, including rRNA, tRNA, and mRNA. While the distribution and function for most ribonucleotide modifications are undefined, the enzymes responsible for depositing RNA modifications are dynamic and sensitive to metabolic alterations, potentially regulating the temporal response to stress or the onset of human diseases such as cancer.

Our group investigates the mechanisms by which RNA modifications regulate protein synthesis and how these mechanisms affect cell fate decisions such as cell proliferation, survival, and differentiation in cancer and stress conditions. By integrating RNA biology, transcriptomics, and cell biology, we aim to uncover novel mechanisms of gene expression regulation and generate new tools that can be harnessed to develop anti-cancer therapies.

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

Current Projects

  • Mechanisms and regulation of RNA acetylation in cancer cells
  • Regulation of stress response by RNA modifications
  • Targeting RNA-modifying enzymes and RNA modifications for therapeutic purposes


See Dr. Arango's publications.


Contact Dr. Arango at 312-503-0732.

 Hossein Ardehali Lab

Role of mitochondria and metabolic processes in cancer growth, cardiac disease and immunological processes


Research Description

Our lab focuses on three major areas of research:

Role of hexokinase enzymes in immune function, cancer growth and stem cell differentiation

Hexokinase (HK) enzymes phosphorylate glucose to trap it inside the cell. There are 5 mammalian HKs (named HK1-5), with two of them having a hydrophobic region at their N-terminus that allows them to bind to the mitochondria. We have made mouse models and developed in vitro systems to allow us to study the role of mitochondrial binding of HKs in glucose metabolism. We have determined that HK1 binding to the mitochondria determines whether glucose is used for anabolic processes (ie, pentose-phosphate pathway) or catabolism (ie, glycolysis). Thus, the non-enzymatic function of this protein and its subcellular location determines the fate of glucose. We are now studying this process in T-cells, vascular cells and cancer cells. We are also in the process of generating several mouse models of hexokinase enzymes, including HK2 without the mitochondrial binding domain and HK3 knockout mice. We will study these models in different disease and physiological conditions.

Characterization of cellular and mitochondrial iron regulation

Our lab has identified a novel mitochondrial protein, ATP-Binding Cassette-B8 (ABCB8), which plays a role in mitochondrial iron homeostasis and mitochondrial iron export. Mice with ABCB8 knocked out in the heart develop cardiomyopathy and mitochondrial iron accumulation. In addition, we have shown that a pathway involving mTOR and tristetraprolin, treatment with doxorubicin (an anticancer drug that also causes cardiomyopathy) and SIRT2 protein also impact cellular and/or mitochondrial iron regulation. Current studies in this area include: 1) further characterization of ABCB8 in iron homeostasis in other organs and disorders, 2) characterization of the mechanism for iron regulation by SIRT2, 3) identification of the mechanism by which mTOR is regulated by iron through epigenetic changes, 4) role of iron in viral infection, particularly HIV, 5) characterization of the effects of iron on mitochondrial dynamics and 6) identification of novel mitochondrial-specific iron chelators.

Role of mRNA-binding proteins in cellular and systemic metabolism

TTP is a protein that binds to AU-rich regions in the 3’ UTR of mRNA molecules and causes their degradation. It has been studied extensively in the field of inflammation. We recently showed that it also plays a role in cellular iron conservation. We have also shown that TTP is a key mediator of cellular metabolic processes. Our studies have demonstrated that TTP regulates glucose, fatty acid and branched-chain amino acid metabolism in the liver and muscle tissue. We also have evidence that TTP directly regulates mitochondrial electron transport chain (ETC) by targeting specific proteins in the ETC complexes. Finally, recent studies demonstrated that TTP also regulates systemic metabolism by targeting FGF-21 expression. We have both TTP Floxed mice (for the generation of tissue specific TTP knockout mice) and TTP knockout mice in the background of TNF-alpha receptor 1/2 knockout mice (to reduce the inflammatory burden).  Current studies include: 1) role of TTP in liver metabolism of fatty acids and glucose, 2) effects of TTP on mitochondrial proteins, 3) mechanism of TTP regulation of branched-chain amino acid levels and 4) role of TTP in cardiac metabolism.

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


See Dr. Ardehali's publications in PubMed.


Dr. Ardehali

 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.


See Dr. Brat's publications in PubMed.


Email Dr. Brat

 Paul Burridge Lab

Investigating the application of human induced pluripotent stem cells to study the pharmacogenomics of chemotherapy off-target toxicity and efficacy

Research Description

The Burridge lab studies the role of the genome in influencing drug responses, known as pharmacogenomics or personalized medicine. Our major model is human induced pluripotent stem cells (hiPSC), generated from patient's blood or skin. We use a combination of next generation sequencing, automation and robotics, high-throughput drug screening, high-content imaging, tissue engineering, electrophysiological and physiological testing to better understand the mechanisms of drug response and action.

Our major effort has been related to patient-specific responses to chemotherapy agents. We ask the question: what is the genetic reason why some patients have a minimal side effects to their cancer treatment, whilst others have encounter highly detrimental side-effects? These side-effects  can include cardiomyopathy (heart failure or arrhythmias), peripheral neuropathy,  or hepatotoxicity (liver failure). It is our aim to add to risk-based screening by functionally validating genetic changes that predispose a patient to a specific drug response.

Recent Findings

  • Human induced pluripotent stem cells predict breast cancer patients’ predilection to doxorubicin-induced cardiotoxicity
  • Chemically defined generation of human cardiomyocytes

Current Projects

  • Modeling the role of the genome in doxorubicin-induced cardiotoxicity using hiPSC
  • Investigating the pharmacogenomics of tyrosine kinase inhibitor cardiotoxicity
  • hiPSC reprogramming, culture and differentiation techniques
  • High-throughput and high-content methodologies in hiPSC-based screening

For lab information and more, see Dr. Burridge’s faculty profile and lab website.


See Dr. Burridge's publications on PubMed.


Contact Dr. Burridge at 312-503-4895.

Lab Staff

Postdoctoral Fellows

Malorie Blancard, Hananeh Fonoudi, Mariam Jouni, Davi Leite, Tarek Mohamed, Disheet Shah

Graduate Students

Liora Altman-Sagan, Raymond Copley, K. Ashley Fetterman, Phillip Freeman, Donald McKenna, Emily Pinheiro, Marisol Tejeda, Carly Weddle

Technical Staff

Ali Negahi Shirazi

 Debabrata Chakravarti Lab

Epigenome and 3D chromatin organization dysregulations define human cancers and reproductive diseases

Research Description

Dr. Chakravarti’s research is focused on understanding epigenetic and transcriptional regulation of human tumorigenesis.  One of his research projects is focused on understanding the mechanisms that drive the development of uterine fibroids and endometriosis that affect an alarmingly high number of all women.  In another project, Dr. Chakravarti’s research team investigates molecular underpinning of contribution of transcription factors, cofactors and epigenomic and 3D genome reorganization regulation of prostate Cancer that affects a large number of men worldwide.  In a third project the laboratory determines the role of protein cofactors in regulation of cell cycle genes. Thus, our work interfaces both fundamental and translational research on diseases that affect humankind.  It is our hope that when combined with results from others, our research will contribute to the development of future therapeutics.  Dr. Chakravarti gratefully acknowledges continuous funding support from the NIH and key roles of his lab members and collaborators in the overall success of the Chakravarti Laboratory.

Dr. Chakravarti also enjoys teaching.  He has continuously taught both medical and graduate students.  He serves on numerous Ph.D thesis committees.  He has trained a large number of graduate students and postdoctoral fellows some of whom are now independent investigators at this and other institutions.

For more information, please see, visit the Dr. Chakravarti's faculty profile.


See Dr. Chakravarti's publications in PubMed.
Associate Editor: Endocrinology 2017-present; Editorial Board:  Molecular Endocrinology 2011- present, Mol. Cell. Biol. 2014-present
The Editor of a Book volume on “Regulatory Mechanisms in Transcriptional Signaling” in Progress in Molecular Biology and Translational Science (Vol 87), published in Aug 2009, Academic Press, Chakravarti, D. Editor

Contact Us

Dr. Chakravarti


 Cheng Lab

Dr. Cheng’s lab investigates cancer stem cell biology, cellular signaling and therapy responses in human brain tumors, particularly glioblastoma (GBM).

Research Description

Our lab broadly studies cancer stem cell biology, cellular signaling, RNA biology, and therapy responses in human brain tumors, in particular, glioblastoma (GBM). We have a range of different projects currently underway in glioma cell lines, gliomas stem-like cells (GSCs), patient-derived xenograft (PDX) GBM model, human iPSC-derived glioma organoid model, orthotopic glioma xenograft model in mice, and clinical glioma tumor specimens. Our current research focuses on novel mechanisms/cellular signaling of GSC biology, tumorigenesis, progression, and therapy responses of GSCs and GBMs.

Roles of RNA alternative splicing and RNA-binding proteins in glioma

RNA alternative splicing (AS), an evolutionarily conserved co-transcriptional process, is an important and influential determinant of transcriptome and proteome landscapes in normal and disease states such as cancer. AS is regulated by a group of RNA binding proteins (RBPs) that bind to the cis-acting elements in proximity to a splice site thus affecting spliceosome assembly. In cancers, altered expression of or mutations in RBPs result in dysregulated AS that impacts cancer biologic properties. We have established AS/RBP networks that are dysregulated in both adult and pediatric gliomas through bioinformatic analysis of both public and our own datasets of clinical glioma tumors. We are investigating the biological significance of AS/RBPs dysregulation in glioma progression and therapy response by using human iPSC-derived glioma organoid model and GSC brain xenograft models in animals. In addition, we are exploring novel therapeutic approaches of targeting glioma-associated AS/RBP networks to treat GBMs.

Roles of Non-coding RNAs in glioma 

Non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), act as transcription repressors or inducers of gene expression or functional modulators in all multicellular organisms.  Dysregulated ncRNAs plays critical roles in cancer initiation, progression and responses to therapy. We study the mechanisms by which deregulated expression of lncRNAs or circRNAs influence GBM malignant phenotypes through interactions with signaling pathways. We study the molecular consequences and explore clinical applications of modulating ncRNAs and related oncogenic signaling pathways in GBM.  We are establishing profiles of ncRNAs in clinical gliomas and patient-derived GSCs, and study mechanisms and biological influences of these ncRNAs in regulating GSC biology and GBM phenotypes. 

Aberrant DNA and RNA structures in therapy-resistant GBM

Standard of care treatment for GBM includes the DNA damaging agent temozolomide (TMZ), which has a known mechanism of action to target and mutate guanine bases. With this knowledge in hand, we sought to determine the effects of guanine (G) mutations in DNA and RNA secondary structure. G’s are important for creating structures like g-quadruplexes in both DNA and RNA which can affect changes in translation or be used as docking sites for DNA repair and RNA binding proteins. Using whole genome sequencing data along with isogenic drug sensitive and resistant lines, we are investigating the role of G mutations in DNA and RNA secondary structure to determine potential therapeutic avenues with the help of a chemical biologist to create novel drugs to target these TMZ-induced aberrant pathways.

Targeting autophagy to treat glioma

Autophagy is an evolutionarily conserved process that removes unnecessary or dysfunctional components through a lysosome-dependent regulated mechanism, thus serving as a protective mechanism against stressors and diverse pathologies including cancer. We study mechanisms by which phosphorylation, acetylation and ubiquitination of autophagy-related proteins regulate GSC and GBM phenotypes and autophagic response, which, in turn contributes to tumor cell survival, growth and resistance to therapy. We investigate whether disruption of these post-translational processes in autophagy-related proteins inhibits autophagy and enhances the efficacy of combination therapies in GBMs. In collaboration with a medicinal chemist, we are characterizing a next generation of novel autophagy inhibitors that specifically target a key autophagy regulator that we recently reported.

Multi-omics and GBM non-responsiveness to immunotherapies

GBM is categorized as a “cold” tumor that does not respond to current immunotherapies using various immune-checkpoint blockers. Although extensive efforts have been made to sensitize GBM to immunotherapies, the mechanistic studies to determine alternative therapies from understanding the underlying signaling and clinical trial results are still disappointing. We are interested in utilizing the information of multi-omics of clinical gliomas, in particular, proteomics profiling in relation to genomic and epigenomic profiling, to identify potential protein targets that could be the major modulators through post-translational modifications in these “cold” GBM tumors. We will also consider the involvement of tumor microenvironment and immune cells in these conditions. These studies are a brand-new direction that are high-risk and high-reward to turn “cold” GBM tumors to immunotherapy responsive tumors.

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


View Dr. Cheng's complete list of publications in PubMed.

Contact Us

Shi-Yuan Cheng, PhD at 312-503-5314

Visit us on campus in the Lurie Building, Room 6-119, 303 E Superior Street, Chicago, Illinois 60611.


 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.


See Dr. Choi's publications on PubMed.


Contact Dr. Choi.

 Lillian Eichner Lab

Transcriptional dependencies in cancer at the intersection of epigenetics, signaling and metabolism

Research Description

The Eichner lab studies transcriptional dependencies in cancer development, progression and resistance mechanisms. We endeavor to elucidate in vivo transcriptional dependencies at the intersection of epigenetics, signaling, and metabolism to reveal and harness therapeutically targetable transcriptional vulnerabilities in cancer.

Project 1

LKB1 (STK11) is among the most frequently mutated genes in Non-Small Cell Lung Cancer (NSCLC), where it is inactivated in about 20 percent of cases. Leveraging immune-competent genetically engineered mouse models to answer key questions in vivo, our work has revealed key insights into the molecular mechanisms driving this disease. We have identified that transcription plays an important and previously underappreciated role in mediating LKB1 function. Future work will continue utilizing mechanistic understanding to explore novel in vivo transcriptional dependencies and therapeutic liabilities of LKB1 mutant tumors.

Project 2

We have identified critical roles of the druggable epigenetic regulator Histone Deacetylase 3 (HDAC3) in lung tumors. We found that HDAC3 directly represses the secretory component of the cellular senescence program, the SASP, and restrains recruitment of T-cells into tumors in vivo. Future work will continue defining the molecular mechanisms mediating HDAC3’s contribution to tumorigenesis, and further explore epigenetic regulation of the senescence program.

For lab information, publications and more, see Dr. Eichner's faculty profile and laboratory website.


See Dr. Eichner's publications on PubMed.


Contact Dr. Eichner.

 Elizabeth Eklund Lab

The Eklund lab investigates myeloid leukemia and approaches to chemotherapy resistant disease.

Dr. Eklund’s laboratory studies are focused on understanding the molecular events that lead to development of myeloid leukemias (acute myeloid leukemia and chronic myeloid leukemia) and to the evolution of drug resistance in these diseases.  The goal is to identify potential molecular therapeutic targets that would delay or prevent drug resistance and relapse in AML and CML.  In related projects, the laboratory is investigating Fanconi Anemia, a genetic disease with defective DNA repair.  Patients with Fanconi Anemia frequently develop leukemia and provide a model for understanding the role of DNA repair in leukemogenesis.


View lab publications via PubMed.

For more information, visit the faculty profile page of Elizabeth Eklund, MD.

Contact Us

Contact Dr. Eklund at 312-503-3208 or the Eklund Lab at 312-503-3208.

Lab Staff

Ling Bei, MD
Research Associate

Elizabeth Hjort
Graduate Student

Liping Hu, PhD
Post Doctoral Fellow

Weigi Huang, MD
Research Assistant Professor

Chirag Shah, PhD
Research Associate

Hao Wang, PhD
Research Assistant Professor

 Daniel Foltz Lab

Epigenetic control of centromere assembly and chromosome segregation.

Research Description

My research program is focused on the important basic question of how chromosomes are segregated during cell division to ensure the complete and accurate inheritance of the genome. Chromosome instability is a hallmark of cancer and can drive tumorigenesis. Therefore, how centromere specification is controlled is a basic biological question with great therapeutic potential. Centromeres are specified by the incorporation of a histone variant CENP-A in a centromere specific nucleosome. The stable inheritance of this locus is controlled by an epigenetic pathway and does not depend on the underlying DNA sequence. My research program is using a combination of cell biology, biochemical purification and in vitro reconstitution of centromeric chromatin to discover the mechanisms of epigenetic inheritance and CENP-A function during mitosis. A key to understanding the epigenetic inheritance of centromeres is determining the process by which new CENP-A nucleosomes are deposited. Our lab is studying how activity of the CENP-A chromatin assembly factor HJURP is coupled to existing centromeres. Non-coding RNAs, as well as chromatin modifying enzymes have been implicated in the process and we are exploring how these factors contribute to specific assembly of the CENP-A nucleosomes. We have identified novel post translational modifications of the CENP-A amino-terminus and we are working to determine how these modifications contribute to genomic stability and accurate chromosome segregation. Our immediate goal is to determine the mechanism of epigenetic centromere inheritance, with a long-term goal of delineating the role of this process in tumorigenesis so as to translate our basic understanding of the enzymes and proteins involved in this process into therapeutic approaches for genomic instability in cancer.

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


See Dr. Foltz's publications on PubMed.


Contact Dr. Foltz at 312-503-5684.

 Ruli Gao Lab
Single cell sequencing technologies and bioinformatics for delineating cellular mechanisms of human diseases

Research Description

Dr. Ruli Gao's laboratory at Northwestern University Feinberg School of Medicine harbors both single cell sequencing technologies and computational methodologies under one roof.  Dr. Ruli Gao has significant contribution in tumor evolution fields by developing and applying single cell sequencing technologies and bioinformatic algorithms (Nature Genetics, 2016; Cell, 2018; Nature Communications, 2017; Nature Biotechnology, 2021).  The ongoing research projects in Gao Lab include: 1) Construction of single cell mosaic mutation atlas of human organs by developing novel computational methods for analyzing large scale human cell atlas datasets, 2) Delineating cellular mechanism of chronic heart transplant failure by developing novel single cell third generation sequencing technologies to dissect the donor and host cell identities and their contributions to transplanted heart failure, 3) Tracking tumor evolution and neovascular adaption of brain metastatic tumors by applying novel single cell DNA and RNA sequencing technologies to deconvolute tumor evolution and dissect the ecological systems of human brain, and 4) Developing human tumor cell atlas of rare cancer types using high throughput single cell sequencing methods to analyze tumor and immune cell populations.


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


See Dr. Gao's publications in PubMed.


Contact Dr. Gao at 312-503-3796.


 Yogesh Goyal Lab

Single-Cell Biology of Development and Disease

Research Description

We are interested in understanding the control principles governing biological processes at various scales, from tissue morphogenesis in development to cell-fate decisions in single cells. In particular, individual cells within a genetically identical population constantly undergo fluctuations in their molecular state which may enable them to adopt new fates in response to stimuli. As opposed to hardwired responses encoded in the genome, this dynamic ability of cells to react, either alone or in concert with each other, to external and internal cues is broadly referred to as “plasticity”. Leveraging our unique interdisciplinary approach, we combine novel frameworks, both experimental (e.g. single-cell profiling, spatiotemporally-resolved lineage tracing, multiplexed single-molecule RNA imaging, optogenetics) and computational (stochastic modeling, statistical analysis of large datasets), to track and control state-to-fate mappings in the context of animal development and cancer progression. Working across multiple mammalian model systems (cell lines, developmental and tumor organoids, mouse models), we will ask how diverse non-genetic variabilities drive fate choices and self-organization in development and disease.

To learn more about specific projects, please visit our Lab Website.



See the Goyal Lab’s publications on the Goyal Lab Website.


Dr. Goyal.

 Craig Horbinski Laboratory

Studying the effects of altered glioma metabolism in the microenvironment.

My translational work focuses on the effects of altered glioma metabolism in the microenvironment. Mutations in isocitrate dehydrogenase 1 or 2 (mutant IDH1/2) are present in a large proportion of gliomas, and are known to alter tumor metabolism and DNA methylation. Additionally, I serve as the Director of the Nervous System Tumor Bank (NSTB) for the Northwestern Brain Tumor Institute. The NSTB provides all NBTI researchers with patient-derived biospecimens and neuropathological support.

For more information, please visit the Horbinski Laboratory website.

 Dai Horiuchi Lab

Understanding the cellular events that influence the aggressiveness of tumors and patient clinical outcome

Research Description

The major focus of the Horiuchi lab, established on April 1, 2015, is on the mechanisms of tumor maintenance and progression in breast cancer and to identify novel therapeutic targets and treatment strategies. To achieve these goals, we utilize a collection of human breast cancer cell lines, preclinical animal models and high-throughput screening approaches along with state-of-the-art bioinformatics through collaboration with experts in the field.

We are currently focused on the following areas:

  1. Mechanisms of tumor maintenance and progression medicated by proto-oncogenes (i.e., MYC transcription factor, PIM family of serine/threonine kinases, etc.), their activators and effectors and the tumor microenvironment.
  2. Biology and therapeutic targetability of novel molecular factors that determine patient clinical outcome.

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


See Dr. Horiuchi's publications on PubMed.


Contact Dr. Horiuchi at 312-503-4085 or the lab at 312-503-4349.

Lab Staff

Technical Staff

Lauren Begg, Adrienne Orriols

 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.


See Dr. Hou's publications in PubMed.


Dr. Hou

 Sui Huang Lab

Seeking to understand the nature and function of a unique nuclear structure, the perinucleolar compartment (PNC), and its relationship with the malignant phenotype

Research Description

Our studies seek to understand the nature and function of a unique nuclear structure, the perinucleolar compartment (PNC), and its relationship with the malignant phenotype. Our work looks to address the function of the PNC and its significance during malignant transformation in multiple ways.

  • Determine the correlation between PNCs and cancer in tissues. In collaboration with Dr. Ann Thor at Evanston Hospital, Northwestern University, we have initiated detection of PNC in breast cancer tissues.
  • Investigate the function of the PNC, its relationship with the nucleolus and rRNA synthesis. We are in the process of isolating and identifying additional proteins and RNAs in the PNC.

Identification of activities taking place in the PNC will shed light on the understanding of the function of this structure and its relationship to the nucleolus and the transformed phenotype.

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


See Dr. Huang's publications on PubMed.


Contact Dr. Huang at 312-503-4269 or the lab at 312-503-4276.

Lab Staff

Temporary Staff

Chen Wang

Visiting Scholar

Nobuhide Ueki

 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.


See Dr. Ji's publications on PubMed.


Contact Dr. Ji at 312-503-2187.

Lab Staff

Postdoctoral Fellows

Qianru Li, Haiwang Yang

Graduate Students

Emily Stroup, Sheng Wang

 Shana Kelley Lab
New Technologies for Disease Biology

Research Description

The Kelley lab utilizes an interdisciplinary approach that integrates nanoscience, bioanalytical science and engineering, focusing on high-throughput single-cell profiling and the application of new technology platforms of the characterization of pathways relevant to cancer progression and treatment.


 Dong-Hyun Kim Lab

Therapeutic Micro/Nanoparticles and their hybrid derivatives for treatment of various types of cancer.

Research Description

Image-guided medicine is rapidly growing to improve treatment regimens as advancing medical imaging, including magnetic resonance imaging (MRI), computed tomography (CT), radiography, ultrasound, positron emission tomography (PET), and single photon emission computed tomography (SPECT). A combination of modern nanoplatforms with high performance in imaging and therapeutics may be critical to improve medical outcomes. One of emerging fields is the image guided therapy using various nanoparticles. Those are including basic bench, preclinical in vitro/in vivo and clinical researches combining synthesis of multifunctional nanoparticle and tracking/navigation tools to improve accuracy and outcomes of the therapeutics. Most of the emerging interventional technique such as heat activated targeted drug delivery, image guided ablation (microwave or HIFU), percutaneous injection gene/bacteria therapy, transcatheter treatments for tumor specific local therapy, serial biopsy, thrombolytic therapy, and so on, can be combined with nanotechnology in clinic. Careful design/selection/synthesis of multifunctional imaging/therapeutic nanomaterials with therapeutic agents will be critical for the translational optimization these new image guided medicine techniques. The DHKIM Lab for Biomaterials​ of Image Guided NanoMedicine has focused on developing various therapeutic/imaging carriers for the treatment of various cancers. Micro/Nanoparticles and their hybrid derivatives have been exploited as vectors for drug/therapeutic delivery and molecular imaging agents of MRI, CT, ultrasound and luminescent/fluorescents. We are working closely with clinicians, medical scientists, biologist and imaging professionals to translate new therapeutic approaches using multifunctional carriers and diagnostic imaging technique to the clinical setting.

For more information, please see Dr. Kim's faculty profile or visit the Kim Lab Website


See Dr. Kim's publications in PubMed.


Email Dr. Kim

Lab Manager: Xiaoke Huang

Phone Kim lab 312-926-3279

 Julie Kim Lab

The role of progesterone receptor in uterine diseases

Research Description

Progesterone is essential for the regulation of normal female reproductive function.  Its mode of action is diverse and dependent on the target tissues.  In my lab we are interested in delineating the molecular mechanisms of progesterone action through its receptor, PR in the uterus.  This is done in the context of normal endometrial differentiation, specifically, decidualization, as well as in uterine pathologies, such as endometriosis, endometrial cancer and uterine fibroids.  Interestingly, in these three diseases, progesterone responsiveness is aberrant.

Endometrial cancer is the most common gynecologic cancer diagnosed in the United States with an estimated 40,100 new cases and about 7,500 deaths in 2008.  As risk factors for endometrial cancer increase, the incidence of this disease will also rise, with a paradigm shift to younger ages. In our laboratory, we investigate the role of progesterone receptor in endometrial cancer to understand why progestin therapy is not an effective treatment in all cases of endometrial cancer.

Endometriosis is an estrogen-dependent disorder affecting up to 10% of the female population and 30-50% of infertile women, with no cure and limited therapies. It is often associated with debilitating pelvic pain and infertility. This disease has also been referred to as a “progesterone resistant” disease since the ectopic and eutopic tissues do not respond to progesterone as it does in normal endometrial tissues. Our laboratory is investigating progesterone resistance in endometriosis and identifying specific biological targets for the future development of alternative therapies.

Leiomyoma, also known as uterine fibroids, are benign tumors originating from the myometrium. These tumors can range from a few millimeters to over 20 cm in size. Leiomyomas are common and can occur in up to 77% of women while up to 20% of women suffer from significant morbidity, pain and discomfort and excessive menstrual bleeding. Leiomyomas are the primary indication for over 200,000 hysterectomies in the United States. In our laboratory we are investigating how progesterone promotes growth of leiomyomas by focusing on the non-genomic signaling of progesterone on the PI3K/AKT pathway. These studies are translated to the identification of important signaling molecules that can be targeted using small molecule inhibitors.

For more information, please see Dr. Kim's faculty profile or the Kim Lab website.


See Dr. Kim's publications in PubMed.


Contact Dr. Kim at 312-503-5377 or the Kim Lab at 312-503-4762.

 Shannon Lauberth Lab

Decoding the Cancer Epigenome

Research Description

The Lauberth Lab is located in the department of Biochemistry and Molecular Genetics at Northwestern University Feinberg School of Medicine and is located in the Simpson Querrey Biomedical Research Center on Northwestern’s campus in downtown Chicago.

Our primary research focus is to make advances in basic and translational studies in the cancer epigenetics field. The laboratory utilizes a combination of approaches that include cutting-edge high-throughput NGS technologies, state of the art microscopy techniques, quantitative proteomics, biochemistry, and cell-based/genetic assays. We also employ powerful cell-free assays that fully reconstitute transcription on chromatin templates and are powerful in discerning direct (causal) effects of epigenetic and transcriptional regulatory mechanisms.

Current Projects

The general transcription machinery functions as signal transducers

Through an exciting collaboration with Nullin Divecha’s group (University of Southampton), we discovered a new role of the basal transcription TFIID complex component, TAF3 in transducing nuclear phosphoinositide signals into gene expression changes that are required to build muscle tissue. This work was published in Molecular Cell.

p53 mutant enhancer selection and regulation imparts transcriptional plasticity to cancer cells in response to chronic immune signaling

My lab has made important contributions in revealing mechanistic insights into how chronic immune signaling drives alterations in the cancer cell transcriptome. We have demonstrated a functional crosstalk between the second most frequently identified p53 mutant and the master proinflammatory regulator NFkB that shapes an active enhancer landscape to reprogram the cancer cell transcriptome in response to chronic TNFa signaling. These studies also revealed insights into mutant p53-dependent gene regulation by describing new ways in which mutant p53 is recruited to specific classes of enhancers through various binding partners since mutant p53 does not directly engage with DNA. This new mechanism underlying the tumor-promoting roles of mutant p53 was published in Nature Communications.

Mutant p53 Co-Opts Chromatin Pathways at Enhancers to Drive Cancer Cell Growth

Our studies have advanced our understanding of cancer epigenetics by establishing an interplay between p53 mutants and chromatin regulators that leads to aberrant enhancer and gene activation in human cancer. Specifically, through global analyses, we demonstrated a requirement for mutant p53 in regulating the prominent histone mark, monomethylation of histone H3 lysine 4 (H3K4me1) that demarcates enhancer regions. This is an important finding that provides new mechanistic insights into how H3K4me1 levels are altered, which is a frequent event in various human cancers. Also, by implementing cell-based and our unique cell-free assays, we revealed mechanistic insights into the cooperativity between epigenetic regulators, MLL4 and the histone acetyltransferase p300 in promoting joint epigenetic aberrations that support enhanced transcriptional activation by mutant p53. These important findings were published in the Journal of Biological Chemistry.

eRNAs regulate the expression of tumor promoting genes

Our recent research efforts have resulted in new insights into the functions of eRNAs, which is particularly significant since these findings are among the few studies to date that have identified roles for these noncoding transcripts. Through global profiling analyses, we identified eRNAs that are synthesized by various p53 mutants, and by depleting several of these eRNAs, we identified their direct roles in the regulation of tumor promoting gene expression. We also revealed that these eRNAs function through the chromatin recognition bromodomains (BDs) of the extra-terminal motif (BET) family member BRD4. We further characterized a mechanism in which eRNAs are required to increase BRD4 binding to acetylated histones and promote enhanced BRD4 and RNAPII recruitment at specific enhancers that, in turn augments enhancer and tumor promoting gene activation. We also extended the implications of our findings by revealing that the BDs of all BET family members and several non-BET family members also directly interact with eRNAs. These findings provide a previously unrecognized convergence between eRNAs and histone posttranslational modifications in regulating the binding of chromatin reader proteins and highlight a mechanism in which eRNAs play a direct role in gene regulation by modulating chromatin interactions and transcription functions of BRD4. A manuscript describing these findings has been published in Nature Structural & Molecular Biology (NSMB).

We have also published several reviews on enhancer regulation and function and the mechanisms underlying eRNA functions that you can find by viewing our publications.

For more information, please see Dr. Lauberth's faculty profile and laboratory website.

Select Publications

Ohguchi H, Park PMC, Wang T, Gryder BE, Ogiya D, Kurata K, Zhang X, Li D, Pei C, Masuda T, Johansson C, Wimalasena VK, Kim Y, Hino S, Usuki S, Kawano Y, Samur MK, Tai YT, Munshi NC, Matsuoka M, Ohtsuki S, Nakao M, Minami T, Lauberth S, Khan J, Oppermann U, Durbin AD, Anderson KC, Hideshima T, Qi J. Lysine Demethylase 5A is Required for MYC Driven Transcription in Multiple Myeloma. Blood Cancer Discov. 2021 Jul;2(4):370-387. doi: 10.1158/2643-3230.BCD-20-0108. Epub 2021 Apr 10. PMID: 34258103; PMCID: PMC8265280.

Sartorelli, V., Lauberth, S.M. Enhancer RNAs are an important regulatory layer of the epigenome. Nat Struct Mol Biol 27, 521–528 (2020).

Rahnamoun H, Orozco P, Lauberth SM. The role of enhancer RNAs in epigenetic regulation of gene expression. Transcription. 2020 Feb;11(1):19-25. doi: 10.1080/21541264.2019.1698934. Epub 2019 Dec 11. PMID: 31823686; PMCID: PMC7053929.

Rahnamoun, H., Lee, J., Sun, Z. et al. RNAs interact with BRD4 to promote enhanced chromatin engagement and transcription activation. Nat Struct Mol Biol 25, 687–697 (2018).

Rahnamoun H, Hong J, Sun Z, Lee J, Lu H, Lauberth SM. Mutant p53 regulates enhancer-associated H3K4 monomethylation through interactions with the methyltransferase MLL4. J Biol Chem. 2018 Aug 24;293(34):13234-13246. doi: 10.1074/jbc.RA118.003387. Epub 2018 Jun 28. PMID: 29954944; PMCID: PMC6109924.

Rahnamoun, H., Lu, H., Duttke, S.H. et al. Mutant p53 shapes the enhancer landscape of cancer cells in response to chronic immune signaling. Nat Commun 8, 754 (2017).

Stijf-Bultsma Y, Sommer L, Tauber M, Baalbaki M, Giardoglou P, Jones DR, Gelato KA, van Pelt J, Shah Z, Rahnamoun H, Toma C, Anderson KE, Hawkins P, Lauberth SM, Haramis AP, Hart D, Fischle W, Divecha N. The basal transcription complex component TAF3 transduces changes in nuclear phosphoinositides into transcriptional output. Mol Cell. 2015 May 7;58(3):453-67. doi: 10.1016/j.molcel.2015.03.009. Epub 2015 Apr 9. PMID: 25866244; PMCID: PMC4429956.

Lauberth SM, Nakayama T, Wu X, Ferris AL, Tang Z, Hughes SH, Roeder RG. H3K4me3 interactions with TAF3 regulate preinitiation complex assembly and selective gene activation. Cell. 2013 Feb 28;152(5):1021-36. doi: 10.1016/j.cell.2013.01.052. PMID: 23452851; PMCID: PMC3588593.

Lauberth SM, Bilyeu AC, Firulli BA, Kroll KL, Rauchman M. A phosphomimetic mutation in the Sall1 repression motif disrupts recruitment of the nucleosome remodeling and deacetylase complex and repression of Gbx2. J Biol Chem. 2007 Nov 30;282(48):34858-68. doi: 10.1074/jbc.M703702200. Epub 2007 Sep 25. PMID: 17895244.

Lauberth SM, Rauchman M. A conserved 12-amino acid motif in Sall1 recruits the nucleosome remodeling and deacetylase corepressor complex. J Biol Chem. 2006 Aug 18;281(33):23922-31. doi: 10.1074/jbc.M513461200. Epub 2006 May 17. PMID: 16707490.

View all of Dr. Lauberth's publications on PubMed.


Contact Dr. Lauberth at 312-503-4780.

Lab Contact Information

Northwestern University Feinberg School of Medicine
Simpson Querrey 7-400B
303 E. Superior Street
Chicago, IL 60611

Lab Staff

Gabriel Lopez
Research Technologist

Jessica Xu
Graduate Researcher

Anita Wang
Lab Coordinator

Nicholas Chin
Temporary Staff

Dylan Jann Pedersen
Temporary Staff

 Isabelle Caroline Le Poole Lab

Immune recognition of melanoma-associated antigens, aiming to develop immunotherapeutics for benign and malignant disease.

Research Description

Role for HSP70i in driving autoimmune responses. This stress protein is included as a component of some anti-tumor vaccines based on its chaperone and adjuvant functions. In human samples, we found that HSP70i is upregulated in vitiligo skin, that HSP70i can associate with melanosomes under stress and that the heat shock protein is increasingly secreted by vitiligo melanocytes.

Development of an immunotherapeutic vaccine for patients with lymphangioleiomyomatosis (LAM). This devastating disease involves development of slow growing tumors in the lungs of female patients with mutations in TSC1 or TSC2. As tumor cells of smooth muscle cell origin transdifferentiate to express melanoma associated antigens, we propose to target melanosomal antigens using T cell receptor transgenic, autologous T cells.

Development of a chemopreventive approach towards melanoma.  The concept carries similarity to ‘elective surgery’ available for some other cancers. This strategy is further supported by the immune response that is indirectly elicited by dying melanocytes targeted by topically applied bleaching phenols. We have contributed to elucidating the mechanism by which phenolic agents can induce melanocyte death, expanded the arsenal of reagents to include those which specifically target the stem cell population and studied the immune response that follows.

Restoring tolerance in newly developed mouse models of autoimmune vitiligo.  Contrary to the existing problem of overzealous regulatory responses that interfere with anti-tumor immunity, patients with autoimmune disease activity generally lack effective regulatory responses. So whereas anti-CD25 therapy to deplete Tregs is popular as a pretreatment for patients undergoing anti-tumor immunotherapy, the opposite holds true in autoimmune disease. We propose to manipulate Treg homing in particular, and recently demonstrated elevated CCR4 expression in circulating Treg from melanoma patients whereas its ligand is highly expressed in tumors; the opposite holds true in vitiligo.

For more information, see the faculty profile for Dr. Le Poole, PhD.

Email Dr. Le Poole.

 Xiao-Nan Li Lab

Understanding tumor biology and implementing preclinical drug testing of malignant brain tumors

Research Description

Our research work focuses on molecular neuro-oncology and experimental therapeutics of malignant brain tumors.  Our goal is to develop more effective and less toxic therapies for children with malignant brain tumors to significantly improve the clinical outcomes.  1) Clinically relevant and molecularly accurate animal models: We have optimized a protocol for to implant a patient’s tumor cells directly into the matched location in mouse brains.  Our laboratory has developed >130 patient derived orthotopic xenograft (PDOX or orthotopic PDX) models of pediatric brain tumors, including high-grade glioma/glioblastoma (GBM), medulloblastoma (MB), ependymoma (EPN), diffuse intrinsic pontine glioma (DIPG), atypical teratoid/rhabdoid tumor (ATRT), Embryonal tumors with multilayered rosettes (ETMR), CNS germinoma, and pleomorphic xanthoastrocytoma (PXA), as well as ~20 models of adult GBM and meningioma. 2) All the models are subjected to detailed histopathological and comprehensive molecular characterizations through global gene expression (RNAseq, single cell RNAseq), whole genome sequencing, DNA copy number analysis, whole genome DNA methylation analysis during serial in vivo subtransplantations to confirm thee cellular and molecular fidelities of the patient-specific PDOX models.  3) Recognizing the need of in vitro model system, we are also utilizing our PDOX model system to develop long term cultures/cell lines as monolayer, 3D neurospheres and organoids. 4) Using this unique in vitro and in vivo model system, we are actively engaged in the understanding of tumor biology and the testing of new therapeutic strategies.

Current Projects

  • Understanding the mechanisms of brain tumor invasion of pediatric GBM
  • Discovery of cellular and molecular drivers of medulloblastoma metastasis
  • Investigating the regulation of cell cycle progression, particularly from quiescent G0 to active G1 phase
  • Implementing unbiased high-throughput combinatory drug screening against highly malignant brain tumors using a novel drug library composed of 17,000 drugs and investigational agents
  • Identifying cellular origins and molecular drivers of therapy resistance and tumor relapse
  • Evaluating therapeutic efficacy and elucidation of mechanisms of action of novel anti-cancer therapies in vivo in PDOX models for the initiation of clinical trials.

For more information, visit the faculty profile of Xiao-Nan Li, MD, PhD.


See Dr. Li's publications.


Email Dr. Li

 Huiping Liu Lab

Understanding and targeting cancer stem cells and exosomes in metastasis using cutting-edge technology and novel therapeutics

Liu Lab photo

Research Description

The Liu lab studies the molecular and cellular mechanisms underlying cancer stem cells (CSCs) and metastasis through four ongoing interactive basic and translational research projects: (1) to understand CSCs, circulating tumor cells (CTCs) and their interactions with immune cells in metastasis; (2) to dissect the role of secreted and circulating exosomes in CSC functions; (3) to target CSCs with novel therapeutics, exosomes and nanoparticles in combination with immunotherapy; (4) to develop CTC and circulating exosome-based biomarkers for cancer diagnosis, therapy response and predictive prognosis.

Recent Findings

  1. CSCs seed metastases of breast cancer.
  2. A rapid, automated surface protein profiling of single circulating exosomes in human blood. (PMID: 27819324)
  3. Micro-206 inhibits stemness and metastasis of breast cancer by targeting MKL1/IL11 pathway. (PMID: 27435395)
  4. Differentiation and loss of malignant character of spontaneous pulmonary metastases in patient-derived breast cancer models. (PMID: 25339353)
  5. MicroRNA-30c inhibits human breast tumor chemotherapy resistance by regulating TWF1 and IL-11.(PMID: 23340433)

Current Projects

  1. Identify how CSCs crosstalk between themselves and interplay with immune cells in circulation thus developing innovative anti-CSC targeting therapeutics.
  2. Single cell RNA sequencing of CSCs and metastatic tumors.
  3. Dissect the role of exosomes in CSC functions and regulation of exosome functions by CSCs.
  4. Develop CSC-targeting novel microRNA therapeutics and exosome delivery tools.
  5. Discover CTC and circulating exosome-based clinical biomarkers for cancer diagnosis, treatment monitoring and prognosis.

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


See Dr. Liu's publications on PubMed.


Contact Dr. Liu at 312-503-5248.

Lab Staff

Research Faculty

Yuzhi Jia

Postdoctoral Fellows

Nurmaa Dashzeveg, Lamiaa El-Shennawy, Andrew Hoffmann

Graduate Students

Hannah Mubarak, Emma Schuster, Erika K. Ramos, David Scholten

Visiting Scholars

Valery Adorno-Cruz

 Yan Liu Lab

Hematopoietic stem cell self-renewal and pathogenesis of myeloid malignancies

Research Description

The Liu laboratory is interested in investigating the molecular mechanisms governing normal and malignant hematopoiesis, with an emphasis on understanding hematopoietic stem cell (HSC) self-renewal and pathogenesis of myeloid malignancies, including myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Our long-term goals are to identify novel regulators of HSC self-renewal, understand the molecular mechanisms regulating their function, and develop novel therapeutic strategies to eliminate leukemia stem cells (LSCs) and improve leukemia treatment. We utilize molecular, genetic, immunological, biochemical, and pharmacological approaches as well as unbiased genome wide studies, including RNA-seq, ChIP-seq, ATAC-seq, and cytokine arrays, to investigate the molecular basis of HSC self-renewal and leukemogenesis. Major areas of focus include: 1) The role of tumor suppressor p53 in CHIP progression and pathogenesis of MDS; 2) Phosphatase PRL2 in HSC self-renewal and leukemogenesis; 3) Polycomb Repressive Complex 1 (PRC1) in HSC self-renewal and terminal differentiation.

For more information, visit Dr. Liu's faculty profile page.


View Dr. Liu's publications at PubMed.


Email Dr. Liu



 Daniela Matei Lab

Mechanisms of ovarian cancer metastasis and novel therapeutics for ovarian cancer

Research Description

My laboratory studies mechanisms of ovarian cancer metastasis and novel therapeutics for ovarian cancer. The general theme is translation between bench and clinic; with laboratory research forming the foundation for clinical experiments. 

One direction of investigation relates to the interaction between cancer cells and the peritoneal stroma.  We described the functions of tissue transglutaminase as an interacting partner of b-integrins and regulator of peritoneal metastasis.  Based on new mechanistic insight into the roles of this enzyme in ovarian cancer, we discovered and began characterizing new small molecule inhibitors for the transglutaminase-fibronectin-integrin interaction that are being developed as anti-cancer agents. We are studying these new inhibitors in-vitro and in in-vivo models of ovarian cancer metastasis.

Another area of research focusses on the characteristics and therapeutic vulnerabilities of ovarian cancer stem cells.  We used small molecule inhibitors that target ALDH1A1 to block the tumorigenic capacity of these cancer-initiating cells.  We are studying how ALDH1A1 inhibitors alter stem cell specific signaling and how ALDH1A1 is involved in maintaining the cancer stem cell properties. 

More recently we identified new metabolic alterations involving fatty acids desaturation in cancer stem cells.  We have targeted lipid metabolism using small molecule inhibitors and are studying the mechanisms by which these metabolic changes contribute to the maintenance and tumorigenicity of cancer stem cells.  Future goals are to refine the use of ALDH and fatty acid desaturases inhibitors to target cancer stem cells residual after chemotherapy and to eradicate the disease.

Another important direction of investigation is epigenetic modulation as a method of resensitization to platinum in ovarian cancer.  We successfully brought to the clinic the concept that epigenetic modulation re-sensitizes chemotherapy-resistant ovarian tumors to carboplatin.  I led a randomized multi-institutional clinical trial testing the effects of DNA hypomethylating agents and carboplatin compared to standard chemotherapy.  We are now analyzing the genome and epigenome of platinum resistant ovarian cancer using specimens from this trial.  We have identified several pathways that are associated with platinum resistance and respond to hypomethylating agents.  We have designed a new strategy to target pathway-specific DNA methylation and are testing the effects of this intervention on cell signaling and gene expression profiles in ovarian cancer cells.  


View Dr. Matei's publications on PubMed


Email Dr. Matei

Phone 312 503-4853

 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

Meghani K, Cooley LF, Choy B, Kocherginsky M, Swaminathan S, Munir SS, Svatek RS, Kuzel T, Meeks JJ. First-in-human Intravesical Delivery of Pembrolizumab Identifies Immune Activation in Bladder Cancer Unresponsive to Bacillus Calmette-Guérin. Eur Urol. 2022 Aug 22:S0302-2838(22)02553-2. 

Cooley LF, Glaser AP, Meeks JJ. Mutation signatures to Pan-Cancer Atlas: Investigation of the genomic landscape of muscle-invasive bladder cancer. Urol Oncol. 2022 Jul;40(7):279-286.

Folgosa Cooley L, Weiner AB, Meng X, Woldu SL, Meeks JJ, Lotan Y. Survival by T Stage for Patients with Localized Bladder Cancer: Implications for Future Screening Trials. Bladder Cancer. 2021 Jan; 7(1): 23-31.

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. 

For more information visit Meeks Lab

 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.


View Dr. Mendillo's publications at PubMed


Email Dr. Mendillo

Phone 312-503-5685

 Hidayatullah G. Munshi Lab

The Munshi lab is interested in the role of fibro-inflammatory stromal reaction in pancreatic cancer progression.

The Munshi Lab is focused on understanding the role of the key collagenase MT1-MMP (MMP-14) and members of the Snail family transcription factors in pancreatic cancer progression using transgenic mouse models. We are also interested in understanding how the pronounced fibrotic reaction induces epigenetic changes to contribute to chemotherapy resistance. We have shown that the collagen microenvironment induces histone acetylation and that targeting 'readers' of histone acetylation marks using BET inhibitors can limit growth of pancreatic cancer cells. We plan to evaluate the efficacy of BET inhibitors in our mouse models with the eventual goal of testing this class of inhibitors in patients with pancreatic cancer.


View lab publications via PubMed.

For more information, visit the faculty profile page of Hidayatullah G Munshi, MD.

Contact Us

Contact Dr. Munshi at 312-695-6180 or the Munshi Lab at 312-503-0312.

Lab Staff

Christina Chow
Post Doctoral Fellow

Holly Hattaway
Research Technician

Krishan Kumar
Senior Research Associate

 Marcus Peter Lab

The lab of Dr. Marcus E. Peter studies various forms of cell death including apoptosis, which is a fundamental process to regulate homeostasis of all tissues and to eliminate unwanted cells specifically in the immune system.

Another interest lies in the study of RNA interference and based on toxic RNAs to development a novel form of cancer treatment. 


View lab publications via PubMed.

For more information, visit the faculty profile page of Marcus Peter, PhD or the laboratory's website.

Contact Us

Contact Dr. Peter at 312-503-1291 or the Peter Lab at 312-503-2883.

Lab Staff

Quan Gao
Postdoctoral Fellow

Monal Patel
Postdoctoral Fellow

Qadir Syed
Postdoctoral Fellow

Ashley Haluck-Kangas
Graduate Student

Will Putzbach
Graduate Student

Bryan Bridgeman
Research Technician

Calvin Law
Research Technician

Andrea Murmann
Research Assistant Professor 

 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.


View Dr. Shilatifard's publications on PubMed.


Email Dr. Shilatifard

Phone 312-503-5223

 Vipul Shukla Lab

Deciphering alternative DNA codes in normal and cancer genomes

Research Description

Our lab applies state-of-the-art genetics, genomics, molecular biology and cell biology techniques to decipher the functions of cytosine modifications and structural conformations as alternative DNA codes in the genome. Decades of research have established how specific DNA sequences control genomic states associated with transcription, chromatin modifications and topological compartmentalization. However, besides helical, linear sequences, the DNA in the genome commonly adopts unusual, non-helical structural conformations and we want to understand the significance of these alternative structural conformations in normal cellular physiology and associated pathologies. As first-steps towards understanding the functions of alternative DNA structures, our lab is studying their abundance in normal and cancer genomes, epigenetic mechanisms regulating their localization and dynamics, and cellular pathways controlled by these structures. These studies have broad implications on many established paradigms in genome biology and will address fundamental questions related to origins of several different cancers with the ultimate goal of identifying vulnerabilities that could be therapeutically targeted.

Our lab also holds strong interest in understanding basic molecular mechanisms regulating immune responses. We are particularly interested in understanding how changes in the metabolic outputs, that are associated with distinct stages of B (and T) cell differentiation impacts their epigenetic landscapes. We aim to uncover these mechanisms with the ultimate objective to design approaches by which we could engineer the desired epigenetic states in immune cells to enhance the fidelity of immune responses.

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


View Dr. Shukla's publications on PubMed.


Email Dr. Shukla


 Alexander Stegh Lab

Dr. Stegh’s lab aims to define and target 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.


Email Alexander Stegh, MD, PhD 

Phone: 312-503-2879

Twitter: @ahstegh

 Lu Wang Lab

Investigating mutations in epigenetic factors that contribute to human cancer development

Research Description

Human Cancer Development: Understanding the Important Functions of Epigenetic Factor Mutations

Mutations and/or translocations within genes that encode for epigenetic factors, such as histone protein lysine methyltransferases (KMTs), lysine demethylases (KDMs), and DNA methyltransferases (DNMTs) are all common mechanisms involved in driving tumorigenesis (Cancer Cell. 2019, Feb 11; 35(2):168-176). We utilize state-of-the-art technologies that are designed to conduct epigenetic-related experiments, which allow us to directly uncover the underlying mechanisms of how mutations in epigenetic factors contribute to human cancer development (Nat Med. 2018, Jun; 24(6):758-769).

Novel Cancer Treatment Options: Targeting Dys-Regulated Epigenetic Factors

Misregulation of histone/DNA modifiers have emerged as a common therapeutic target option for treatments of different human diseases, including cancer. (Genes Dev. 2017, Oct 15; 31(20):2056-2066), Cancer Cell. 2014, Jan 13; 25(1):21-36, Sci Adv. 2015 Oct 9; 1(9):e1500463). Currently, several protein methyltransferases and demethylases have been identified, but their physiological significance has just begun to be elucidated. Our goal is to understand the relationship between dys-regulated epigenetic factors and cancer development through the use of these advanced technologies, such as CRISPR screening and experiments involving small inhibitor molecules. As a result, this could lead us to generate potential cancer treatment options by identifying the druggability of selected epigenetic factors, in order to develop a novel and more precise use of a drug that can be translational to clinical applications.

For lab information and more, see Dr. Wang’s faculty profile and lab website.


See Dr. Wang’s publications.


Contact Dr. Wang.

Lab Staff

Technical Staff

Aileen Szczepanski

 Gayle Woloschak Lab

Studying radiation-induced mutations in radiation-induced cancers; DNA-TiO2 nanoparticles; Radiosensitivity/motor neuron disease.

Research Description

Gayle E Woloschak, PhD
Gayle E Woloschak, PhD

The Woloschak Lab members focus their research on three main areas.

The Janus Project: Studying radiation-induced mutations in radiation-induced cancers

This 30 year, $200 million set of experiments were performed at 150 laboratories and then terminated before the data were completely analyzed. Funded by the Department of Energy and National Aeronautic and Space Administration, department radiobiologists will continue the data analyses.

Members of the Woloschak laboratory have assumed responsibility from Argonne National Laboratory for archiving tissue associated with 30,000 mice and 4,000 dogs that received various doses and dose-rates of radiation.

These studies examined the effects of dose-rate on radiation-induced toxicities and radiation-induced cancer. They are analyzing cancer cells from these tissues to find differences in mutational spectra that occur in tumors induced in radiation-exposed animals compared to those that occur in spontaneous tumors. Recent scientific concerns about very low dose exposures makes this effort particularly important.


  • University of Chicago
  • Bundewehr Radiobiology Institute in Munich
  • Argonne National Lab

DNA-TiO2 nanoparticles

The researchers have combined the functional properties of the biomolecule DNA and the inorganic compound TiO2. The project is oriented to investigating the functional use of these nanocomposites for intracellular manipulation, imaging and gene silencing.

Radiosensitivity/motor neuron disease

The project's purpose is to better understand the molecular basis for the combined abnormalities from a molecular-cellular perspective. Chip-based mRNA studies, gene promoter analyses, immunohistochemistry and standard molecular approaches are being used.

Learn More

For lab information and more, see Dr. Woloschak's faculty profile and Woloschak Lab site.


See Dr. Woloschak's publications in PubMed.


Contact Dr. Woloschak at 312-503-4323 or via email.

Research Assistant Professor

Tatjana Paunesku, PhD/ email

Additional Resources

  • Feinberg School of Medicine. Annual Report: Excellence in Research: The Bionanoprobe Penetrates More Deeply. Chicago, Feinberg School of Medicine, 2013.

 Rendong Yang Lab

Integrating genomics, big data, and computing to drive innovations in human genetics, precision oncology, and cancer immunotherapy

Research Description

The Yang laboratory is interested in the integrative analysis of large-scale, multi-dimensional genomic data to understand the initiation and progression of diseases. The research projects involve in the development of highly accurate and sensitive computational methods for analyzing large-scale genomic data, especially in the area of detecting and analyzing genetic variations and somatic mutations using next generation sequencing data. Current work in the lab is to explore the functional consequences of somatic alterations in cancer patients, to identify driver alterations, and to understand the genetic mechanisms of cancer progression and drug resistance by integrating multi-dimensional data from large-scale cancer studies such as The Cancer Genome Atlas (TCGA). Example projects span from technique-driven research that aims developing algorithms for a wide range of applications to hypothesis-driven investigation of specific biological problems where the main goal is the discovery and advancement of biological knowledge.

For more information visit Dr. Yang's lab website:


Wang TY, Liu Q, Ren Y, Alam SK, Wang L, Zhu Z, Hoeppner LH, Dehm SM, Cao Q, Yang R. A pan-cancer transcriptome analysis of exitron splicing identifies novel cancer driver genes and neoepitopes. Molecular Cell. May 2021.

Ting-You Wang, Rendong Yang. ScanITD: Detecting internal tandem duplication with robust variant allele frequency estimation. GigaScience, Volume 9, Issue 8. August 2020. 

Yingming Li, Rendong Yang, Christine M. Henzler, Yeung Ho, Courtney Passow, Benjamin Auch, Suzanne Carreira, Daniel Nava Rodrigues, Claudia Bertan, Tae Hyun Hwang, David A. Quigley, Ha X. Dang, Colm Morrissey, Michael Fraser, Stephen R. Plymate, Christopher A. Maher, Felix Y. Feng, Johann S. de Bono, Scott M. Dehm; Diverse AR Gene Rearrangements Mediate Resistance to Androgen Receptor Inhibitors in Metastatic Prostate Cancer. Clin Cancer Res 15 April 2020. 

Ting-You Wang, Li Wang, Sk Kayum Alam, Luke H Hoeppner, Rendong Yang. ScanNeo: identifying indel-derived neoantigens using RNA-Seq data. Bioinformatics, Volume 35, Issue 20, 15 October 2019, Pages 4159–4161. 

See Dr. Yang's publications on PubMed.


Contact Dr. Yang.

 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.


 See Dr. Yue's publications on PubMed.


Contact Dr. Yue at 312-503-8248.

Lab Staff

Postdoctoral Fellows

Tingting Liu, Yu Luan, Baozhen Zhang

Lab Manager

Qiushi Jin

Graduate Students

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

Technical Staff

Lena Stasiak

 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.


Email Dr. Zhang

Phone 312-503-1040

 Youyang Zhao Lab

The Zhao Lab studies the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury as well as endothelial and smooth muscle cell interaction in the pathogenesis of pulmonary vascular diseases.

Research Description

Recovery of endothelial barrier integrity after vascular injury is vital for endothelial homeostasis and resolution of inflammation. Endothelial dysfunction plays a critical role in the initiation and progression of vascular diseases such as acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and atherosclerosis. A part of the research in the lab, employing genetically modified mouse models of human diseases, endothelial progenitor cells/stem cells, and translational research approach as well as nanomedicine, is to elucidate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury and determine how aging and epigenetics regulate these processes (J. Clin. Invest. 2006, 116: 2333; J. Exp. Med. 2010, 207:1675; Circulation 2016, 133: 2447).  We are also studying the role of endothelial cells in regulating macrophage functional polarization and resolving inflammatory lung injury. These studies will identify druggable targets leading to novel therapeutic strategies to activate the intrinsic endothelial regeneration program to restore endothelial barrier integrity and reverse edema formation for the prevention and treatment of ARDS in patients.

Pulmonary hypertension is a progressive disease with poor prognosis and high mortality. We are currently investigating the molecular basis underlying the pathogenesis.  We have recently identified the first mouse model of pulmonary arterial hypertension (PAH) with obliterative vascular remodeling including vascular occlusion and formation of plexiform-like lesions resembling the pathology of clinical PAH (Circulation 2016, 133: 2447). Our previous studies also show the critical role of oxidative/nitrative stress in the pathogenesis of PAH as seen in patients (PNAS 2002, 99:11375; J. Clin. Invest. 2009, 119: 2009). With these unique models and lung tissue and cells from idiopathic PAH patients, we will define the molecular and cellular mechanisms underlying severe vascular remodeling and provide novel therapeutic approaches for this devastating disease. 

The Zhao lab employs the state-of-the art technologies including genetic lineage tracing, genetic depletion, genetic reporter, and CRISPR-mediated in vivo genomic editing as well as patient samples to study the molecular mechanisms of acute lung injury/ARDS, and pulmonary hypertension and identify novel therapeutics for these devastating diseases. Current studies include 1) molecular mechanisms of endothelial regeneration and vascular repair following inflammatory lung injury induced by sepsis and pneumonia; 2) how aging and epigenetics regulate this process; 3) how endothelial cells regulate macrophage and neuptrophil function for resolution of inflammation and host defense; 4) stem/progenitor cells in acute lung injury and pulmonary hypertension and cell-based therapy; 5) mechanisms of obliterative pulmonary vascular remodeling; 6) molecular basis of right heart failure; 7) pathogenic role of oxidative/nitrative stress; 8) lung regeneration; 9) drug discovery; 10) nanomedicine.


View publications by Youyang Zhao in PubMed.

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


Email Dr. Zhao

Contact Dr. Zhao’s Lab at 773-755-6355

Lab Staff

Zhiyu Dai, PhD.
Research Assistant Professor

Xianming Zhang, PhD.
Research Assistant Professor

Narsa Machireddy, PhD.
Research Assistant Professor

Junjie Xing, PhD.
Research Scientist

Colin Evans, PhD.
Research Scientist

Varsha Suresh Kumar, PhD.
Research Scientist

Xiaojia Huang, PhD
Research Scientist

Hua Jin, PhD
Postdoctoral fellow

Yi Peng, PhD
Research Scientist

Mengqi Zhu, M.S.,
Graduate Student

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